Endurance in Sport (The Encyclopedia of Sports Medicine, Vol. 2)

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IOC MEDICAL COMMISSION SUB-COMMISSION O N PUBLICATIONS I N THE SPORT SCIENCES Howard G. Knuttgen PhD (Co-ordinator) Boston, Massachusetts, USA Francesco Conconi MD Ferrara, ltaly Harm Kuipers MD, PhD Maastricht, The Netherlands Per A.F.H. Renstrom MD, PhD Stockholm, Sweden Richard H. Strauss MD Los Angeles, California, USA






Blackwefl Science

0 i ~ z , ~ o International oo Olympic

Committee Published by Blackwell Science Ltd Editorial Offices: Osney Mead, Oxford 0x2 oEL 25 JohnStreet, London WCrN zBL 23 Ainslie Place, Edinburgh EH3 6AJ 350 Main Street, Malden MA02148 5018, USA 54 University Street,Carlton Victoria 3053, Australia 10, rue Casimir Delavigne 75006 Paris, France Other Editorial Offices: Blackwell Wissenschafts-Verlag GmbH Kurfiirstendamm 57 10707Berlin, Germany Blackwell Science KK MG Kodenmacho Building 7-10 Kodenmacho Nihombashi Chuo-ku, Tokyo 104, Japan First published 1992 Reprinted 1993,1995 Second edition zoo0 Set by Excel TypesettersCo., Hong Kong Printed and bound in Great Britain by MPG Books Ltd, Bodmin, Cornwall The Blackwell Science logo is a trade mark of Blackwell Science Ltd, registered at the United Kingdom Trade Marks Registry Part title illustration by Grahame Baker

The rights of the Authors to be identified as the Authors of this Work has been asserted in accordance with the Copyright, Designs and Patents Act 1988. All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by the UK Copyright, Designs and Patents Act 1988, without the prior permission of the copyright owner.

Acatalogue record for this title is available from the British Library ISBN 0-632-05348-8 Library of Congress Cataloging-in-publicationData Endurance insport/edited byR.J. Shephard & P.-0. Astrand. - 2nd ed. cm. (Volume I1 of the p. Encyclopaediaof sports medicine) "An IOC MedicalCommission publication, in collaboration with the International Federation of Sports Medicine." Includes bibliographical references and index. ISBN 0-632-05348-8 1. Endurance sports. 2 . Exercise Physiologicalaspects. 3. Physical fitness. I. Shephard, Roy J. 11. Astrand, Per-Olof. 111. IOC Medical Commission. Iv.International Federation of Sports Medicine. V. Series:Encyclopaediaof sports medicine; v. 2. RCizzo.E53E53 2000 613.7'14~21 99-38456 CIP


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7 Skeletal Muscle Blood Flow and Endurance Exercise: Limiting Factors and Dynamic Responses, 84

List of Contributors, ix Forewords, xiii


Preface to the First Edition, xiv Preface to the Second Edition, xvi






Part 211: Biological Bases of Endurance Performance and the Associated Functional Capacities Determinants of Endurance Performance, 21

Influence of Endurance Training and Detraining on Motoneurone and Sensory Neurone Morphology and Metabolism, 136 V.R.


& A.


Muscular Factors in Endurance, 158 H.J.




Endocrine Factors in Endurance, 184 M.S.




Body Size and Endurance Performance, 37 EISENMANN

& R.M.


Pulmonary System and Endurance Exercise, 52 T.J.



Part 2: Basic Scientific Considerations


A . P . AAKER,


9 Cellular Metabolism and Endurance, 118


Endurance Sports, 9




Semantic and Physiological Definitions, 3



8 Endurance Exercise and the Regulation of Visceral and Cutaneous Blood Flow, 103

Part I: Definitions R.J.




& J.A.


The Athlete's Heart, 68

13 The Importance of Carbohydrate, Fat and Protein for the Endurance Athlete, 197 T.E.


Part 2b: Psychological Aspects of Endurance Performance 14 Psychology in Endurance Performance, J.S.







25 Personality Structureof the Endurance Performer, 366

Part 2c: Genetic Determinants of Endurance Performance


15 GeneticDeterminantsof

Endurance Performance, 223 C . B O U C H A R D , B. WOLFARTH,

RIVERA, J. G A G N O N & J.-A.



Part 2d: Physical Limitations of Endurance Performance 16 BiomechanicalConstraintsand Economy of Movement in Endurance Performance, 245 K.R.


17 Endurance in Hot and Cold Environments, 259 G.W.

M A C K & E.R.


Part 3: Measurements in Endurance Sport 18 Factors to be Measured, 271 P.-o. ASTRAND 19 Sport-SpecificTesting in Laboratory and Field, 273 A. D A L M O N T E , M .


Assessment of Environmental Extremes and Competitive Strategies,287 K.B.



Maximal Oxygen Intake, 301 R.J.



26 Perception of Effort During Endurance Training and Performance, 374 B.J. NOBLE & J.M.


Part 4: Principles of Endurance Preparation 27 Influencesof Biological Age and Selection, 397 P.-o. ASTRAND 28 Endurance Conditioning, 402 J.


29 Food and Fluids Before, During and After Prolonged Exercise, 409 R.J. M A U G H A N

30 Haemoglobin, Blood Volume and Endurance, 423 N . G L E D H I L L & D . WARBURTON

31 Smoking, Alcohol, ErgogenicAids, Doping and the Endurance Performer, 438 M.H.


32 Psychological Preparation of Endurance Performers, 451 S.



Anaerobic Metabolism and Endurance Performance, 311 R.J.


33 Prevention of Injuries in Endurance Athletes, 458 P.A.F.H.



23 Metabolism in the Contracting Skeletal Muscle, 328 I. H E N R I K S S O N

24 Body Composition of the Endurance Performer, 346 5 . G O I N G & V. M U L L I N S

34 Monitoring for Overtraining in the Endurance Performer, 486 D.G. D.





Part 5: Specific Population Groups and Endurance Training 35 Endurance Training and Children, 507 T.W.



36 Endurance Training for Women, 517 M.L.



47 Cardiovascular Benefits of Endurance Exercise, 688 A.R.



37 Pregnant Women and Endurance Exercise, 531 L.A.

48 Cardiovascular Risks of Endurance Sport, 708


R.J. S H E P H A R D

38 The Elderly and Endurance Training, 547 M.L. J.F.





49 ReproductiveChanges and the Endurance Athlete, 718 A.B.

39 Endurance Training for Persons with Disabilities,5 65 K.H.




50 Endurance Exerciseand the Immune Response, 731 D.C.

Part 6: Environmental Aspects of Endurance Training 40 Hyperthermia, Hypothermia and Problems of Hydration, 591 T.D.




52 Overuse Syndromes, 766 MALLOCH

& J.E.


53 Countering Inflammation, 800 H . N O R T H O F F & A . BERG


42 Air Pollutants and Endurance Performance, 628 L.J.

51 Other Health Benefits of Physical Activity, 747



41 Problems of High Altitude, 614 R.I.


Part 8: Specific Issues in Individual and Team Sports


54 Energetics of Running, 813 43 Endurance Performersand Time-Zone Shifts, 639 T. REILLY,




55 Swimmingas an Endurance Sport, 824 L.


Part 7: Clinical Aspects of Endurance Training 44 Medical Surveillance of Endurance Sport, 653 R.J.


45 Considerations for Preparticipation CardiovascularScreening in Young CompetitiveAthletes, 667 B.].


46 Lung Fluid Movements in Endurance Sport, 682 N.H.


56 Rowing, 836 N.H.


57 Cross-CountrySki Racing, 844 U.


58 Cycling, 857 G. NEUMANN

59 TheTriathlon, 872 G.G.




60 Canoeing, 888 A. D A L M O N T E , P.



63 The Physiology of Human-Powered Flight, 942 E.R.

61 Endurance Aspects of Soccer and Other Field Games, 900 T. REILLY

S C H O E N E & T.F.


Index, 947 HORNBEIN


64 Endurance in Other Sports, 945 P.-0.

62 Mountaineering, 931 R.B.

N A D E L & S.R.

List of Contributors

AARON P. AAKER MS, DepartmentofMedical


Physiology, University of Missouri-Colombia, Colombia, MO, U S A

Exercise Science, University of South Carolina, Columbia, SC, U S A



Physiology 8 Pharmacology, Karolinska Institute, Stockholm,Sweden

Center, University of California, Los Angeles, CA, U S A

JOEY C. EISENMANN MA,Instituteforthe GREG AT KIN SON PhD, Reasearch Institute for Sport and Exercise Sciences, Liverpool John Moores' University, Liverpool, UK

Study of YouthSports, 213 IM Sports Circle, Michigan State University, East Lansing, MI, U S A

PIERRO FACCINI PhD,Instituteof Sports Science, LOIS BERG MD, Department ofPrmention, Rehabilitation and Sports Medicine, University of Freiburg, Freiburg, Germany

Italian National OlympicCommittee,Rome, ltaly

MARCEL LO FAINA PhD, Institute of Sports Science, ltalian National Olympic Committee,Rome, Italy

LF BERGH PhD, DefenceResearch Institute, S-17~90, Stockholm,Sweden

CLAUDE BOUCHARD PhD,Pennington Biomedical Reasearch Center, Louisiana State University, Baton Rouge, LA, U S A

STEVEN R. BUSSOLARI PhD,Departmentof Aeronautics and Astronautics, Massachusetts Institute of Technology,Cambridge, M A , U S A

LAWRENCE J . FOLINSBEE PhD,National Center for Environmental Assessment, US.Environmental Protection Agency,Research Triangle Park, NC, U S A

AARON R. FOLSOM MDMPH,Divisionof Epidemiology, School of Public Health, University of Minnesota, Minneapolis, M N , U S A

ARTUR FORSBERG DPE,Swedish Nationalcenter for Research in Sports, Stockholm,Sweden

J O A N F. CARROLL PhD,Departmentof Integrative Physiology, University of North Texas Health Science Center, Fort Worth,T X ,U S A

JENNIFER L. COPELAND MSc,Facultyof Kinesiology, University of New Brunswick, Fredericton, New Brunswick, Canada

JACQUES GAGNON PhD,PhysicalAclivity Sciences Laboratory, Division of Kinesiology, Faculty of Medicine, Universiti Lava/, Ste-Foy, Quebec, Canada

NORM A N G L E D HIL L PhD, Department of Kinesiology and Health Science, Bethune College, York University, Toronto, Ontario, Canada

JEROME A. DEMPSEY PhD,Departmentof Preventive Medicine, University of Wisconsinat Madison, 504N Walnut,Madison, Wl, U S A




SCOTT G O I N G PhD, DepartmentofPhysiology, University of Arizona, Tucson, AZ, USA

J AC K G 00DM A N PhD, Faculty of Physical Education &Health, University of Toronto, Toronto, Ontario, Canada

A N N E B. LOUCKS PhD,Department ofBiologica1 Sciences, Ohio University, Athens, OH, USA

DAVID T. LOWENTHAL MDPhD, Department of Medicine, Pharmacology, Exercise and Sport Sciences, University of Florida and Gregg VA Medical Center, Gainsville,FL, USA

TERRY E. G R A H A M PhD,HumanBiologyand Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada

JAMES E. GRAVES PhD, DepartmentofExercise

GARY W. MACK PhD,John B. Piercehboratory, and Department of Epidemiology and Public Health, Yale University School of Medicine, 290 Congress Avenue, New Haven, CT, USA

Science, Syracuse University, New York, USA

ROBERT M. MALINA PhD,lnstituteforthe HOWARD J. GREEN PhD,Departmentof Kinesiology, University of Waterloo, Waterloo, Ontario, Canada

Study of Youth Sports, 213 IM Sports Circle, Michigan State University, East Lansing, MI, USA

ANDREW J . MALLOCH MBChB,Sports LENNART GULLSTRAND PhD,Boson Institute of Sport, S-18147, Lidingo, Sweden

J A N HENRIKSSON MDPhD, Department of Physiology &Pharmacology,Karolinska Institute, Stockholm, Sweden

TOM F. HORNBEIN PhD,Departrnentof Medicine, University of Washington, HarborviewMedical Center, Seattle, WA, USA

AKI H I K O IS H I H A R A PhD, Laboratoy of Neurochemisty, Faculty of Integrated Human Studies, Kyoto University, Kyoto, Japan

Medicine Center, University of British Columbia, BC, Columbia

BARRY J. M A R O N MD,MinneapolisHeart Institute Foundation, 920 East 28th Street, Minneapolis, MN, USA

RON A L D J . M AUG H A N PhD, Department of Biomedical Sciences, University Medical School, Aberdeen, UK

G I OVANN I MI RRI PhD, Institute of Sports Science, Italian National Olympic Committee, Rome, Italy

A N T O N I 0 D AL MONTE PhD, Italian National J O H N M. J O H N S O N PhD,Departmentof Physiology, University of Texas Health Science Center, Sun Antonio, TX, USA

Olympic Committee, Institute of Sports Science, Via dei Campi Sportivi, Rome, Italy

ALAN R. MORTON EdDFACSM, Departmentof PEKKA KANNUS MDPhD,Tampere Research Station of Sports Medicine, Tampere, Finland

Human Movement 8 Exercise Science, The University of Western Australia, Nedlands, WA, Australia

DAVID KEAST PhD, Department ofMicrobiology,


The University of Western Australia, Queen Elizabeth 11 Medical Centre, Nedlands, WA, Australia

Nutn'tional Sciences, university of Arizona, Tucson, AZ, USA

M . H . LAUGHLIN PhD,Departmentof Veterinary Biomedical Sciences & Medical Physiology, and Dalton CardiovascularResearch Center, University of MissouriColombia, MO, USA

LARRY M. LEITH MAPhD,FacultyofPhysical Education &Health, University of Toronto, Toronto, Ontario, Canada

ETHAN R. NADEL PhD,IohnB.Pierce Laboratory and Departments of Cellular and Molecular Physiology, and Epidemiology and Public Health, Yale University School of Medicine, New Haven, CT, USA (Dr E.R. Nadel unfortunately passed away during production ofthis volume.)


GEORG N E U M A N N M D , DepartmentofSports Medicine, Institute for Applied Training Science, Leipzig, Germany

DAVID c . N I E M A N PhD, DepartrnentofHealth, Leisure and Exercise Science, Appalachian State University, Boone, NC, U S A

TIMOTHY D. NOAKES M D , Department of Exercise and Sports Science, University of Cape Town,and Sports Sciencelnstitute of South Africa, Newlands, South Africa

BRUCE J . NOBLE PhD, Purdue University, Madison, Wl, U S A


T H O M A S RE ILLY PhD DSc, Research Institute for Sporf G. Exercise Sciences, Liverpool Iohn Moores’ University, Liverpool, UK

PER A.F.H. RENSTROM MDPhD,Department of Orthopaedic Sports Medicine, Karolinska Hospital, Stockholm,Sweden

MIGUEL A. RIVERA PhD, Departmentsof Physiolog/ and Physical Medicine and Sports Medicine, University of Puerto Rico Medical School, San Iuan, Puerto Rico

DAVID G . ROWBOTTOM PhD,Schoolof Human Movement Studies, Queensland University of Technology,Kelvin Grove, QLD, Australia

J 0 H N M . N 0 B L E PhD, HPER Building, University of Nebraska at Omaha, Omaha, NE, U S A

H I N N A K NORTHOFF MD, Dcpartmentof Transfusion Medicine, University of Tiibingen,Abteilung Transfusionsmedizin, Tiibingen, Germany

T H O M A S W. R O W L A N D M D , Departmentof Pediatric Cardiology, Baystate Medical Center, Springfield, M A ,U S A

R O L A N D R. R O Y PhD,Brain ResearchInstitute, Universityof California, Los Angeles, C A , U S A

MARY L. O’TOOLE PhD, Departmentof Obstetrics and Gynaecology and Women’sHealth, Saint Louis University, St Louis, M O , U S A

JAMES W.E. RUSH PhD, Departmentofveterinary Biomedical Sciences and Dalton Cardiovascular Research Center, University of Missouri-Colombia, M O , U S A

KENT B. PANDOLF PhD, U.S.ArmyResearch lnstitute ofEnvironmenta1Medicine, Natick, M A , U S A

MARK A. PEREIRA PhD, Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis, M N , U S A

KENNETH H . PITETTI PhD, Departmentof Public Health Sciences, College of Health Professions, Witchita State University, Witchita,KS, U S A

MICHAEL L. POLLOCK PhD,Centerfor Exercise Science, College of Medicine, University of Florida, Gainsville, FL, U S A (Dr M.L. Pollock unfortunately passed away during the production of this volume.)

PIETRO E. DI PRAMPERO M D P h D , Department of Biomedical Sciences, University of Udine, Udine, ltaly

J O H N S . RAGLIN PhD,Departmenf of Kinesiology, Indiana University, Bloomington,IN, U S A

EDWARD S. SCHELEGLE PhD,Schoolof Veterinay Medicine, Department of Anatomy,Physiology nnd Cell Biology, Universityof California, C A , U S A

ROBERT B. S C H O E N E M D , Departmentof Medicine, University of Washingfon,Harborvim Medical Center, Seattle, WA,U S A

WILLIAM G . SCHRAGE MS,Departmentof Medical Physiology, Universityof Missouri-Colombia, Colombia,MO, U S A

NIELS H . SECHER MDPhD,Department of Anaesthesia, Rigshospitalet, Blegdamsveg 9, Copenhagen, Denmark

ROY J . S H E P H A R D MDPhDDPE,Professor Emerrtus of Applied Physiology, PO Box 521, Brackendale, British Colombia, Canada



JEAN-AIME SIMONEAU PhD, Physical Activity Sciences Laboratory, Division of Kinesiology, Faculty of Medicne, Universit6Laval Sfe-Foy,Quebec, Canada (Dr ].A.Simoneau unfortunately passed away during the production of this volume.)

T H O M A S J. WETTER MS, Deparfmentof Preventive Medicine, University of Wisconsinat Madison, Madison, Wl, U S A

MELVIN H. WILLIAMS PhD, Department of Exercise Science,Old Dominion University,Norfolk, VA, USA

G O R D O N G . SLEIVERT PhD,Human Peyformance Centre, School of Physical Education, University of Otago, Dunedin, New Zealand

KEITH R. WILLIAMS PhD, Departmentof Exercise Science, University of California at Davis, Davis, CA, USA

J A N SVEDENHAG MDPhD, Departmentof Clinical Physiology, St Goran's Hospital, Stockholm, Sweden

GREGORY S. WILSON PED, Departmentof Human Kinetics and Sports Medicine, University of Evansville, Evansville, IL, USA

JACK E. TAUNTON MDPhD,SportsMedicine Center, university of British Colombia, Vancouver,BC, Canada

B ERN W O L FA RTH PhD, Department of Rehabilitation and Preventive Sports Medicine, Freiburg University,Freiburg, Germany

MARK S. TREMBLAY PhD,Facultyof Kinesiology,Universityof New Brunswick, Fredericton, New Brunswick,Canada

LARRY A . WOLFE PhD, School ofPhysical6 Health Education, Department of Physiology, Queen's University,Kingston, Onfario,Canada

S U Z A N N E TUFFEY PhD, Sport Psychology Director, U S ASwimming,Colorado Springs, CO, U S A

D ARREN WAR B URTON MSc,Faculty of Physical Education and Recreation, University of Alberta, Edmonton, Alberta, Canada

CHRISTOPHER R. W O O D M A N r h D , Department of Veterinary Biomedical Sciences, and Dalton Cardiovascular Research Center, University ofMissouriColombia, Colombia,MO, U S A

ANDREW J . YOUNG PhD,Thermaland JIM WATE R H O USE Dl'hil, Research Institute for Sport and Exercie Sciences, Liverpool John Moores' University,Liverpool, UK

Mountain Medicine Division, US.Army Research lnstitute of Environmental Medicine, Natick, MA, USA


Nine years have passed since the publication of Volume II Endurance in Sport for the IOC Medical Commission Encyclopaedia of Sports Medicine Series. Reflecting the tremendous research activity that has taken place relative to the topic of endurance, Professors Shephard and Astrand have succeeded in collecting the input of 85 authors of international renown to produce a completely revised second edition of this publication. Endurance in Sport includes basic and applied scientific informationon cellular metabolism, genetics, physiological function, environment, laboratory testing, and conditioning programs as related to endurance performance. Special attention is given to children, women, the elderly, and the disabled. Special attention is also given to a variety of Olympic sports in separate chapters dealing with such activities as running, swimming, rowing, skiing, cycling, and team sports. This publication in its new and expanded edition will prove to be of great value as an authori-

tative reference to scientists, clinicians, and graduate students around the world for many years to come. Prince Alexandre de Merode Chairman IOC Medical Commission

This new edition will offer all those involved in the field of sport sciences updated information indispensable to an improved perception of sport in general, just as the first edition did nine years ago. This new volume will enhance the intrinsic value of the IOC Medical Commission’s collection of Sports Medicine Encyclopaedias. I hope it will be just as successful as the first edition. Juan Antonio Samaranch Marqub de Samaranch


Preface to the First Edition

Relatively brief physical activities such as a 1500-m race have sometimes been characterized as ’endurance sport’. However, in this book we have deliberately focussed our attention upon events where the competition itself and/or the required training lasts for 1 hour or longer. There were several reasons for thisdecision. Certainly, we were instructed to do this by the series editors, since they are currentlyplanning other volumes that will cover shorter periods of activity. However, we are not exactly famous for following arbitrary directives from editors, and our eventual compliance with the 1-hour criterion was assured by more persuasive arguments. Firstly, we both view international competition as the ultimate challenge to the various regulatory systems of the body, physiological, biochemical, biomechanical and psychological.If the body finds difficulty in regulating the constancy of the milieu inthieur over a 4-min mile, how much greater is the challenge to accommodate the metabolic, thermal and other demands of a marathon race run in the heat of summer, or the Vasa Loppet in the depths of winter, and how much more exciting it is to unravel details of the adaptive mechanisms that allow such feats to be accomplished! We recognize that there have been a number of previous monographs looking at various physiological aspects of prolonged exercise, but much of the work described in such texts has been conducted in the laboratory. There remains a dearth of scientific information on the stresses encountered and the adaptive responses demanded by actual participa-


tion in the various potential forms of prolonged athletic competition. The present volume was thus conceived to fill this void in a comprehensive fashion. In completing such a major undertaking, we have been fortunate to draw upon more than 60 of the world’s authorities in all areas of the sport sciences. The volume thus offers a broad international perspective upon the challenge of human participation in endurance events. The material is divided into seven sections: (I)a brief definition of fundamental terms and concepts, (2)a full review of basic scientific considerations that ranges over anatomy, biomechanics, physiology, biochemistry, nutrition, humoral and immune function, psychological factors, genetics and environmental constraints, (3) methods of measuring the various determinants of endurance performance in the field and in the laboratory, (4) optimal principles of preparation for various types of endurance competition, (5) endurance training in special population groups, (6) prevention of medical and surgicalproblems during endurance training and competition, with a discussion of the potential health benefits of such activities, and (7) an exploration of issues specific to individual types of endurance performance ranging from cross-country skiing to human-powered flight. The material is presented in a format that will be accessible to all with some background in the sport sciences. It is anticipated that the volume will appeal particularly to sport scientists and physicians involved in the preparation of endurance com-


petitors, but the broad picture of human regulatory mechanisms during extended exercise will also attract the interest of a much wider audience in physiology, biochemistry and psychology, and this volume will undoubtedly become required reading


for many graduate programmes in medicine and the science of sport. Roy J. Shephard, Toronto Per-Olof Astrand, Stockholm 1991

Preface to the Second Edition

The first edition of Endurance in Sport was designed to offer state-of-the-art information on current topics of clinical and scientific importance for endurance sport, provided by a panel of international experts in a form that would be appropriate for professional personnel working with athletes and sports teams. For our purpose, endurance sport was arbitrarily defined as an event where the competition itself or the associated training lasted for 1 hour or longer. We recognized that relatively brief physical activities such as a 1500-m race were sometimes characterized as 'endurance sport'. The 60-minute criterion was established in discussion with the IOC Publications Advisory Committee, who were planning other volumes covering competitions of shorter duration. Nevertheless, the editors of the present volume were also intrigued by the ultimate challenge that prolonged international competition presented to the body systems regulating physiological, biochemical, biomechanical and psychological variables. If the body found difficulty in regulating the constancy of the milieu intbieur over a 4-minute mile, how much greater was the challenge to accommodate the metabolic, thermal and other demands of a marathon race run in the heat of summer, or the Vasa Loppet in the depths of winter. We immediately recognized that a number of monographs and specialist symposia had looked at various physiological aspects of prolonged exercise, but we also noted that much of the work described had been conducted in the laboratory. There remained a dearth of authoritative scientific information on the stresses encountered and the adap-


tive responses demanded by actual participation in the various potential forms of prolonged athletic competition. The book Endurance in Sport was thus conceived to fill this void. The information was directed to individuals and groups representing a wide range of disciplines, particularly sports scientists, sports physicians, medical doctors in family practice, physical therapists and athletic trainers, and the growing number of graduate students in the sports sciences and other health-related professions. The first edition was generously received by critics, and achieved a very large world-wide distribution relative to its size and cost. However, almost 8 years have elapsed since the appearance of the first edition, and in order that potential readers might still have access to state-ofthe-art information, it was thought important to embark upon a second edition. This has followed the same general plan as the first edition, although the volume has necessarily undergone considerable expansion. Many new international experts have been recruited, and all of the remaining chapters have been thoroughly revised and updated. The volume thus offers a broad and current perspective on the challenges associated with human participation in endurance events. The material is now divided into eight main sections: (i) a brief description of fundamental terms and concepts; (ii) a full review of the basic scientific principles underlying the optimization of endurance performance, including anthropometry, biomechanics, physiology, biochemistry, nutrition, humoral and immune function, psychological factors, and genetic and environmental constraints;


(iii)methods of measuring the various determinants of endurance performancein the field and in the laboratory; (iv) principles of preparation for various types of endurance competition; (v) the response to endurance training in various special population groups; (vi) environmental aspects of endurance training; (vii)the prevention of medical and surgical problems during endurance training and competition, with a discussion of the potential health benefits of such activities; and (viii) an exploration of issues specific to various types of individual and team endurance performance, ranging from cross-country skiing, mountaineering and human-powered flight to soccer and other team games. The material is once again presented in a format


that will be accessible to all with some background in the sports sciences. Although the volume will continue to appeal particularly to sport scientists and physicians involved in the preparation of endurance competitors, the broad analysis of human regulatory mechanisms during prolonged exercise will attract the interest of a much wider audience in physiology, biochemistry and psychology. It will continue to be required reading for many graduate programmes in medicine and the science of sport. Roy J. Shephard, Toronto Per-Olof Wstrand, Stockholm 1999






Semantic and Physiological Definitions ROY J . SHEPHARD

Physical activity, exercise and physical fitness The distinction between such terms as physical activity, exercise and physical fitness has been sharpened through the contributions of Caspersen et al. (1985) and Bouchard and Shephard (1994). as discussed below.

Physical activity Physical activity may be considered as any form of body movement that makes a significant metabolic demand. Thus defined, it encompasses not only preparation for, and participation in, competitive sports, but also other aspects of an athlete's life, such as the pursuit of a strenuous physical occupation, the undertaking of household chores (including the care of children and ageing relatives, and in some countries the production of food), certain methods of transportation (walking, cycling, the operation of hand-propelled watercraft) and engaging in voluntary leisure activities that are unrelated to the individual's primary sport interests.

Exercise Physical exercise is usually considered as the voluntary component of a person's physical activity inventory, although in the case of professional athletes it may be a form of employment. It is occasionally spontaneous and playful, but more usually it is performed with a specific objective in view (such as preparation for competition, rehabilitation

following injury or the maintenance of personal fitness). Some forms of play and recreational exercise contribute to the primary performance of a major athlete, either by developing biological function (for example, the adoption of a landbased training programme when a rower cannot exercise on water, Wright ef al. 1976) or by offering relaxation and psychological dAente between competitive seasons. However, other physically active pursuits are disadvantageous to the performance of an athlete, encouraging an inappropriate development of physique, occupying time that should have been allocated to more specific forms of training and sometimes (through a process of 'negative transfer') degrading established psychomotor skills.

Physical fitness The concept of physical fitness has been discussed in detail elsewhere (Shephard 1977,1994). Its definition remains controversial, but in the context of high-performance sport, it implies an optimal combination of those physical, physiological, biochemical, biomechanical and psychological characteristics that contribute to competitive success. The physical fitness of an athlete is usually highly specific to a given class of competition, although in the pentathlon and decathlon the successful contestant requires a more broadly based type of fitness. Further, an optimal combination of biological characteristics does not guarantee success in any given event; for example, psychological hardiness has sometimes allowed a very successful competitive




performance by a person with a body form that is very unfavourable from a biomechanical or a physiological standpoint. Repeated bouts of vigorous physical activity normally enhance fitness. But this is not inevitably the case. An inappropriate type of conditioning can induce disadvantageous changes. For example, an overemphasis upon strength training can handicap a distance runner by causing an excessive increase in body mass. Moreover, if the intensity and/or duration of training are excessive, a combination of physiological and psychological reactions leads to a deterioration of fitness (the situation of ’staleness’or ’overtraining’), with microinjuries of muscle, suppression of immune function and an increased vulnerability to infections (Shephard 1997). Argument continues as to how far physical fitness is inherited, how far it is determined by a person’s family environment, and how far it can be acquired through an appropriate conditioning programme (Bouchard & Malina 1983; Bouchard & Perusse 1994). Plainly, body build makes a major contribution to success in many events; body fat content can increase with overeating and severe malnutrition can stunt growth, but in general the shape of the human body is an immutable inherited characteristic. With respect to physiological characteristics such as peak oxygen transport, an attempt can be

made to partition observed interindividual differences into components of variance attributable to constitution, a constitutional susceptibility to training, domestic environment (for example, a household where high-level competition is the expected norm) and a residual response to training that could have been elicited through adequate motivation of any growing child or young adult (Bouchard & Perusse 1994). A clarification of the relative contributions of genes and environment to competitive success is important for the coach, who must decide whether to allocate resources to talent scouting or to improvement of training methods (Fig. 1.1).Unfortunately, results obtained through comparisons between twins and other closely related family members have to date proved rather unstable. Some authors have inferred that physical fitness has a large genetic component, but others have found that constitution has only a minor influence on the determinants of endurance performance. It is possible that completion of the human genome project will resolve this issue. But given current uncertainty in the partition of variance for easily quantified biological data such as maximal oxygen intake, it is hardly surprising that little is known about the contribution of inheritance to other more subjective determinants of endurance fitness.

Fig. 1.1 Diagram illustrating the relative importance of athletic selection and rigorous training to the development of a competitor with a large maximal oxygen intake. Assumptions are made that: (i) the peak effect of training is a 20% increase in oxygen transport; and (ii) the constitutional variance in maximal oxygen intake is normally distributed, with a standard deviation of bml.[kgmin]-’. From Shephard (1978),with permission.


Force, work and power: the choice of units The terms force, work and power have a longstanding mechanical significance; they have been defined in a biological context by Ellis (197i), Knuttgen (1984) and Knuttgen & Komi (1992). Force

Early reports expressed peak muscle force in pounds weight or kilograms force. Force is more properly expressed in newtons (N), the SI unit of force (Ellis 1971;Table 1.1). For example, a mass of 1 kg exerts a force of 9.81N when in unit gravitational field. Gravitational acceleration (and thus the weight of an object) varies with changes in its latitude or altitude, reflecting corresponding differences in the object’s distance from the centre of the Earth. The effects (up to 3%) are large enough to have an appreciable influence on sport performance. Work

Work is the product of force and distance. If a force of I N is sustained over a distance of 1m, 1 newtonmetre, or 1 joule (J) of work is performed. OIder texts on nutrition express work and stored food energy


in calories; under standard conditions, I calorie is equal to 4.186J. The body must perform work whenever physical activity is undertaken. Stores of potential energy are modified, viscous work is performed against internal or external resistance, and the kinetic energy of the body and associated equipment is altered. Body stores of chemical energy are used to effect these changes, and reserves are later replenished through the consumption of food. Metabolic energy expenditure is still commonly expressed in kcal.min-I or kJ.min-’, although in the future these may be replaced by the SI unit (Watts). Likewise, the SI unit of heat accumulation or dissipation in unit time is the Watt. The athlete may increase the potential energy stores of the body and/or sports equipment by performing sustained work against gravity, for example when propelling a bicycle up a steep hill. The accumulated potential energy may be calculated as the product of the vertical ascent (in metres) and the mass of the rider plus machine (in newtons). The potential energy of individual body segments may also change in the course of a bout of physical activity, for example when an arm and racquet are raised in a tennis serve. A good example of external viscous work is encountered when cross-country skis glide over a snow-covered surface. The external viscous work

Table 1.1 Recommended standard international (SI, SystPme International (d’Unites))units of force, work and power (based on recommendations of The International Bureau of Weights and Measures 1970,Ellis 1971and Knuttgen & Komi 1992). Mass Force Distance Time Velocity Acceleration Torque Angle Angular velocity Work Power Pressure Volume Amount of substance

= kilogram (kg)

= newton (N) (1 kgms$; a mass of 1 kg exerts a force of 9.81 N in a standard gravitational field) = metre (m) = second (s) = metres per second ( m s ’ ) = metres per second2(m& = newton-metre (N.m) = radian (rad) = radians per second ( r a d s d ) = force x distance = N.rn = joule (J) = work/time = Js’ =watt (W) = force/area = N.m-’ = pascal (Pa) = Iitre (1) = mole (mol)



performed by the ski competitor may be calculated as the distance travelled times the resisting force (the product of gravitational acceleration, the mass of the competitor plus skis and the coefficient of sliding friction for a given wax, temperature and snow condition). The body accumulates kinetic energy when its speed of movement is increased, as when a runner accelerates from the blocks. A single limb and associated equipment may also gain kinetic energy (for example, as the arm and racquet accelerate during a tennis serve).The developed force is proportional to the product of the mass of the moving part plus equipment and its acceleration; the work performed is again the product of this force and the distance over which it has operated. Work may be performed not only in accelerating the body or its parts, but also in deceleration (for instance, the eccentric muscle contractions that control the descent of the body when running downhill).







Energy expenditure (watts)

Fig. 1.2 Relationshipbetween rate of energy expenditure and power availablefor performanceof sport. The intercept on the abcissa reflects the resulting rate of energy expenditure, and the slope of the line indicatesnet efficiency (20% in the example illustrated).Adapted from Shephard (1982),with permission.


Mechanical efficiency

The quantity of work performed in unit time has the dimensions of power. It is best expressed in watts (I W = 1N.m.s-’, or 1J.s-’). A distinction must be drawn between the external power output, readily measured on a device such as a cycle ergometer, and the internal energy consumption. The latter is usually at least four times as great, reflecting not only energy consumed by the muscles engaged in the primary task, but also the resting energy consumption, unavoidable ancillary costs of the activity (such as increases of energy expenditure in the heart and the respiratory muscles) and (particularly if the regimen includes resistance exercise) the energy costs of synthesizing additional lean tissue.

Like most human-designed machines, the body is an imperfect device for converting stored food energy into external work. The gross mechanical efficiency expresses the ratio of the external work performed to the food energy that has been consumed. Commonly, resting energy expenditure is deducted from the gross energy cost to yield a net efficiencyvalue.The net efficiency vanes from around 25%* when operating a machine such as a bicycle or a cycle ergometer (Fig. 1.2) to a figure as low as 1%in a novice swimmer. In activities such as swimming, the difference in mechanical efficiency (and thus the energy cost of a given performance) between a novice and a highly skilled international competitor is at least four-fold, and a novice can make very substantial gains of performance from an upgrading of technique, even if the individual shows no increase of maximal oxygen intake. The difference between the external work performed and the food energy that is consumed nor-

Other units

In general, the SI system of units (Ellis 1971) is now well accepted by exercise physiologists. However, two exceptions are the systemicblood pressure (still commonly expressed in mmHg rather than in kPa; ioommHg = 13.3kPa), and oxygen transport (still expressed in 1.min-’ STPD rather than as mmo1.s-I; 1 1 = 44.6mmol).

* The mechanical efficiency can sometimesrise above the theoretical ceiling of 25% suggested by biochemical analyses (Shephard 1982).for instance if stored energy is recouped from sources such as the stretched tendons of a runner during a stride rebound.


mally appears as heat. In many circumstances, the endurance athlete has problems in dissipating the waste heat, but in some types of event (such as distance swimming in very cold water), heat production helps to conserve body core temperature.

Strength and endurance Physically demanding sports may be broadly classified into events that demand great strength (well typified by competitive weightlifting) and events that demand tremendous endurance (for example, participation in an ultramarathon run). The first type of competition requires an unusual development of the skeletal muscles (particularly fasttwitch, type I1 muscle fibres), but performance in the second category of event is favoured by the predominance of slow-twitch, type I fibres (Fig. 1.3). Endurance performance depends on an ability to supply the active muscle fibres with adequate amounts of oxygen and essential nutrients, to eliminate metabolic heat, carbon dioxide and other waste products and to sustain homeostasisin the body as a whole. Strength events are examined in a companion volume in this series (Komi 1992).The present book is thus limited almost exclusively to a discussion of


endurance activities, typically events that require an hour or more of physical activity. In many classes of prolonged athletic competition, central factors (particularly the pumping ability of the heart) appear important to success, but in some events (for example, the dinghy sailor who must make repeated 'hiking' movements to counterbalance a small boat), an ability to sustain load-bearing muscle contractions (isometricmuscle endurance) is a critical factor. In other instances (such as a prolonged tennis tournament) repeated powerful arm movements (isotonic muscular endurance) are needed for success. The distance runner requires, above all, cardiovascular endurance. A large blood flow to the working muscles must be sustained as preloading of the heart is reduced by sweating and an extravasation of fluid into the active tissues, and peripheral resistance is diminished by a rising core temperature (Saltinet al. 1972). In ultra-long distance events, performance is threatened by other factors-a depletion of intramuscular and hepatic glycogen reserves, a dispersal of the sarcoplasmic calcium ion reserves needed to initiate muscle contraction and an escape of intracellular potassium ions that threatens the electrical function of the muscle membranes.

Fig. 1.3 Bar chart illustrating the preponderanceof slow-twitch (type I) muscle fibres among successfulendurance competitors. From Dirix et al. (1988),with permission.



Finally, irrespective of the type of event, there is a need for psychological toughness-a motivation to endure and to excel in the face of pain and discouragement. Individual competitors may have an advantage in any of these domains, giving them an unusual endurance relative to their rivals.

Acknowledgement Dr Shephards studies are funded in part by research grants from the Defence and Civil Institute of Environmental Medicine, Toronto, ON.

References Bouchard, C. & Malina, R. (1983) Genetics of physiologicalfitness and motor performance. Exerciseand Sports Sciences Reviews 11,306-339, Bouchard, C. & Peruse, L. (1994)Heredity, activity level, fitness and health. In: Bouchard, C., Shephard, R.J. &Stephens, T. (eds) Physical Activity,Fitness and Health, pp. 106-1 18.Human Kinetics, Champaign, IL. Bouchard,C. &Shephard, R.J. (1994) Physical activity, fitness and health: The model and key concepts.In: Bouchard, C., Shephard, R.J.& Stephens, T. (eds) Physical Activity,Fitness and Health, pp. 77-88. Human Kinetics, Champaign, IL. Caspersen, C.J.,Powell, K.E. &Christenson, G.M. (1985) Physical activity, exercise and physical fitness: definitions and distinctions for health related research. Public Health Reports ioo,12&13 1. Dirix, A,, Knuttgen, H.G. & Tittel, K. (eds)

(1988) The Olympic BookoJSports Medicine. Blackwell Scientific Publications, Oxford. Ellis, G. (1971) Units, Symbolsand Abbreviations. A Guide for Biological and Medical Editors and Authors. Royal Society of Medicine, London. International Bureau of Weights and Measures (1970) SI. The International Systems of Units (Approved translation). Her Majesty's Stationery Office, London. Knuttgen, H. (1984) Instructions to authors. Medicine and Science in Sports and Exercise 16, xviii-xix. Knuttgen H.G. & Komi, P.V. (1992) Basic definitions for exercise.In Komi, P.V. (ed.) Strengthand Power in Sport, pp. 3-6. Blackwell Scientific Publications, Oxford. Komi, P.V. ( 1 9 9 ~Strength ) and Power in Sport. Blackwell Scientific Publications, Oxford.

Saltin, B., Gagge, A.P., Bergh, V. & Stilwijk, J.A.J. (1972) Body temperature and sweating during exhausting exercise. fournal of Applied Physiology 32,635-643. Shephard, R.J. (1977) Endurance Fitness, and edn. University of Toronto Press, Toronto. Shephard, R.J. (1978) The Fit Athlete. Oxford University Press, Oxford. Shephard, R.J. (1982) Physiologyand Biochemistry of Exercise. Praeger Publications, New York, NY. Shephard, R.J. (1994) Aerobic Fitness and Health. Human Kinetics, Champaign, IL. Shephard, R.J. (1997)Physical Activity, Training and the Immune Response. Cooper Publications, Carmel, IN. Wright,G.R.,Bompa, T. &Shephard, R.J. (1976) Physiologicalevaluation of a winter training programme for oarsmen. Journal of Sports Medicine and Physical Fitness 1 6 , ~ - 3 7 .



Endurance Sports PER-OLOF ASTRAND


Intermittent exercise

Which sport events call for endurance? Certainly running a marathon, cycling 18okm and, still more so, participating in the triathlon. What about running ioooo m? Rather arbitrarily, physical activity that lasted for i h or longer was taken as a guide in this volume. However, each training session for a ioooo-m race usually lasts for many hours. A tennis match can last for 4 h or more. Team sports are activities with intermittent exercise: the regulation time in team handball is two periods of 30min, in basketball 2 x 20min, in American football 4 x 15min, and in Australian football 4 x 25 min; volleyball consists of three sets and the time for a set is from 15 to 3omin, field hockey is 2 x 35min, water polo is 4 x 5min and netball is 4 x 15min; in ice hockey, where the effective time is 3 x zomin, individual players except for the goalkeeper participate for only part of this time. The total time taken for a game is often much longer than the 'regulation time'. In a world cup soccer championship held in Italy, many matches were not settled after two 45-min periods; two 15-min periods were added, with short breaks in between. The physiological response to continuous exercise can be very different when compared with the response to intermittent exercise, i.e. short bursts of intensive exercise. This chapter describes the physiology of intermittent exercise (bouts of less than 1 min), interval exercise (2-6-min bouts) and continuous exercise (over longer periods of time).

A man was able to exercise at a high work rate, 412 W, but after 3 min of continuous cycling he was exhausted @strand et al. 1960). When exercising intermittently for imin and resting for zmin, etc., the same man was able to continue for 24 min before being totally exhausted, with a blood lactate concentration of i5.7mM. On another day, the periods of exercise were reduced to 10s and the rest periods to 20s. He could then complete the intended work production of 247kJ within 3omin with no severe feeling of strain. On this occasion, his blood lactate concentration did not exceed zmM, indicating an almost balanced oxygen supply to his heavily stressed muscles (Fig.2.ia). With periods of exercise and rest of 30s and 60s, respectively, intermediate results were obtained. Thus, if 10-s exercise bouts were interrupted by 20-5 rest periods, the engaged muscles and their metabolic processes could be subjected to great demands without undue fatigue. How can we explain the fact that a power which demands an oxygen consumption exceeding the subject's maximal oxygen intake, measured at the 'lung level', can be performed without noticeable support from anaerobic processes? Figure 2.i(b) attempts to give an answer. When a person exercises intermittently in 10-s periods there is a vasodilatation of the vessels supplying active muscles; this will secure a good blood supply, and therefore a good oxygen supply, during exercise as well as during rest intervals. In addition, there is an oxygen store in the myoglobin which can be consumed during the bout of exercise. During the




Fig. 2.1 (a) Blood lactate concentration in a total work production of 247 kJin 30 min. The exercise was accomplished with a power of 412 W, the exercise periods being io,30 and 60s, and the rest periods 20,60 and 1205,respectively.The lower shaded area shows lactate concentration at rest. (b)Oxygen requirement for 10s and 60s power of 412 W. The schematic drawing indicates the basal metabolic rate (BMR), the calculated hactions of oxygen bound to myoglobin and transported by the blood, and the oxygen deficit. From Astrand et al. (1960).

following rest interval, this depot is quickly refilled with oxygen. The calculated oxygen store in this experiment was approximately 0.41. With the period of exercise prolonged to 60s, it was calculated that 1.91 of oxygen were 'missing' (Fig. 2.1b) and therefore anaerobic processes must have been contributingto exercisemetabolism.

In another experiment, by running for 10s and resting for 5 s, a subject was able to prolong the total exercise plus rest period to 3omin at a speed that would normally have exhausted him after about qmin of continuous running. During exercise, there is a reduction in adenosine triphosphate (ATP) and phosphocreatine concentrations; however, this


can be restored during the period of rest, evidently by aerobic processes. If intermittent exercise is performed at the same work rate as continuous exercise, less glycogen is utilized and the lactate concentration in the muscles is much lower. Thirteen times more ATP can be replenished when glycogen is metabolized aerobically, compared with the efficiency of anaerobic breakdown of glycogen to lactate (for references to these studies, see Astrand & Rodahl1986, pp. 304-707). If maximal effort is extended to I min, followed by rest for 4min, and the sequence is repeated four or five times, very high lactate concentrations can be attained both in the active muscles (>25 mh4.kg-l wet muscle) and in the blood (> zomM.l-'); indeed the pH in arterial blood can drop to 7.0. It is very fatiguing to train using this protocol, and such a regimen is usually not introduced until a month or two before the competitive season.

Interval exercise Figure


illustrates interval exercise, performed


with the intent of bringing oxygen intake, heart rate and cardiac output up to maximal values. After warming up, maximal rates can be reached within I min. When running, well-trained and highly motivated athletes can maintain maximal oxygen intake for some zomin, but a more 'normal' time is well below iomin. One hundred per cent of maximal oxygen intake can be attained even if speed and perceived exertion are submaximal. If oxygen demand exceeds the individual's maximal oxygen intake, the deficit must be covered by anaerobic processes, with the consequence that muscle and blood proton (and lactate) concentrations increase. We cannot explain the mechanisms, but marked proton accumulations interfere negatively with performance and are correlated with fatigue. Training at maximal oxygen intake is an effective way of improving maximal aerobic power (see Wenger & Bell 1986). The balancing act is to find a work rate just high enough to tax this maximum without requiring too much anaerobic support. On a cycle ergometer, a power demand of 300 W may cause exhaustion after 5min, but 250W is enough to

Fig. 2.2 Heart rate and oxygen uptake recorded in two subjects during training with alternating ymin periods of running (shaded areas) and rest (unshaded areas). The efforts were not maximal, but the oxygen uptake reached maximal values, as did the heart rate. From Saltin et al. (1968).



engage the oxygen transport system at maximal power (Astrand & Rodahl 1986, p. 300). When running on a treadmill at a speed of 13kmmix-', the maximal time for one subject was 4min. His speed could be reduced by several kmmin-I without reducing maximal oxygen intake (see Astrand & RodahJ 1986, p. 443). These examples illustrate how maximal aerobic power can be attained at submaxima1 work rates. There are no studies indicating that an aerobic training regimen is more effective if combined with hypoxia and anaerobic conditions. There is an ongoing discussion about training at high altitude (see Chapters 30 and 41). In endurance events, a period of several weeks of acclimatization is an essential part of the preparation for competition at an altitude of 2000m or higher (see Jackson & Sharkey 1988). It is unfortunate that organizers of world cups, world championships and the Olympic games give in to pressure groups for economic reasons and select high-altitude locations for competition. Data indicate that athletes with a very high oxygen intake per kilogram of body mass are particularly handicapped at high altitudes, due to limitations in the peak oxygen diffusing capacity of the lungs (see Shephard et al. 1988). In addition, countries that lack good sports facilities at high altitudes face an economic handicap in preparing for competition. Performance at sea-level is, as far as we know, not enhanced by a period of acclimatization at high altitude. Thus, following the 1968 Olympic Games in Mexico City (altitude zgoom), no world records in middle- and long-distance running events were broken when world-class runners returned to sealevel conditions after spending several weeks at high altitude. As discussed in Chapter 3, there is convincing evidence that the central circulation limits maximal oxygen intake. It therefore makes sense that stress on this system should elicit a positive adaptation. Nevertheless, training at less than 100%of maximal oxygen intake will also improve maximal oxygen transport (see Chapter 28). Peak blood pressures, heart rate and cardiac output are attained at approximately the same work rate as when oxygen intake reaches its maximum. However, stroke volume has already reached a maximum when


Maximal oxygen intake

Stroke volume 4 - - - - '

Heart rate

Rate of exercise (m.5-l; W)

Fig. 2.3 Schematicdiagram showing some of the major cardiovascular responses to exercise of increasing intensity up to a maximum. From Astrand and RodahI (1986).

oxygen intake is 40-50% of maximum (Fig. 2.3). Cross-country running and skiing offer 'natural' forms of interval training, with peak efforts when going uphill and moderate demands when travelling on the horizontal or downhill. During the periods between bouts of vigorous exercise, walking or jogging at a rate of up to about 50% of maximal oxygen intake ( Pohax) will speed up the rate of removal of lactate, which is a substrate in aerobic metabolism. Lactate is definitely not a waste product! From a theoretical point of view if 'anaerobic training' includes intermittent exercise, subjects should rest in the periods between bursts of physical activity, because then the removal rate of lactate is slow.

Continuous exercise The endurance time is limited in types of exercises that demand maximal oxygen intake. Therefore, if


continuous exercise is performed for 10-zomin or longer, as in running, cycling, skiing, swimming or canoeing, the intensity must be submaximal. The skeletal muscle cells of endurance-trained individuals are characterized by a high density of mitochondria and therefore a high concentration of the enzymes involved in aerobic metabolism. In fact, fast-twitch (type 11) and slow-twitch (type I) muscle fibres have similar metabolic profiles in such subjects. Capillary density is also high and, at any given time, more blood is available for the exchange of gases, nutrients and waste products with the tissues. Promotion of the oxidation of free fatty acids has a glycogen-saving effect (see Chapter 13).It was mentioned above that the central circulation seems to be the limiting factor for maximal aerobic power. In endurance events, peripheral factors are quite decisive. An 6lite marathon runner has a high maximal oxygen intake per kilogram of body mass and a good running economy, and she or he can run at a high percentage of maximal aerobic power without accumulation of protons and lactate (see Sjodin & Svedenhag 1985).As indicated in Fig. 2.4, marathon runners are not necessarily champions in terms of their maximal oxygen intake. Other qualities, just mentioned, are very important for success. Elite marathon runners and cross-country skiers have a high percentage of slow-twitch fibres, about 80%, compared with about 50% in unselected subject groups. It is still an open question whether the high percentage of slow-twitch fibres is a consequence of adaptation to endurance training or is an innate, inherited characteristic (see Chapters 9, 11 and 15). Coggan et al. (1990) found that master athletes in endurance events, with a mean age of 63 years, had a similar distribution of fibre types to younger runners with a mean age of 26 years (60% type I and very few type IIb fibres in the gastrocnemius muscle). One interpretation of their finding could be that years of endurance training do not modify fibre distribution (from type I1 to I). The literature related to exercise physiology reveals a great interest in the anaerobic threshold concept, i.e. the work rate or percentage of maximal oxygen intake that can be attained at a given blood lactate concentration (Chapter 22). Alternative methods of establishing the threshold are non-


Fig. 2.4 Maximal oxygen intake in track athletes who represented the Swedish national team. From Svedenhag and Sjodin (1984).

invasive. With increasing work rate, pulmonary ventilation increases linearly with oxygen intake to a point where ventilation increases non-linearly (the ventilation per litre of oxygen intake increases). There are data indicating that this 'ventilatory threshold' occurs at a work rate associated with an increase in blood lactate concentration. However, other reports do not support the idea of similar ventilatory and lactate thresholds (Loat & Rhodes 1993). There are also large individual variations in the responses (for discussion, see Astrand & Rodahl 1986, pp. 327-330; Orok et al. 1989; Chapter 22). Droghetti ef al. (1985) found a linear relationship between power output and heart rate up to a certain submaximal rate, beyond which the increase in heart rate slowed down. This deflection point where non-linearity in the heart rate response was found correlated significantly with the anaerobic threshold ('Conconi test'). Other researchers have been unable to confirm this finding (see Francis ef al. 1989).



For a physiologist, the anaerobic threshold concept is not simple to interpret: should one consider a threshold for a single muscle fibre, a muscle group, regulatory systems (e.g. the centres generating impulses that activate the respiratory muscles), the behaviour of blood lactate concentration (which does not necessarily mirror events within a muscle), or some other lactate- and pH-dependent functions? How important is the establishment of a threshold as a guide in coaching? Can data obtained in the laboratory be applied to field situations? When running is performed outdoors, physiological responses at a given speed are modified by track conditions, terrain and wind. If heart rate is taken as a guide to demands on the oxygen transport system, one must keep in mind that a hot environment and dehydration can dramatically increase the heart rate at a given oxygen intake (Chapter 40). After all, the experienced endurance athlete knows quite well the speed that can be tolerated without undue fatigue caused by proton and lactate accumulation. However, naining becomes much more sophisticated when the coach can give instructionsbased on blood lactate data. Recommendations about the intensity of endurance training are often based on a percentage of maxima1 oxygen intake or heart rate. Perceived exertion is also used as a guide (see Purvis & Cureton 1981; Chapter 26). From a practical viewpoint, few coaches have access to laboratories that can measure pulmonary ventilation, oxygen intake or lactate concentration, particularly in developing countries. Therefore heart rate recordings or, if equipment is not available, just recording the time taken for a fixed number of heart beats, are often the only objective measurements available. Taking group mean values, 50% of corresponds to about 65% of maximal heart rate; 80% of corresponds to about 87%of maximal heart rate. If heart rate is calculated as a percentage of 'heart rate reserve', the value comes, on average, very close to the corresponding percentage of Vo,. One can generalize and take 60 beats.min-' as the resting heart rate. If the maximal heart rate is igo beats.&-', then the 'reserve' is 190 - 60 = 130beats.mh-'. If the purpose is to train at 80%of 'heart rate reserve', the required

value is 104 beabmin-'. Adding the resting heart rate of 60 beatsmin-', we end up with a heart rate of 104 + 60 = 164 beats.min-*. In the example given above, 80% of Pomx should correspond to 87% of the maximal heart rate: 87% of igo = 165 beats m i d . If the individual's maximal heart rate is not known, an age group mean value is often used. However, because this mean value has a standard deviation of f 10beatsmin-' it is quite useless as a guide. In healthy, trained people, the individual's maximal heart rate can easily be established with a stopwatch. After warming up, the subject runs at a speed close to maximum for a couple of minutes and then makes a 1-min spurt, preferably uphill. Immediately afterwards the subject sits down and a stopwatch is used to record the time taken for exactly 10 beats, with palpation over the carotid artery or the radial artery, or on the chest over the heart. Because the heart rate drops rapidly, it is important that counting of the heart rate should start immediately after exercise (make a countdown of '5-4-3-2-i-o', and on 'o', start the stopwatch). A table can be constructed to convert the lo-beat time to heart rate in beatsmin-'. A similar protocol can be applied when the exercise is skiing, cycling, swimming or rowing; the peak heart rate in these activities is similar to that of running. Again it should be emphasized that exercise in a hot environment and resulting dehydration will gradually increase the heart rate at a given submaximal oxygen intake.

Conclusion This volume concentrates on a scientific analysis of endurance sports, focusing particularly on events with continuous activation of large muscle groups for I h or more. However, it is important to include also a basic discussion of training for many sports events of short duration because they may demand hours of daily exercise. In this chapter, the physiological responses involved in three different types of training have been discussed. I Intermittent exercise with repeated bursts of vigorous activity of short duration (less than 1min, followed by rest). Intermittent exercise in periods of 10s or less can be performed almost exclusively


aerobically, thanks to unloading and recharging of myoglobin oxygen stores. 2 Interval exercise, where repeated 3-6-min periods of vigorous activity are interspersed with periods of walking or jogging. Such exercise can effectively load the oxygen transport system up to maximum. A balancing act is needed to find a power level that is high enough to tax this maximum while requiring only a modest contribution from the anaerobic breakdown of glycogen. 3 Continuous, relatively long duration exercise at submaximal oxygen intake. This type of training seems effective as a stimulus to increase the mass


and density of mitochondria in skeletal muscle. The oxidation of free fatty acids is thus enhanced, with a glycogen-saving effect. A simple method of establishing an individual’s maximal heart rate is described, and a formula is given by which the percentage of maximal oxygen intake can be converted to the percentage of maximal heart rate. Other chapters give more detailed discussion of muscular endurance, including the ’anaerobic threshold’ (Chapter 22), endurance conditioning (Chapter 28) and training for specific sport events (Chapters 54-64).

References Astrand, P.-0. & Rodahl, K. (1986) Textbook of WorkPhysiology. McGraw-Hill, New York. Astrand, I., Astrand, P.-O., Christensen, E.H. & Hedman, R. (1960)Myoglobin as an oxygen-storein man. Acta Physiologica Scandinavica 48,454-460. Coggan,A.R, Spina, R.J.,Rogers, M.A. et al. (1990) Histochemical and enzymatic characteristicsof skeletal muscle in master athletes. Journal of Applied Physiology 68,1896-1901. Droghetti, P., Borsetto, C. & Casoni, I. (1985)Noninvasive determination of the anaerobic threshold in canoeing, cross-countryskiing, rolling and ice skating, rowing and walking. Europ ean Journal of Applied Physiology 53, 299-303. Francis, K.T., McClatchey, P.R., Sumsion, J.R. & Hansen, D.E. (1989)The relationship between an aerobic threshold and

heart rate linearity during cycling ergometry. European Journal of Applied Physiology 59,273-27. Jackson,C.G.R. & Sharkey, B.J. (1988)Altitude, training and human performance. Sports Medicine 6 , 2 7 ~ 2 8 4 . Loat, C.E. & Rhodes, E.C. (1993)Relationship between the lactate and ventilatory thresholds during prolonged exercise. SportsMedicine 15,104-115. Orok, C.J., Hughson, R.L., Green, H.J. & Thomson,J.A. (1989) Blood lactate responses in incremental exercise as predictors of constant load performance. European Journal of Applied Physiology 59, 262-267. Purvis, J.W. & Cureton, K.J. (1981)Ratings of perceived exertion at the anaerobic threshold. Ergonomics 16,595400. Saltin, B., Blomqvist,G., Mitchell, J.H., Johnson, R.L. Jr, Wildenthal, K. & Chapman, C.B. (1968) Response to sub-

maximal and maximal exercise after bed rest and training. Circulation 38 (Suppl. 71,178. Shephard, R.F., Bouhlel, E., Vandenvalle, H. & Monod, H. (1988)Peak oxygen intake and hypoxia: influence of physical fitness. International Journal of Sports Medicine 9,279-283. Sjodin, B. & Svedenhag, J. (1985)Applied physiology of marathon running. Sports Medicine 2,8399. Svedenhag, J. & Sjodin, 8.(1984)Maximal and submaximal oxygen uptakes and blood lactate levels in elite male middleand long-distance runners. International Journal of Sports Medicine 5,255261. Wenger, H.A. & Bell, G.J. (1986)The interactions of intensity, frequency and duration of exercise training in altering cardiorespiratory fitness. Sports Medicine 3,346-356.




Part 2a Biological Bases of Endurance Performance and the Associated Functional Capacities

Chapter 3 Determinants of Endurance Performance ROY J. SHEPHARD

General considerations This section of the monograph examines the basic determinants of endurance performance: physical, biological, psychological and genetic. In essence, competitive success depends on the individual's ability to maximize biological function, technical skills and psychological preparedness, thus optimizing his or her potential to perform athletically useful work against the inevitable constraints imposed by body form and environment. Much of the focus of this section is upon biological factors. Nevertheless, the psychological makeup of the individual is a major determinant of the athlete's willingness to maximize biological function by continuing rigorous training over many months. Psychological hardiness also allows a person to sustain an all-out competitive effort in the face of physical pain and discouragement. Genetic factors contribute to the individual's initial physical and physiological status, as well as modulating a competitor's responsiveness to training; constitution seems a significant determinant of the susceptibility of both whole organs and specific enzyme systems to conditioning programmes. Finally, the immediate physical circumstances (for example, a change in the type of equipment that is permitted, or the choice of a high-altitude location for training or competition) can substantially influence the physical performance that is achieved for a given expenditure of metabolic energy. Because the human body obeys the basic laws of thermodynamics, the energy that is needed to perform external work must be derived from the

physical or chemical stores of the body. Individuals differ greatly in the mechanical efficiency with which they can convert the chemical energy of foods into athletically useful work. Such discrepancies reflect inherent differences in body build, the progressive acquisition of technical skills and the learning of competitive tactics such as the choice of a moderate aerobic pace rather than a faster speed that demands costly and inefficient anaerobic effort. Realization of the individual's potential in terms of technical skills and the learning of optimal tactics are important goals of prolonged, sport-specific training. Discounting special cases such as an athlete who is reducing reserves of potential energy by releasing a stretched tendon or descending a hill, the active muscle fibres meet their immediate energy needs through the breakdown of a small local reserve of high-energy phosphate compounds (the phosphagens adenosine triphosphate (ATP) and creatine phosphate (0)). During a bout of physical activity, the ATP is usually degraded to adenosine diphosphate (ADP) and occasionally to adenosine monophosphate (AMP), whereas CP is converted to creatine. Each gram molecule of phosphate that is liberated by the breakdown of these several phosphagens yields a 'free' energy of about 46 kJ.mo1-I. This can be applied to the actin-myosin interaction that is needed to initiate a muscle contraction. Unfortunately, the total usable store of high-energy phosphagens is only about 30 mmol.kg-' muscle (wet weight), a reserve that can be exhausted by 2 s or less of all-out effort. The endurance competitor must therefore resynthesize ATP and CP repeatedly, 21



using energy derived from the metabolic breakdown of other food reserves (Newsholme 1983; Shephard 1984). Prolonged athletic performance depends not only on the extent of local food stores within the active muscles, but also on the ability to mobilize reserves held elsewhere in the body and to transport them to the working tissues. Furthermore, the cardiorespiratory system must be equal to the task of transporting the oxygen needed for aerobic metabolism, and of removing the waste products of metabolism (carbon dioxide, heat and such substances as lactate). Moreover, function must be sustained in regions of the body other than muscle as exercise proceeds. For instance, an inadequate blood flow to the brain may lead to a poor competitive performance because of mental confusion or impaired muscular coordination. Likewise, in sports that demand forward planning or teamwork, either an excessive rise in core body temperature or a drop in blood sugar concentration may lead to impaired thinking, irritability and a lack of cooperation between team members. The next section of this chapter discusses factors influencing the transport of oxygen, carbon dioxide, lactate, heat and metabolic fuels in terms of a generalized conductance equation. Ultimately, fatigue develops as various homeostatic mechanisms fail. A final section of the chapter thus looks at physiological, psychological and medical aspects of fatigue, discussing whether the primary site of fatigue is central or peripheral.

Conductance theory The physiological and biochemical systems involved in metabolism are arranged as a tightly interlinked sequence of transport mechanisms extending from the environment to the enzymes of the mitochondria1 cristae within the active muscle cells (Shephard 1977,1994). The various links in the transport chain can be conceptualized as a series of conductances. A conductance (@ is the reciprocal of the corresponding resistance (Y):&= i/r, or r = i/S.Thus, it is conventional to think of the gas transporting function of the chest bellows as the respiratory minute volume that can be sustained during vigorous exercise (a

maximum of perhaps iool.min-'). It is possible to think of an electrical or mechanical analogue for any conductance. The electrical analogue is governed by Ohm's law, with the electrical driving pressure or voltage (e) across an individual link in the system being proportional to the product of flux (I) and resistance (e = Ir, ore = I/@, The overall resistance of the system is then given by reciprocal summation of the individual conductances: R = l / G = l / g , + l / g , + 1 / ~ 3 . ..+l/gn One purpose of such a conductance analysis is to identify potential bottlenecks in the processes of transport and metabolism. Performance can then be bettered as these bottlenecks are eliminated through an appropriate combination of initial selection and extensive conditioning of the competitor. We shall look first at the conductance chain for the transport of oxygen, and will then examine more briefly analogous systems for the transport of carbon dioxide, lactate heat and metabolic fuels between the working muscles and the external environment (Shephard 1976,1982).

Oxygen conductance When analysing any of the conductances in the human model, the driving pressure must be expressed in dimensionless units. For example, ambient air normally contains about 20.9% oxygen, and the partial pressure of oxygen in the active muscle fibres is close to zero. Thus, the total driving pressure (E) from ambient air to the muscle mitochondria may be expressed as 209ml.l-l, or the corresponding fraction of an atmosphere (0.209). To apply this concept in a practical sense, let us assume that an endurance competitor can develop a maximal oxygen flux of 6 lemin-'. The overall conductance for oxygen (6= I/E) is then 6/0.209,or z8.71.min-'. If the driving pressure from the atmosphere to alveolar gas is 0.06 of an atmosphere, and the maximal alveolar ventilation during exercise is iool.min-', then the overall oxygen flux can be derived from the product of the regional pressure gradient and the corresponding conductance (I = e&, 100 x 0.06, or again 6l.min-'). It is more difficult to analyse data describing the



Ambient air e



(100 1.rnin-l)



(1.2 (25) Imin-')

- Mitochondria

-1 = - 1+ T 1



- _1



-100+30 Go, = 23.1 1.rnin-l

Fig. 3.1 Diagram illustrating in terms of electrical conductances the main barriers to the transport of oxygen from ambient air to the working muscles. The total pressure gradient ( E ) from ambient air to the muscle mitochondria (0.209atm) is distributed between ventilation (e = 0.06), muscle blood flow (e = 0.149)and the residual intramuscular gradient (e = 0.009), the distribution being determined by the reciprocal of the individual conductances (for ventilation,g, = 100 l.min-', and for muscle blood flow,g, becomes 30Lmin-' after allowing for an average solubility coefficient of 1.2;see Fig. 3.2).

transfer of oxygen from the alveolar spaces of the lungs to the pulmonary capillaries, and from the muscle capillaries to the muscle sarcoplasm, because the driving pressure changes continually, over the respiratory cycle in the case of the lungs, and at both sites the pressure gradient decreases progressively along the length of the capillaries. In both the lungs and the skeletal muscles, equilibration is almost complete on reaching the venous end of the capillaries. An accurate modelling of gas exchange in either capillary bed would require an integration of pressure gradients along individual capillary pathways, and an averaging of integrals across parallel pathways. But because equilibration is almost complete at the venous end of the capillaries, both in the lungs and in muscle, to a first approximation the overall process conducting oxygen from ambient air to the muscle sarcoplasm can be simplified to a series arrangement of respiratory and cardiovascularconductances (Fig.3.1). There is a change of phase on passing from alveolar gas into the bloodstream. Thus, it is necessary to introduce an appropriate solubility factor (technically, an air-liquid partition coefficient) in order to describe the cardiovascular conductance relative to the chosen measure of driving pressure. This solubility factor corresponds to the average slope of the oxygen dissociation curve between arterial and muscle venous blood. During vigorous endurance

I 0



40 80 120 Oxygen pressure (rnI.I-')

Fig. 3.2 Graph illustrating the calculation of an average blood solubility factor (air-liquid partition coefficient) for oxygen during a bout of maximal aerobic exercise.At the arterial point on the oxygen dissociation curve, an oxygen pressure of 140ml.l-' is associated with a blood oxygen content of 190m l t ' , while at the venous point the corresponding figures are 18and 40ml.l-'. The slope between the arterial and venous points during maximal aerobic activity thus averages 150/122,or 1.2.

exercise, a linear average value of 1.2 may be assumed (Fig. 3.2). A peak muscle blood flow of 25 l.mir-' thus yields a bloodstream conductance of 3ol.min-'. Plainly, when considering oxygen transport, the cardiovascular conductance is the smallest element



s c I E NT I F I c c o N s I D E R A T I o N s

in the chain. Thus, the cardiovascular resistance is the most important bottleneck, a point that is confirmed by looking at the corresponding driving pressures (0.06 of an atmosphere for the respiratory part of the circuit, close to zero for pulmonary gas exchange, 0.14 for the circulation and 0.009 for events within the muscle itself).Because the driving pressure at the venous end of the muscle capillaries has dropped to very near zero, it is unlikely that peripheral factors such as the activity of metabolic enzymes have a major influence on the peak rate of oxygen consumption during sustained endurance effort. The overall oxygen conductance can be approximated by reciprocal summation of the respiratory and cardiovascular components. In our example, it amounts to 23.1 1.min-I (see Fig. 3.1). Carbon dioxide conductance Similar general principles govern the transport of carbon dioxide from the working muscles to ambient air (Fig. 3.3). However, the gradient of driving pressure is in the opposite direction to that for oxygen. In a normal, well-ventilated environment, the partial pressure of carbon dioxide in ambient air remains close to zero. However, in the case of the underwater athlete, inefficiencies of carbon dioxide absorbing systems can quickly lead to a significantbuild-up of carbon dioxide pressures within a closed-circuit breathing system. Local toxic effects of carbon dioxide set a ceiling to driving pressures at the muscular end of the system. Specifically, a rising hydrogen ion concentration

= Ambientair

Muscle sarcoplasm e


0.056 Muscle flow ( 5 (25) 1.rnin-l)


-1= - +1 _ 1 6 92


- _1 -loo+



Gco, = 55.6 Imin-'

in the working muscles inhibits key enzymes of glycogen metabolism such as phosphorylase and phosphofructokinase. Very high concentrations of carbon dioxide also have an adverse effect on cerebral function. If the gradient is expressed in ml.l-', the limiting pressure at sea-level is perhaps iooml.l-' (0.10 of an atmosphere), but when underwater, the rise in ambient pressure necessarily causes this ceiling to decrease as the ambient pressure rises. The total flux of carbon dioxide is usually a little less than that for oxygen. At the beginning of an endurance event, the respiratory quotient (the ratio of carbon dioxide output to oxygen intake) is likely to exceed 0.9, signifying that carbohydrate metabolism is providing most of the food the body requires. Thus, if the maximal oxygen transport is 6l.min-', the initial maximal flux of carbon dioxide is 6.0 x 0.9, or 5.41.min-I. However, the body reserves of glycogen become exhausted if an event continues for longer than about ioomin. The main source of energy then becomes fat. At this stage, the respiratory quotient may drop to 0.8 or lower, corresponding to a maximal carbon dioxide flux of 4 . 8 l . d - ' . Note also that as the respiratory quotient falls, there is a progressive decrease in the quantity of energy transformed for each litre of oxygen that has been transported; the yield is 10%poorer for fat than for carbohydrate metabolism. The blood solubility factor is larger for carbon dioxide than for oxygen. As with oxygen, we are in essence dealing with the corresponding blood dissociation curve. Over the normal operating range from the venous end of the muscle capillaries to

Ventilation (100 1.rnin-l)

Fig.3.3 Diagram illustrating the conductance of carbon dioxide from the exercising muscles to the atmosphere. The total pressure gradient from the working muscles to ambient air ( E , o.iooatm) is distributed between ventilation (e = 0.056) and muscle blood flow (e = 0.044) according to the reciprocal of the individual conductances (for ventilation,g, = iool.min-', and for muscle blood flow, g2= 125 Lmin-' after allowing for a solubility coefficient of 5.0).


arterialized blood, the curve for carbon dioxide may be approximated by a linear solubility coefficient of 5.0. Thus, in our hypothetical example, the overall conductance for carbon dioxide becomes i / i o o + 1/5(25), or 55.51.min-I.Given also that the peak flux is smaller for carbon dioxide than for oxygen, it is unlikely that carbon dioxide transport will limit most types of competition, despite the fact that the overall pressure gradient is smaller for carbon dioxide than for oxygen. Exceptions are found in the underwater environment and in patients with chest disease (situations where the alveolar ventilatory conductance may be reduced by an increase in gas density, and spasm of the airways or a poor distribution of inspired gas, respectively).

Lactate conductance Lactate is normally converted to pyruvate, and is then broken down to carbon dioxide and water via the Krebs cycle. However, it tends to accumulate in the active muscles whenever the local oxygen supply is inadequate to support aerobic metabolism (Shephard 1982).Lactate that cannot be metabolized locally either passes from the active muscles into the bloodstream (Fig. 3.4) and thence to the liver (where glucose and glycogen can be synthesized from the lactate residues), or it diffuses locally to other better oxygenated tissues (where it can be converted back to pymvate and then metabolized through the Krebs cycle) (Gladden 1989). The pressure driving lactate from the muscle sarcoplasm into the bloodstream is the local concentra-


tion within the active tissues, acting on a 30-40 kD lactate transporting protein (McCullagh & Bonen 1995). The rate of transport is also influenced by the local tissue pH (Bonen & McCullagh 1994). The maximal intramuscular lactate concentration (30-40mmol.1-*) is set by the rising local hydrogen ion concentration and the resultant inhibition of glycolytic enzymes (Shephard 1984). The peak arterial concentration in young adults is typically 10-15 mmol.l-', although lower values are seen in young adolescents and in elderly individuals. Arterial concentrations as high as 30mmol~1-'have been reached when conditions have allowed equilibration between muscle and blood (for instance, when several brief bouts of exhausting large muscle work have been repeated over the space of 20min). Peak lactate values are usually larger in athletes than in sedentary individuals, and at any given level of training they are also greater in individuals who have a high proportion of Type I muscle fibres (Pilegaard et al. 1994). Bangsbo et al. (1994) further noted that during 'active' recovery (a period of light exercise following endurance exercise), lactate concentrations decreased more rapidly than with passive recovery. The main basis for this was an increase of metabolism within the muscle rather than a speeding of bloodstream transport to other parts of the body. The flux of lactate from the active muscle to the bloodstream and other, better oxygenated muscles typically reaches a rate of about iommol.min-' during maximal effort, although some authors have suggested figures as low as 2mmol.min-' Muscle membranes

Muscle membranes (0.33 Imin-')

Muscle flow (20 1.min-l) Hepatic membranes

Fig. 3.4 Diagram illustrating possible pathways for the conductance of lactate from the working muscles. The pressure gradient E is a lactate concentration of 40mmol.l-', extending from the muscle sarcoplasm to the sites of lactate metabolism in resting muscle and liver. The main gradient (and thus the smallest conductance) is from muscle sarcoplasm into the bloodstream.



(Shephard 1976). Taking the iommol.min-' figure, and assuming a muscle blood flow of 201.min-', the arteriovenous concentration gradient would reach the typically observed experimental value of 0.5mmol.I-~, compared with a gradient of 30 mmol .I-' from muscle sarcoplasm to the capillary bed. Based on these driving pressures, we may conclude that the conductance term describing the outward transport of lactate from muscle into the bloodstream and other muscle fibres is only about one-sixtieth of that describing bloodstream transport, the equivalent of a local blood flow of 0.33lamin-'. The reverse conductance of lactate, from the bloodstream into resting or moderately active muscle, proceeds more rapidly than the efflux, probably reaching a peak rate of about 40 mmol. min-'. These figures still remain relatively imprecise, and there have been suggestions that the bottleneck in lactate transport across the muscle cell membrane can be reduced substantially if the local hydrogen ion gradient is manipulated by the administration of bicarbonate solutions. There is thus a temptation to enhance athletic performance by 'bicarbonate doping' (Gledhill 1984). Over medium distances, this may confer an advantage of about 3%, but such a practice may not confer any advantage in long-distance events, since an increase of blood bicarbonate slows the transfer of lactate from the blood into resting muscle (Grainer et al. 1996).Bicarbonate is a normal body constituent,so there is little possibility of regulating this practice by blood or urine testing.

Heat conductance During vigorous exercise, metabolic heat follows a pathway from muscle to skin (Fig.3.5). It is then normally dissipated by a combination of sweating and convection (Nadel1977,1987).The driving pressure is a temperature difference, measured between the active deep tissues and either the skin surface (in a partial analysis) or the ambient air (in a total analysis). There is competition between muscle and skin blood flow when vigorous exercise is being performed in a hot environment. Skin blood flow usually peaks at 5 lamin-' or less. When the data are analysed in terms of a conductance analogue, it is necessary to apply a solubility factor describing the heat-carrying capacity of the blood (its specific heat, about 3.4 kJ.1-I per degree centigrade).The total heat conductance of the body is then approximated by reciprocal summation as (1/20 + 1/5) 1 / 3 4 or 14kJ.l-'-min-' per degree centigrade. Assuming a net mechanical efficiency of 25%,75% of body metabolism appears as heat. Further, each litre of oxygen that is consumed generates some 21 kJ of heat. If the oxygen flux is 61-min-l,the total heat flu is then 0.75 (6.0) 2ikJmin-', or about 95 kJmin-'. Given also a total conductance of 14 kJ.min-' per degree centigrade, a thermal gradient of about 7°C is necessary for circulatory transfer to the skin surface of all the heat that is produced by the working muscles. A core temperature in excess of 41°C is regarded as a dangerous level of hyperthermia. The implication is that the skin temperature should not exceed 34°C if a prolonged bout of

Muscle sarcoplasm e


Ambient air 40°C

Muscle flow (3.4 (20) klmin- )


Barrier layer (3.4 ( 5 ) kJmin- )


Barrier layer


Fig. 3.5 Diagram illustrating pathways for the conductanceof heat from the working muscles. The total pressuregradient (measuredin degrees centigrade) depends on the ambient air temperature (25'C in the example).The bloodstream conductanceof heat is given by the product of blood flow and a 'heat solubility factor' of 3.4 kJ.l-'."C-'.If transfer of heat across the barrier layer of still air around the body is expressed in the same units, it can be seen that normally this is the smallest of the three conductances, and thus it has the largest influenceon heat loss fromthe body.



strenuous physical activity is to be performed under warm conditions. The peak oxygen intake is more commonly 4 lmin-' rather than 6 1.min-I during prolonged endurance events; this reduces the total heat flux from 95 to about 65kJ-min-'. Moreover, some heat is conducted directly from muscle through the overlying tissues, without transfer to the bloodstream. The required skin temperature can thus rise to around 35.8"C rather than 34°C. Nevertheless, it may remain difficult for an athlete to achieve thermal homeostasisif an event is performed under hot and humid conditions. A rising core temperature commonly becomes an important factor limiting sustained physical activity in a warm environment. Finally, it is worth noticing that under temperate environmental conditions, a major portion of the overall thermal gradient is from the skin surface to ambient air.A thin film of stationary air (the 'boundary layer') offers a major barrier to heat dissipation. Assuming an air temperature of 25"C, the thermal gradient from skin to air (10.8"C in our example) is more than twice that from core to skin (5.2OC), implying that the barrier to heat exchange is at least twice as great for the boundary layer as for the maximal circulatory conductance. Heat transfer across the boundary layer changes dramatically from the laboratory treadmill (where there is normally little air movement or displacement of the body) to the athletic field (where body movement greatly reduces the effectiveness of the barrier layer, particularly for competitors such as cyclists, skiers and speed skaters. The conductance of heat across the barrier layer depends on the density and thermal conductivity of gases in the body's immediate microenvironment.Conductance falls with the decreaseof gas density which occurs at high altitudes, but it is greatly increased in the diver who is using not only a high-pressure breathing system, but also a gas mixture that contains a substantial fraction of helium (a gas with a high thermal conductivity). The thermal conductivity of water is much larger than that of air, and boundary layer effects are also much less important when a person is immersed in water. The outward heat flux is thus much greater when swimming than when on land, and a distance



swimmer may encounter physiological problems due to a fall in core body temperature over the course of competition.

Conductanceof metabolites Depending somewhat upon the state of training of the individual, carbohydrate provides about twothirds of the energy needed by an endurance athlete at the beginning of an endurance event. Intramuscular reserves of glycogen are used at a rate of about 2-4 grnin-' (about 16mmoLmin-' of the equivalent glucosyl units), while a further igmin-' (5.3mmol.min-' of glucosyl units) is transported from the liver to the active tissues. There is no evidence that performance is limited by the transport of metabolites to the working muscle, at least until the local reserves of glycogen have dropped to quite low levels (Hultman 1971; Karlsson 1979; Conlee 1986; Greenhaff et aZ. 1993; see Chapter 13). At this stage, corresponding to the running of a distance of perhaps 3-35 km,the speed of a distance competitor shows an appreciable decline, and contestants speak of 'hitting the wall'. The rate of muscle glycogen depletion depends on the tactics that are adopted by the competitor. Fat metabolism is oxygen dependent, so that the choice of an over-rapid pace increases the likelihood of local oxygen lack, boosting the proportion of energy that must be obtained from carbohydrate rather than fat in the early part of a race. The ideal plan is for the competitor to operate just below his or her anaerobic threshold. The experienced participant in endurance events adopts this pattern of exercise, reserving a burst of anaerobic activity for the final sprint to the finishing line. Endurance training also influences the situation; as conditioning increases the activity of the aerobic enzymes, the contestant is able to obtain a larger fraction of the needed energy by metabolism of fat (Greenhaff et aZ. 1993). On occasion, an attempt is made to eke out the carbohydrate reserves of the athlete by the drinking of a glucose or glucose/polymer solution during competition (Murray 1987; Shephard & Leatt 1987). The maximum rate of ingestion and absorption of sweetened fluid seems to be achieved when drinking a 5% solution of glucose. The peak intake is


B A sI c

s cI E N T I F I c c o N sI D E RATI o N s

then about 6ooml.h-' (0.5gmin-' glucosyl units, or 92.6mmol.min-*). This makes some contribution to metabolic demand, although it represents only a small fraction of total carbohydrate metabolism, at least until muscle glycogen reserves have been depleted. In very prolonged effort, performance may be limited by the ability to mobilize fat from the adipose tissue and/or the ability to transport fatty acids to the working muscles (Biilow 1987).In view of the limited blood supply of adipose tissue and the variations in the rates of triglyceride metabolism with changes in blood levels of fatty acids, one might suspect the problem is in part a local limitation of vascular conductance within the fat depots. On the other hand, training increases the ability to mobilize triglyceride metabolites, in addition to its effect in increasing the activity of fat-metabolizing enzymes within the working muscle. Presumably, these changes contribute to a sparing of glycogen in the early stages of an endurance competition.

Nature and location of fatigue Acute and chronic forms of fatigue (Simonson 1971; Green 1987; MacLaren et al. 1989)are common complaints of the endurance competitor. The problem may be physiological, psychological or occasionally medical in nature, and it can be local (confined to a particular group of muscles) or general (affecting the body as a whole).

Physiological fatigue Physiological fatigue is seen as a deterioration of performance, either over the course of a specific competition, or as a task is repeated from one day to another. For example, the pace of a runner may become slow, or the force of repeated maximal isotonic muscular contractions may diminish. There are usually associated signs of failing homeostasis; for example, the cardiorespiratory system is marked by a rising heart rate, respiratory rate, respiratory minute volume or respiratory gas exchange ratio at any given intensity of effort, and there are parallel increments in blood lactate and core temperature. However, there remain substantial interindividual

differences in the limiting values for each of these variables, and often there is only a limited relationship between subjective reports of tiredness and changes in objective measures of fatigue. For many people, there is a substantial gap between the physiologically possible and the psychologically acceptable, a gap that can be narrowed by either hypnosis or the roar of a cheering crowd. The proximal cause of fatigue may be central (a lack of appropriate signals to drive the active muscle fibres, resulting in a decrease of motor unit discharge, fibre recruitment and tension development), or peripheral (a failure of force generation due to problems in replenishing the high-energy phosphate molecules needed to power muscle contractions). There may also be more general problems of homeostasis associated with the accumulation of the waste products of metabolism (lactate, hydrions, phosphate and ammonia), disturbances of the ionic balance across membranes (Simonson 1971; Dawson et al. 1986), progressive fluid depletion, or an excessive accumulation of heat and resulting circulatory collapse (see Chapters 17 and 40). F A I L U R E OF D R I V E M E C H A N I S M S

Muscle contractions are normally initiated by a coordinated volley of impulses originating in the motor cortex and/or the cerebellum. The electrical signal passes through several synapses in the brain and spinal cord, traverses the neuromuscular junction and penetrates the transverse tubules, finally activating the muscle fibre by liberating calcium ions from the sarcoplasmic reticulum. The calcium ions in turn are one key component in a triggering mechanism that initiates the formation of crossbridges between actin and myosin molecules, using energy stored in ATP. In theory, fatigue could originate at any point in the chain of command. The brain has little capacity for vasodilatation, and is thus dependent on the ability of the heart to maintain an adequate perfusion pressure. Moreover, cerebral tissue can only metabolize carbohydrate, so that the progressive decrease in blood sugar which develops after several hours of large muscle activity and/or severe shivering may cause errors of judgement, loss of


teamwork, failure of coordination and a cerebral form of fatigue. In some instances (for example, soccer matches), team performance has improved when players have been given small doses of glucose or sugar at half-time (Shephard & Leatt 1987). A poor coordination of movement is one expression of cerebral fatigue, although it may reflect either a poor circulation to the brain or a low blood sugar level. Clumsiness is exacerbated by changes in the sensitivity of the spindle organs that detect muscle tension, and by attempts to sustain a given level of performance using muscle groups other than those which have been trained to undertake a given task. Evidence for a neural component to fatigue can be seen in both a decrease of discharge frequency in fast-twitch motor units and an altered pattern of movement as a person becomes tired (Green 1987; Bigland-Ritchie 1990; Figs 3.6 & 3.7). Recordings of action potentials from the working muscles show that the slow frequency component of the electromyogram increases as fatigue develops. This could represent an attempt to recruit fibres that are not yet exhausted from some alternative muscle group. Among many suggested causes of the slower average rate of firing we may note: (i) a voluntary inhibition of effort (the peak muscle force of an

Fig. 3.6 Potential sites of central fatigue: I, supraspinal failure; 2, segmental afferent inhibition; 3, depression of motoneurone excitability; 4, loss of excitation at branch points; 5, presynaptic failure. From Green (1987)’with permission.


‘exhausted competitor can often be increased by techniques such as hypnosis or cheering);(ii) a lessening of synchronization of firing between individual motor units; (iii)the recruitment of slowly firing, high-threshold motor fibres; (iv) alterations in the electrophysiological characteristics of the conducting membranes; and (v)an inhibitory feedback from muscular afferents designed to maintain optimal muscle function in the face of a prolonged force transient and a slow relaxation of the contracting muscle (Fitts & Metzger 1993; Nicol & Komi 1996). There is little evidence that the carriage of impulses along the nerve fibres or neuromuscular transmission itself is adversely affected by the fatigue of endurance competition. Fatigued muscles generate the same tension whether they are stimulated directly or via the motor nerve (Fitts & Metzger 1993). Within the muscle, there is sometimes evidence of a slowing of calcium pumping; this process is essential to a recovery of function both at the neuromuscular junction and in the sarcoplasmic reticulum of the active muscle fibres. Hydrogen ion accumulation may competitively inhibit the binding of calcium ions to troponin, thus preventing activation of the muscle cross-bridges; it may also inhibit the shift of the cross-bridges from a low to a high





Fig. 3.7 Potential peripheral sites of fatigue: I, presynaptic failure; 2, inability to develop an action potential at the motor endplate (ACh, acetyl choline); 3, failure of sarcolemma to sustain an action potential; 4, loss of coupling of excitation between t-tubule and sarcoplasmic reticulum; 5 , depressed release of calcium ions from the sarcoplasmic reticulum; 6, reduced binding affinity of the receptor protein troponin on the actin molecule; 7, a failure in the actin-myosin crossbridge cycle; 8, delayed cross-bridge dissociation; 9, depressed reaccumulation of calcium ions by sarcoplasmic reticulum. From Green (1987),with permission.

force state, or it may inhibit the sarcoplasmic reticular AWase involved in calcium ion uptake and release (Fitts & Metzger 1993). Furthermore, both local and general fatiguing exercise lead to a substantial leakage of potassium ions from the active muscle fibres (Sjogaard et al. 1985). The escape

of potassium ions adversely affects the electrical charge on the muscle membrane and conduction of the activating signal along the transverse tubules to the site of calcium release within the muscle fibres (Westerblad et al. 1990; Fitts & Metzger 1993).



We have noted that the release of energy needed for the resynthesis of ATP can be threatened by an inadequate supply of oxygen, an inhibition of the enzymes involved in glycogen breakdown due to an accumulation of carbon dioxide, hydrogen ions or lactate, a product inhibition from the accumulation of phosphate radicals (Dawson et al. 1986), or a depletion of food reserves locally within the active muscle fibres. However, there is surprisingly little correlation between the onset of fatigue and the exhaustion of local reserves of CP and ATP (Thompson & Fitts 1992). A competitor can use 100% of maximal oxygen transport for a few minutes of large muscle effort, but during an extended competition such as a marathon run, fatigue generally develops if the intensity of effort averages more than 75% of maximal oxygen intake (Costill 1972). The probable explanation of this ceiling is that the blood supply to the muscle fibres is non-uniform. Thus, if the intensity of effort exceeds 75% of the overall oxygentransporting capacity, the capillary supply to some parts of the working muscle is no longer sufficient to avert anaerobic metabolism (Antonutto & DiPrampero 1995).One factor that profoundly influences the local blood supply in heavy rhythmic and isotonic activity is the development of a high intramuscular pressure as the muscles contract; this occludes the arterial supply. The problem can be countered by a reduction of intramuscular pressure (for instance, by using a lower gear ratio on a bicycle, or strengthening the active muscles through appropriate training). Such tactics enable a distance competitor to exercise at more than 75%of maximal oxygen intake for long periods without becoming fatigued (Chapter 7). Likewise, in a sport that requires repeated vigorous isotonic efforts, the decrease in peak force over 50 such contractions may be much less marked after suitable training. Carbon dioxide accumulation does not contribute significantly either to local or to general fatigue, except in special circumstances such as prolonged underwater exploration. At depth underwater, the ventilatory component of overall conductance (more important for carbon dioxide output than for



the intake of oxygen) is limited both by the increase in gas density and by the added dead space and external resistance of breathing equipment. Glycogen reserves are almost completely depleted after ioomin of endurance work (Hultman 1971; Conlee 1986; Chapter 13). Stores can also be exhausted by the frequent accelerations and decelerations needed in team sports such as soccer and ice hockey. A third possible scenario is a sequence of 10-12 near-maximal contractions of a given muscle group, particularly if individual efforts have been sustained to the point of fatigue. The transport of fatty acids from depot fat to the working muscles can subsequently sustain an intensity of aerobic activity equivalent to about 50%of the competitor's maximal oxygen intake, but unfortunately, fat metabolism cannot provide fuel for anaerobic activity. The potential to synthesize glucose in the liver (the process of hepatic gluconeogenesis; Wahren & Bjorkman 1981; Winder 1985) draws on such precursor resources as hepatic glycogen, amino acids, glycerol and lactate. Nevertheless, the peak rate of gluconeogenesis is quite limited; the blood glucose may thus drop as low as 3mmol.l-' in some very prolonged events such as ultramarathon running. Once muscle glycogen stores have been depleted, a sensation of intense weakness and fatigue develops whenever postural, isometric or heavy isotonic muscle activity must be performed. F A I L U R E OF H O M E O S T A S I S

With very prolonged activity, a general failure of homeostasis may develop. This can involve the circulation, the kidneys and /or the endocrine glands. Sometimes, there is also an excessive rise or fall of body temperature. A local failure of homeostasis is a further possibility, particularly if one specific group of muscles is engaged in repeated and intensive isotonic or isometric effort. General circulatory problems arise from a decrease in the fraction of the total blood volume stored in the central part of the circulation (Saltin 1964; Senay & Pivarnik 1985; Convertino 1987). Many factors contribute to the depletion of central blood volume, including: (if a dilatation of the peripheral capacitance vessels (the major veins); (ii)



sweating (which may cause a fluid loss of as much as 2l.h-I); (3) exudation of fluid into the active tissues (a loss of fluid which has the potential to decrease total blood volume by up to 20%over 30 min of vigorous physical activity); and (iv) possible exhaustion of the neural and hormonal regulatory systems. Dominant features of central circulatory failure include a decline in blood pressure and cardiac stroke volume with an increase in heart rate for any given intensity of effort. Local circulatory problems arise when blood flow is restricted by a forceful muscle contraction.Perfusion of a given muscle decreases when contractions exceed 15% of the maximal voluntary force for a given muscle group. Occlusion of the local blood supply becomes complete at 70%of maximal voluntary force (Shephard 1982).Because of the effective decrease in local systolic pressure, the situation is worsened if the arm is held above the head (as in rock-climbing or a tennis serve).The perfusion pressure in the upper limb is then decreased because the heart must pump blood to a greater height, but the force of muscle contraction and thus of vascular compression is unchanged by limb position. If subjects compete repeatedly in a very hot environment, a progressive failure of circulatory homeostasis may develop over several weeks (Wyndham& Strydom 1972).The problem seems to involve a chronic depletion of sodium and other mineral ions, with an associated loss of water and thus blood volume. There have been occasional reports of renal failure following prolonged events such as marathon and ultramarathon races. Generally, there is evidence of an associated hyperthermia. The primary cause of the problem seems to be a restriction of visceral blood flow, in an attempt to maintain blood flow to other ‘more vital’ parts of the circulation.However, such a shift in blood flow distribution is not always advantageous; late-stage renal failure has possible links to tissue injury, a generalized septic response, excessive inflammation and the multiple organ dysfunction syndrome (Shephard & Shek 1998). Restriction of visceral flow may allow a penetration of the gut wall by intestinal bacteria, or cause a failureof the adrenal cortex (thefinal stage of Selye’s stress reaction).Damage to the adrenal cortex limits

the production of the hormones regulating potassium and sodium ions (aldosterone)and water and carbohydrate stores (cortisol).If competition is perceived as unusually stressful from a psychological perspective, there can be an interaction between physiological and psychological stress, exacerbating hormonal fatigue. There may be an associated deterioration in immune function (Keast et al. 1988; Shephard 1997).This leaves the athlete temporarily more vulnerable to viral infection. Moreover, any infection can further exacerbate both physical and psychological fatigue. A failure of circulatory homeostasis may be linked with an excessive rise in core body temperature (Nadel 1987). Because the rising core temperature diverts blood flow from the brain and the working muscles to the skin, it exacerbates feelings of fatigue, and precipitates a failure of circulatory homeostasis (Rowel11986). Repeated bouts of prolonged exercise in a hot climate can produce cumulative chronic fatigue; this condition can be associated with mineral ion and water depletion, unless care has been taken to replenish mineral stores between bouts of physical activity. Too low a core body temperature can also induce fatigue. In a cold environment, the local blood flow to the limbs is reduced, an increase of muscle viscosity augments the internal work that must be performed during physical activity, and a cooling of peripheral neural receptors leads to a more clumsy performance of many tasks. Psychological fatigue Although psychological fatigue is hard to pinpoint, it is a very real phenomenon, particularly in athletes who have pursued heavy training to the point of ‘staleness’. The tiredness can arise acutely, but more often its onset is gradual and chronic. Typically, symptoms have a situational or even an emotional rather than a firm physiological basis. Factor analyses of subjective reports from athletes (Kinsman et al. 1973) distinguish three elements: projected fatigue (noted in such sensations as leg weakness, shaking or aching muscles, a pounding heart, shortness of breath and a


dry mouth-many of the somatic manifestations of an anxiety state); task aversion (perceived as sweating, discomfort and a wish to do something other than train or compete); and poor motivation, encompassing feelings of reduced drive, lack of vigour and a want of determination. The athlete becomes bored with the routine of seemingly endless and unchanging training sessions, and there is an adverse reaction to the restrictions imposed by the coach, with the associated loss of social life. Discouragement develops as the rewards of a progressive improvement in performance disappear, despite the ever-increasing demands of training. The affected individual is typically underaroused, and fails to achieve his or her physiological potential. An associated loss of vigilance may increase the risk of accidents. In contrast with physical exhaustion, the psychologically fatigued athlete demands a change rather than a rest. An unpleasant or unfamiliar environment (for example, competition in a foreign country, sleeping in an uncomfortable hotel room at an unaccustomed altitude or temperature, conflict with the coach or a series of defeats) can exacerbate the problem, not by any direct physiological mechanism, but rather by increasing task aversion. Short-term training programmes apparently do little to change the perception of a given intensity of physical effort (Pandolf 1983). However, highly trained athletes undoubtedly habituate themselves to situations that lesser competitors would find psychologically fatiguing. Medical aspects of fatigue Fatiguing effort may induce disturbances of tissue function that are only slowly reversed. Lesions range from a slight muscular stiffness and/or pain, reported for a few days following intensive competition, to chronic tendon injuries, fatigue fractures of bones and disturbances of immune function. The immunosuppression increases susceptibility to intercurrent infections (Chapter 50) and, at least theoretically, augments the risk of various types of tumour. The minor muscle lesions are subcellular in type. It is unclear how far they arise simply from


mechanical overload, how far they are attributable to local hypoxia, and how far they are a consequence of increased local concentrations of reactive species of oxygen (Hellsten 1996;Jackson 1996).Evidence of increased membrane permeability can be found in: (i) modifications of ionic balance (a shift of potassium ions from within the active muscles to extracellular fluid, plasma and inactive tissues); (ii) the liberation of various intracellular enzymes such as lactate dehydrogenase and creatine kinase into the bloodstream; and (iii) the appearance of low molecular weight proteins in the urine (Poortmans 1985; Rogers et al. 1985; Armstrong 1986). The majority of observers have detected evidence of mitochondria1 damage and other ultrastructural changes in fatigued muscle, heart and nerve at electron microscopy (Banister 1971; Oscai & Palmer 1988; McCutcheon et al. 1992). It seems likely that these ultrastructural changes contribute to perceptions of chronic fatigue-particularly in terms of such feelings as stiffness and muscle pain. Some authors have suggested that the subcellular changes are a necessary concomitant of an adaptive response to heavy training, including the increased synthesis of muscle protein. However, the dividing line that separates such phenomena from irreversible tissue injury is fine. Immune disturbances may reflect a decrease in plasma levels of glutamine and other amino acids needed for cell proliferation (Newsholme et al. 1991).inhibitory effects of prostaglandins on natural killer (NK) cell function (Pedersen 1997). and direct influences of mood state upon the immune system (LaPerriPreet al. 1994). In some instances, reports of fatigue may be an indication that an athlete is developing an anxiety state, as a reaction to the stresses of competition or other adverse personal circumstances. Interindividual differences Susceptibility to central fatigue depends largely on the psychological hardiness of the individual and his or her willingness to continue exercise in the face of weakness, pain and other symptoms. The speed of onset of peripheral fatigue is influenced markedly by the relative proportion of type I



and type I1 fibres in the individual's musculature. Subjects with a high proportion of type I fibres are less susceptibleto fatigue (Komi & Tesch 1979).

Central versus peripheral limitations of endurance effort There has been much debate as to whether a typical endurance performance such as distance running is limited by central or peripheral factors (Shephard 1982).The issue is important for both the physiologist and the coach who seek to augment human performance, since it indicates whether investigative effort and conditioning programmes should focus on methods of boosting cardiorespiratory function, or whether attention should be directed towards enhancing the cellular and subcellular processes of metabolism. In forms of exercise that involve activation of a large proportion of the total musculature, the conductance theorem (this chapter) offers persuasive arguments favouring a central limitation of effort. Arguments for a peripheral limitation of function have been considered and rejected (Shephard 1982). Given zokg of active muscle and a peak muscle blood flow of ql.min-', the regional blood flow to the legs of a distance runner averages about 8ooml.min-' per litre of tissue. There are good reasons to believe that the blood vessels in a large muscle could accept three to four times this flow if the heart were able to sustain a greater rate of tissue perfusion (Savard et al. 1987; Reading et al. 1993). In forms of exercise where the volume of active muscle is more limited, the likelihood of a peripheral limitation of effort is correspondinglyincreased (Shephardet al. 1988).During cycling, a surprisingly large proportion of the total effort is sustained by the quadriceps muscle. Poorly trained individuals thus complain that their maximal effort on a bicycle or cycle ergometer is limited by muscular fatigue, rather than by indications of impending cardiovascular collapse such as incoordination, mental confusion or loss of consciousness (Shephard 1977). Because of local hypertrophy of the limb muscles, muscle fatigue is less likely in those who are well trained. Wheelchair athletes, for example, can use

the greatly hypertrophied muscles of their arms and shoulder girdles to develop as large a maximal oxygen intake as an average person can produce when running on the treadmill. Acquired skill is a further important consideration. Thus, the experienced cyclist uses toe clips and oscillatory movements of the body mass against the handlebars to distribute effort over a large fraction of the total muscle mass, avoiding local problems of quadriceps fatigue. During some types of heavy dynamic work, the volume of active muscle is very small. The intensity of effort that is demanded then approaches maximal voluntary force very quickly. Local blood flow becomes entirely occluded, and a peripheral limitation of exercise is the norm (Shephardet al. 1988). Even if a sport does involve use of a large fraction of the total muscle mass, the distinction between a central and a peripheral limitation of endurance performance becomes less clear cut as the determinants of cardiac output are considered. Determinants include preloading of the ventricles, myocardial contractility, the chronotropic response of the heart and the afterloading of the ventricles. Preloading reflects the rate of venous return to the heart. Thus, in wheelchair athletes with muscular paralysis, a loss of the muscle pump may cause blood to accumulate in the paralysed limbs, reducing preloading and restricting cardiac output (Shephard 1990; Glaser 1992). The sympathetically controlled increase of myocardial contractility quickly augments the stroke volume during exercise, and the chronotropic increase in heart rate is also mediated largely via sympathetic P-receptors. However, some authors have argued that local, limb-specific peripheral responses to training can play an important role in modulating the extent of these responses. Perhaps there is less peripheral stimulation of ergoreceptors as the active muscles become stronger, or perhaps there is a reduction of central command to the working muscles and thus a lesser irradiation of impulses to the cardiovascular control centres in the brain. Finally, the extent of afterloading, the force opposing ventricular emptying, is strongly influenced by the exercise-induced rise in systemic blood pressure; this depends in turn on the fraction of the maximal voluntary force



which is exerted by the working muscles, and thus on the local muscular strength (Shephard 1982). From many points of view, the distinction between central and peripheral limitation is thus somewhat arbitrary, and tends to be a matter of semantics.


Acknowledgement The studies of Dr Shephard are supported in part by research grants from the Defenceand Civil Institute of EnvironmentalMedicine, Toronto, ON.

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Chapter 4 Body Size and Endurance Performance J O E Y C. EI S EN MA N N A N D ROBERT M. MALINA


Assessment of body size and physique

Many of the same questions that we ask today about body size and sports performance were addressed a century ago by one of the first 'exercise scientists', Harvard professor of physical training, Dudley A. Sargent (Carter & Heath 1990). The main question was, 'Are there certain structural (anthropometric) requirements for various sports?' The general hypothesis is that body size and physique are important selective factors necessary for elite performance in a particular sport (Tanner 1964; Carter 1970). Successful athletes in many sports or in specific events within a sport often have many morphological characteristics in common. Further, 'ideal' values for a given sport are based upon reported values for elite performers and are often used to predict success in a given sport. Although the ideal values appear to cluster around the mean of a given morphological parameter, interindividual variability is considerable. Given such variability, what are the consequences of body size for endurance performance? This chapter provides an overview of the anthropometric characteristics of endurance athletes in several sports and then discusses the issue of scaling body size for differences in endurance performance. The adult and child endurance athletes are considered. 'Endurance' refers to the ability of the organism to maintain muscular activity for a period of time that depends upon aerobic metabolism as the predominant energy system.

The size and shape of the body can be measured with a series of systematized techniques that comprise anthropometry (Malina 1995). The number of measurements that can be taken on an individual is almost limitless. However, the selection of measurements should depend on the purpose of the study and the specific questions under consideration. In this chapter, we focus on overall body size and physique, although many other measures such as segment lengths, skeletal breadths, circumferences and skinfold thicknesses, and various ratios and proportions have been described for athletes in a variety of sports. Several methodological issues must be considered in reviewing studies of the anthropometric characteristics of athletes. Some include self-report of body size, equipment, inter- and intraobserver measurement reliability, and diurnal variation. These issues may be especially relevant when considering the stature and body mass of Olympic athletes as reported in the descriptive summaries for each sport at specific Olympic competitions. Although anthropometry is quite easy, it is often taken for granted and used without considering its limitations. Physique is an individual's body form, the configuration of the entire body. The assessment of physique is most often expressed as the somatotype, which consists of three components: endomorphy (predominance of roundness of contours throughout the body); mesomorphy (predominance of muscularity); and ectomorphy (predominance of




linearity). It should be emphasized that the somatotype should be treated as a unit, i.e. the contributions of endomorphy, mesomorphy and ectomorphy should be considered together and not in isolation. Most of the somatotype data used in this chapter are from Carter and Heath (1990). The Heath-Carter anthropometric protocol is the method of estimating somatotype most commonly used in studying athletes.

Anthropometric characteristics of adult endurance athletes Mean stature and body mass vary among en-

durance athletes in different endurance sports (Tables 4.1 & 4.2; Fig. 4.1a,b). Although certain events in swimming constitute endurance activity, studies often fail to stratify by distance. Body size and physique differ among dite short-, middle- and long-distance swimmers (Table 4.3). Therefore, only a limited number of studies of swimmers are reported here. Among endurance athletes in a particular sport, mean values are similar.The stature and body mass of rowers and swimmers are the greatest, while body size is smallest in distance runners. Based on a model of the effects of gravity on endurance performance, Tittel and Wutscherk (1992) suggested that

Table 4.1 Age, body size and physique of adult male enduranceathletes. Sample


Age (years)

Stature (m)

Mass (kg)


Cyclists Mexico City Olympics, 1968





1.8-4.9-2.7 0.5-0.8-0.7

British Olympic Squad, 1982





1.6-4.2-2.8 0.3-1.1-0.8

Cuba, 1976-80


21.5 (3.9)



2.0-4.8-2.5 0.4-0.7-0.6

Rowing Mexico City Olympics, 1968




82.6 (7.4)

2.1-5.3-2.4 0.6-0.w.8





Montreal Olympics, 1976 Cuba, 1976-80

2.3-5.0-2.7 0.6-0.9-0.8


22.2 (2.3)



2.3-5.3-2.5 0.6-0.8-0.6

SouthAustralia Heavyweight







1.82 (0.03)


0.5-0.7Q.5 2.1-4.3-3.4 0.2-0.4-0.7


1.81 (0.04)

1.6-4.0-3.4 0.3-0.8-0.7



World Championships, 1985 (lightweight) San Diego State University,1967 USA Olympic Trials, 1968 Singles Eights










2.3-5.9-2.5 0.7-0.8-0.7 2.1-5.3-2.7 0.4-0.5-0.6 Continued



Table 4.1 (Continued) ~~

Age (years)

Stature (m)

Mass (kg)



24.8 (2.3)

1.87 (0.05)

85.6 (5.1)



22.9 (3.0)


65.0 (5.6)



25.3 (4.5)

1.72 (0.05)

59.8 (5.4)



26.4 (4.8)

1.69 (0.06)

56.6 (3.7)

1.5-4.2-3.6 0.2-0.6-0.7 1.4-4.1-3.6 0.5-0.7-0.9 1.4-4.3-3.5 0.5-0.8-0.9

Us, 1977t Distance Marathon


1.76 (0.05)



63.1 (5.3) 62.1 (3.7)

Bulgaria (elite)$ Marathon


1.73 (0.06)

64.3 (6.4)

2.0-4.7-3.0 0.5-9-1.0

Cross-country skiing Czechoslovakia, 1968



70.6 (5.1)

1.7-6.3-2.0 O.h.7-0.7

European, 1976



1.76 (0.05)

69.3 (6.3)


US National Team,


22.8 (1.9)


71.8 (5.4)

2.0-4.5-3.0 0.5-.4-0.3

Bulgaria (elite), 1984






Triathlon USA National Team, 1984


28.9 (3.2)


75.6 (4.3)

1.7-4.3-3.1 0.6-0.3-0.6

28.7 27.2 27.6 30.5 30.5

1.82 1.76 1.79 1.79 1.82

73.8 69.4 72.8 74.7 76.6

1.83 1.80

74.3 78.1


65.0 (9.3)

Sample New Zealand National Team, 1967-68

Distance running Mexico City Olympics, 1968* 800-15oom



US, 19899

9 25 9 8 10

Swimming World Championships, 19911 1500m 25 km





Bulgaria (elite)$


1.5-4.8-3.4 2.5-5.3-2.3 2.1-4.0-3.2 0.6-1.1-1 .I

All values are adapted from Carter and Heath (1990)except as indicated. Mean (SD) except for somatotype where SD is indicated below the mean. * Data from de Garay et al. (1974). t Data from Pollock et al. (1977). $ Data from Toteva (1992). 9 As reported in Roalstad (1989). 7 Data from Carter and Ackland (1994).

s c I E N T I F I c c o N sI D E R A T I o N s



Table 4.2 Age, body size and physique of adult female endurance athletes. Sample

Rowing Montreal Olympics, 1976 World Championships, 1985


Age (years)

Stature (m)

Mass (kg)



23.8 (2.7)


67.4 (5.3)



24.1 (3.7)



57.1 (2.0)

2.4-3.0-3.5 0.8-1.1-1.0

Distance running England, 1983 'elite' marathon

29.4 (7.6)


Brighton Polytechnic, 1986


1.66 (0.04)

54.7 (5.6)

2.8-3.6-4.6 0.5-0.8-0.6

1.67 (0.03)

55.0 (5.8)

2.7-3.6-4.1 1.0-0.g-1.0

San Diego, 1981 Eumenorrhoeic


29.4 (6.6)

1.66 (0.06)

54.2 (5.9)



25.1 (6.3)







University of Texas, 1985-95'

Triathlon Southern California, 1987 US, 1989t



23.5 (4.7)


53.9 (1.1)

3.5-4.3-2.3 0.7-0.5-0.8


24.2 (4.3)

1.62 (0.06)

55.2 (4.6)

3.1-4.3-2.6 1.00.8-0.9

31.3 31.3

1.63 1.68

56.4 58.9

18.7 (0.8)


61.4 (5.0)

34-3.8-3 .O 0.6-0.7-0.8

19.3 22.8

1.72 1.63

63.5 62.2

1.65 (0.04)

52.9 (6.6)

2.4-3,8-3.0 4.4-4.7-1.7 2.7-3.3-3.6 0.8-0.6-0.9

6 8

Swimming University of Texas, 1985-95'


World Championships, 1994 800 m 25


Bulgaria (elite)§



52.2 (3.7)


Cross-country skiing USA, 1976



19.3 (1.2)









All values are adapted from Carter and Heath (1990)except as indicated. Mean (SD)except for somatotype where SD is indicated below the mean. *Unpublished data, Malina. t As reported by Roalstad (1989). $Data from Carter and AckIand (19941. §Data fromToteva (1992).


Adult males 90 0



A Distance runners 8 Triathletes





Swimmers Reference


25 $

endurance athletes are low in endomorphy, ranging from 1.4 in distance runners to 2.5 in rowers for males and from 2.4 in distance runners and rowers (lightweight) to 3.5 in cross-country skiers in females. Mesomorphy is lowest in distance runners and highest in cross-country skiers in both sexes. Ectomorphy is relatively similar in all groups of endurance athletes, but distance runners generally have the highest ratings.

0 00

0 Rowers 85 - o Cross-country skiers



* *


25-34 yrs





18-24 yrs



Anthropometric characteristics of child and adolescent endurance athletes







60 1.65



1.80 1.85 Stature (m)



Ldult females

0 Rowers o Cross-country skiers A Distance runners



Triathletes Swimmers Reference

+ 25-34 yrs 8

18-24 yrs +


8 -













Stature (m)

Fig. 4.1 (a,b) Distribution of male and female endurance athletes based on mean mass and stature.

the lowest values are seen in sports where the body mass acts in an unrestricted manner against gravity, whereas the highest values are in endurance sports that require a greater level of strength. Mean somatotypes for endurance athletes also vary among sports (Tables 4.1 & 4.2).In general,

Two other questions proposed by Sargent that are still of interest today include, 'Are body size parameters of child and adolescent endurance athletes comparable to adult endurance athletes? and 'Can athletic success in adulthood be predicted during childhood or adolescence?' In general, studies of child and adolescent endurance athletes indicate that body size (Table 4.4)and physique (Malina 1994) resemble those of adult endurance athletes in the corresponding sports. However, the ability to predict future athletic ability assumes that growth in body size and physique is stable throughout childhood and adolescence. The stability of stature (r = 0.8) and mass (r = 0.6-0.8) tends to be moderately high to high and stable from the age of 2-3 years until early adulthood (Malina & Bouchard qy),whereas the stability of somatotype during growth is only moderate (r = 0.4-0.6).Therefore, those interested in identifying young athletes on the basis of body size and physique alone need to be aware of the growth- and especially maturityassociated variation related to the timing and tempo of the adolescent growth spurt. Selection at an early age implies the exclusion of other potentially talented youth and, given the limited precision of talent identification and selection programmes, the exclusion factor needs to be considered carefully. Another issue in the area of body size and endurance performance of child and adolescent athletes is whether intensive training during childhood and adolescence perturbs the processes of linear growth and biological maturation. Presently the available data for young athletes, including distance



Table 4.3 Differences in body size and physique of swimmers stratified by distance. Stature (m)

Mass (kg)




1.74 (0.05) 1.62-1.85 1.70 (0.06) 1.56-1.84 1.70 (0.05) 1.61-1.78

64.2 (5.1) 55.114.8 62.2 (5.1) 50.3-72.6 61.4 (5.0) 53.3-70.8

2.8 (0.6)

3.7 (0.6) 2.5-5.0 3.9 (0.7) 2.7-5.7 3.9 (0.7) 2.7-5.1

3.2 (0.7) 1.7-4.7 2.9 (0.7) 1.0-4.4 3.0 (0.8) 1.5-4.5

Sprint (n = 31) Middle (n = 27) Long (n = 6) Ultra (n = 10)

1.74 1.74 1.72 1.63

65.0 64.6 63.5 62.2

3.7 3.7 3.8 4-7

3.2 3.2 3.0 1.7

Mules Sprint (n = 47) Middle (n = 34) Long (n = 10) Ultra (n = 13)

1.86 1.85 1.83 1.80

79.8 79.1 74.3 78.1

4.9 4.7 4.8 5.3

3.2 3.1 3.4

Distance University"

Females Sprint (n = 39) Middle (n = 34) Long (n = 14)

1.7-4.1 3.1 (0.6) 1.9-4.4 3.4 (0.6) 2.3-4.8

World Championships, 1991t



*Unpublished data, Malina. Mean (SD) and range provided. t Means from Carter and Ackland (1994).

Table 4.4 Stature and mass of child and adolescent endurance athletes relative to percentiles (P) of United States reference data. Based on data reported in Malina (1994,1998). Males







Distance running Swimming Cycling Rowing/canoeing

P 50 f P 50-p 90 >P50 >P~o

P 5-p 90 fP5o >P50

2P50 P 5CYp90

onceihr)? Prolonged standing? Mainly sitting? Normal daily activily Do you currently smoke tobacco?' Do you consume alcohol?'










3 1 1 3 3 1

3 3 1 i

PART 4: PHYSICAL ACTIVITY INTENTIONS What physical activity do you intend lo do?

Is this a change from what you currently do?







Jc ~

CONTRAINDICATIONS TO EXERCISE: to be completed by physician Relative Contralndlcetlons

Absolute Contraindications

Does Ihe patient have:

Does the pafienf have: 1. Ruptured membranes, premature labour?





1. History of spontaneous abortion or premature labour in previous pregnancies?





2. Persistent second or third trimester bleedingiplacenta previa?



3. Pregnancy-inducedhypertension pie-eclampsia or toxemia?

2. Mild/moderatecardiovascular or respiratory disease (e.g., chronic hypertension. asthma?)





3. Anemia or iron deficiency? (Hb < 10 gldt)?



4. Incompetent cewix?



4. Very tow body fatness. eating disorder (anorexia. bullmia)? 0


5. Evidence of intrauterinegrowth retardation?



5. Twin pregnancy after 28th week?

6. Multiple pregnancy (e.g., triplets)?



6. Other significant medical condition?

0 0

7. UncontrolledType I diabetes, hypertension or thyroid disease. other serious cardiovascular. respiratory or systemic disorder?


9 0

Please specity:

NOTE. Risk may exceed benefits of regular physical a3Mly. The decisionto be ohvsicellv active or not should be made with aualitied medical advice.



Q Contraindicated

0 RecommendedADDroved

Prescription for Aerobic Activity RATE OF PROGRESS^ The best time to progress is during the second trimester since risks and discomfort of exercise are lowest at that time. It is no1 advisable to begin a new exercise program or increase the amount of exercise prior to the 14th week 01 pregnancy or after the 28th week. Aerobic exercise should be gradually end progressively increased during the second trimester from a minimum of 15 minutes per session to a maximum of approximately 30 minutes per session. WARM-UP/COOL-DOWN: Aerobic activity should be preceded by a brief (10-15 min.) warm-up and lollowed by a short (10-15 mln.) cool-down. Low intensity calesthenics, stretching and relaxation exercises should be included in the warm-upicool-down.




FREQUENCY Begn at 3 times per week and progress to lour or live bmes

INTENSITY Exercise within an appropnate RPE range and/or largel hean rate zone

TIME Attempt15 minules. even if it means reducing the intensity. Rest intervals may be helpful

per week


PRESCRIPTION/MONITORlN~OFINTENSTY: The best way to prescribe and monitor exercise is by ccmbining the heart rate and rating of erceived exertion (RPE Hhcds.

The heart rate zones shown below are appropriate lor most pregnant women. Work during the lower end of the HR range at the start of a new exercise program and in late pregnancy.

Non weight bearing or low-impact endurance

exerase using large muscle groups (e g , walking, staNonary cycling. swmming. aquatic exercises, b w impact aerobics)



Aae. c20 20-29 30-39 240

Check the accuracy of your heart rate target zone by comparing it to the scale below. A range of about 12-14 (somewhat hard) is appropriate for most pregnant womz.1.

Heart Rate Range .__._ 140-155 135-150 130-145 125-140

"TALK TEST". A final check to avoid overexertion is to use the 'talk test". The exercise intensity is excessive if you cannot carry on a vertbal conversation while exercising.

6 7

Very, very light

1 "

9 10 11 12 13 14 15 16 17 18 19 20

Somewhat light Falrlylight Somewhat hard Hard Veryhard Very,veryhard

(The original PARmed-X for PREGNANCY was developed by L.A. Woife, Ph.0. 01 Queen's University,Kingston, Ontario. The mugCutar COndltiOnl~Q component wa> developed by M.F.Monola. Ph.0. of The University of Western Ontario, London, Ontario. II has been revised by an ExpeIlAdvisory Committee assembled by the Canadlan Society for Exercise Physiology and the Fltness Program-HealthCanada (1996).

Transiatlon and reproduction In its entirety is encouraged Disponible en Iranwis sous Ie titre .*Exeminationmedicale sur I'aptitude t~I'activitb physique pour Ies lemmea enceinte6 (X-AAP pour les temmes encein1es)-

To order additional printed copies of the PARmed-X lor PREGNANCY, the PARmed-X andlor the PAR-Q.(for a nominal charge) Contact the:


Canadian Society for Exercise Physiology 185 Somerset St. West. Suite 202 Ottawa. Ontario CANADA K2P OJ2 tel. (613) 234-3755 FAX (613) 234-3565




Prescription for Muscular Conditioning It is important to conditron a// major . . muscle groups during Prenataf and POSfnafaf periods.



upper back Lower back Abdomen

Promotion of good posture Promolion 01 g w d posture Promotion of good posture. prevent low-backpain. prevent diastasis recti, strengthen muscles of labour Promotion of good bladder control. prevention of urinary incontinence Improve muscular support lor breasts Facilitation01 weight-bearing, prevention of varicose veins

Range of Motion: neck, shoulder girdle, back, arms, hips. knees. ankles, etc.

Pelvic floor

("Kegels") Upper body Buttocks. lower limbs

mvscle oroups




Shoulder Shrugs. shoulder blade plnch Modified slanding opposite leg B arm lilts Abdominal tightening. abdominal cud-ups. head raises lying on side or standing posllion 'Wave'. 'elevator" Shoulder rotations. modirii push-ups against a wall Buttocks squeeze,standing leg lilts. heel raises





__.. -.



Precautions lor Resistance Exerclse - __--



- -- -

- -


* emphaos on wrrect posture

loWard shin in the a n t r e of gravity and may increase the arch In the lower bacr this may alsa cause shoulders to slump lomaro -~ - . -. - - - emphasis must be placed on conlinuous breathmg IhrOLghoJt exercse




. increasmg weight ofenlarged breasts and ulerus may cause a






exhale on exertion inhale on ,elaxation Valsaiva Manoevre (holding breatn while working againsl a resistance) causes a decrease in blood pressLre and theretore should be avoided mold exercise in supine posilion past 4 months gestatlon

Health Evaluation Form (to be completed by patient and given to the prenatal fitness professional after obtaining medical clearance to exercise)

PLEASE PRINT (patient's name), have discussed my plans to participate in physical I, activity during my currenl pregnancy with my physician and I have obtained hisiher approval to begin participation. Signed:

Dale: (patient's signature) PHYSICIANS COMMENTS:


Name of Physician. Address:









~ -





M.D (physician's signature)




Advice for Active Living During Pregnancy Pregnacy is a time when women make beneficial changes in their health habits to protect and promote the healthy development of their unborn babies. These changes include adopting improved eating habits, abstinence from smoking and alcohol intake, and participating in regular moderate physical activlty. All of these changes can be carried over into the postnatal period and many health experts believe that pregnancy is a very good time to adopt healthy lifestyle habits that are permanent by integrating physical activity with enjoyable healthy eating and a positive self and body image.

Active Living: see your doctor before increasing your activity level during pregnancy exercise regularly but don't overexert exercise with a pregnant friend or join a prenatal exercise program follow FlTT prlnciples modified for pregnant women know safetey considerations for in pregnancy

Healthy Eating: the need for calories is higher (about 300 more per day) than before pregnancy

Positive Self and Body Image:

follow Canada's Food Guide to Healthy Eating and choose healthy foods from the following groups: whole grain or enriched bread or cereal, fruits and vegetables, milk and milk products, meat, fish, poultry and alternatives drink 6-8 glasses of fluid, including water, each day salt intake should not be restricted limit caffeine intake Le., coffee, tea, chocolate, and cola drinks

remember that it is normal to gain weight during pregnancy accept that your body shape will change during pregnancy enjoy your pregnancy as a unique and meaningful experience

dieting to lose weight may be harmful


Enjoy eating well, being active and feeling good about yourselj. That's VITALIT




6 Avoid prolongedor strenuous exertion during the 1st trimester

6 Persistent uterine contractions (more than 6-8 per hour)



+ + + 6

+ +

Avoid isometric exercise or slraining while holding your breath Maintain adequate nutrition and hydration - drink liquids before and after exercise Avoid exercising in warmlhumid environments Avoid exercise while lying on your back past the 4th month of pregnancy Avoid activities which involve physical contact or danger of falling Periodic rest periods may help to minimize possible low oxygen or temperature stress to the fetus Know the reasons to slop exercise and consult a qualified physician immediately if they occur

'* CAUTION ** It is important to monitor the temperature of heated pools. Maternal body temperature during exercise may be increased more by exercising in a warm environment.



Bloody discharge from vagina Any "gush of fluid from vagina (suggesting premature rupture of the membranes) Unexplained pain in abdomen

+ +

Sudden swelling of extremities (ankles. hands, face)


Persistent headaches or disturbances of vision


Unexplained dizziness or faintness


Marked latigue, heart palpitations or chest pain

Swelling, pain and redness in the calf of one leg (suggesting phlebitis)

6 Failure to gain weight (less than 1 kg per month during

last two trimesters)


Absence of usual fetal movement


Chapter 38 The Elderly and Endurance Training MICHAEL L. POLLOCK, DAVID T. LOWENTHAL, J O A N F. CARROLL A N D JAMES E. GRAVES

Introduction The population in North America and most industrialized countries is living longer. US Census Bureau data (1996) show that from 1980 to 1990 the US population increased by 15.8%in the age range of 65-74 years, 29.5%for those aged 75-84 years and 34.9% for those above 85 years. In 1990, the number of persons in the US over 65 years of age was 31.1 million, but it is projected to reach over 40 million by the year 2010, and over 70 million by 2030. With increased life expectancy, Americans who reach 65 years of age can expect to live an average of 17 additional years (Beck 1989). Stephens (1987)reported that the activity level of elderly persons had increased over the preceding two decades. Even so, it was estimated that at most 10-20% of elderly North Americans participated in regular vigorous physical activity (defined as activity that involved an energy expenditure of 12.5kJ.kg-' body mass, three times per week for a minimum of zomin per session) (Haskell et al. 1985). Further, approximately 37% of North Americans over 65 years of age rated themselves as having a sedentary lifestyle (US Department of Health and Human Services, 1996). Ageing is associated with a dramatic increase in health problems and physical limitations. The physical and physiological limitations to be discussed here are related to changes in aerobic power/maximal oxygen intake body composition, muscular strength and the ability to perform the activities of daily living. We will also discuss how these limitations are related to a variety

of chronic diseases. Many health problems and physical limitations are related to the individual's lifestyle. Thus, sedentary living has a significant adverse effect on health and physical well-being. With the elderly population living longer, the importance of leisure-time activity and regular exercise training is apparent. The purposes of this chapter are to discuss the various health problems and physical/physiological limitations associated with ageing, to review studies dealing with endurance training in the elderly, and to give recommendations for exercise prescription in older individuals. Special concerns of and contraindications to exercise in the elderly will also be addressed.

Physiological and pathological changes related to ageing and exercise science Physical capacity and physiological function decline with age (Dehn & Bruce 1972; Raven & Mitchell 1980; Shephard 1993). The loss of physical capacity has been attributed to age, reduced physical activity, chronic disease and the medications that are used to treat chronic disease. The majority of the elderly do not exercise, and until recently they have not been encouraged to participate in regular exercise. It is unclear therefore whether the reduced state of physical conditioning associated with ageing is a result of deconditioning (a sedentary lifestyle), ageing, or both. Several reports have suggested that the age-associated decline in physical performance and increased incidence of disease can be minimized by regular endurance training (Ordway & Wekstein 1979; Buskirk & Hodgson 1987; Pollock &




Wilmore 1990; US Department of Health and Human Services 1996). Indeed, participation in regular physical activity results in many favourable responses that contribute to healthy ageing (Huang et al. 1998; Mazzeo et al. 1998). Age-associated changes such as a decline in fat-free mass, total body water and intracellular water, and an increase in fat mass (Sidney et al. 1977; Suominen et al. i977a), may alter the physiological responses to exercise and influence drug dynamics and kinetics (Richey & Bender 1975; Epstein 1979). Changes in cardiac function Cardiac performance undergoes direct and indirect age-associated changes. With increasing age, there is a small reduction in the contractility of the myocardium (Becklake et al. 1965; Dock 1966; Gerstenblith et al. 1976) which may be due to a decrease in myocardial responses to catecholamines (Gerstenblith et al. 1976). Plasma norepinephrine concentrations are increased in the elderly, but the cardiovascular responses are diminished (Palmer et al. 1978; Eisdorfer 1980).The myocardium increases in stiffness, which impairs ventricular diastolic filling (Templeton et al. 1979; Weisfeldt 1981). This suggests that exercised-induced increases in heart rate would be less well tolerated in older individuals than in younger populations. The age-associated decline in maximal heart rate (Astrand & Rodahl 1986) is probably less than the 10 beat per decade value commonly reported (Londeree& Moeschberger 1982; Graves et al. 1993). There are multiple causes of this decline, but the most important seems to be a decrement in sympathetic nervous system (adrenergic) reactivity. Reductions in maximal values for cardiac output, stroke volume and stroke index have all been observed with increasing age (Brandfonbrenner et al. 1955; Raven & Mitchell 1980),especially in those individuals with heart disease. The healthy elderly human heart tends to maintain its cardiac output by increasing stroke volume through the Starling effect (Weisfeldt 1981).Nevertheless, cardiac output at the same relative exercise load is lower and arteriovenous 0, difference is greater than in younger persons (Ogawa et al. 1992).

In a young adult, acute exercise results in a redistribution of the cardiac output from inactive to active tissues (Clausen 1977);in particular, there is a reduction in resting splanchnic flow in order to increase perfusion of the exercising muscle. In the elderly, the resting splanchnic blood flow is reduced to a greater extent than cardiac output, thereby allowing other tissues to be perfused adequately (Bender 1965). The reduction in resting splanchnic blood flow limits the availability of blood flow for redirection to skeletal muscle and the skin during exercise. Older persons do not tolerate high ambient temperatures as well as younger persons (Shock 1977). because decreases in cardiovascular and hypothalamic function compromise heat-dissipating mechanisms (Irion et al. 1984). The dissipation of heat is further compromised by the decrease in fat-free mass and intracellular and total body water, and the increase in body fat. Regular endurance exercise favourably alters coronary artery disease (CAD) risk factors, including hypertension, serum concentrations of triglycerides and high density lipoprotein (HDL) cholesterol, glucose tolerance and obesity (US Department of Health and Human Services 1996). In addition, regular exercise raises the angina threshold (Pollock & Wilmore 1990) by improving coronary circulation to the affected myocardium (Laughlin 1994). Coronary artery disease and graded exercise testing In spite of a downward trend in CAD mortality rates over the past two decades, cardiovascular disease is still the leading cause of death among older North Americans; CAD accounts for 80%of all cardiovascular deaths. Fifty per cent of US citizens aged 70 years or more show coronary artery stenoses of 75% or more at autopsy (Gersh et al. 1983). Disease has many atypical manifestations in the elderly. Silent ischaemia may present as confusion, a disturbance of mobility or dizziness. However, angina pectoris remains the most common presenting symptom of CAD. Dyspnoea is also a common presenting symptom in elderly people who have


either a myocardial infarction or transient ischaemia (Gottliebet al. 1988). As many as 50%of North Americans over the age of 65 years have a diagnostically abnormal resting electrocardiogram (ECG). This may reflect agerelated changes in the heart, such as mild thickening of the ventricular wall and fibrosis of the conduction system. Electrocardiographic observation of deep Q waves, 1-2mm of ST segment depression, and T-wave changes associated with symptoms of ischaemia, remain classical features of clinicallysignificant disease (Gottliebet al. 1988). The aforementioned ECG changes may be interpreted as a false-negative graded exercise test, especially if no further ischaemic changes are noted because the exercise test is terminated after an inadequate peak effort. However, further ST segmental depression to 3-4mm, if superimposed on a baseline resting ECG of 1-2mm depression, may connote ischaemia (Bruce 1985). The baseline resting ECG and the patterns observed during graded exercise testing must be interpreted with knowledge of the confounding effects of ageing and underlying conditions, including CAD, hypokalaemia, hypomagnesaemia, hypercalcaemia and hypoxaemia. Peripheral vascular disease and musculoskeletal disorders may also compromise exercise test performance. Individualization of the graded exercise test (treadmillor cycle ergometer)is important, and protocol selection must depend on the individual's capabilities (Wassermanet al. 1994). The use of radionuclide scintigraphy and thallium in graded exercise testing may improve test sensitivity relative to the ECG alone, particularly at lower levels of intensity. However, some decrease in specificity is found, since other concomitant illnesses may cause abnormalities of coronary perfusion and myocardial function. The gold standard for the diagnosis of CAD remains coronary arteriography.


Kannel et al. 1987) showed a mean increase of 20-25 mmHg between the ages of 36 and 74 years in both men and women. In the same study, the diastolic blood pressure tended to fall in both men and women who were older than 60 years of age. Ageing is associated with a progressive increase in the rigidity of the aorta and peripheral arteries (Dustan 1974; Hollander 1976), due to a loss of elastic fibres, increases in the collagenous materials and calcium deposition in the media. As aortic rigidity develops, the pulse generated during systole is transmitted to the arterial tree relatively unchanged. Therefore, systolic hypertension predominates in elderly hypertensive patients. Because of the rise in diastolic blood pressure with isometric or dynamic resistance exercise (Lewiset al. 1985; McCartney 19981,elderly individuals with poorly controlled hypertension and/or left ventricular dysfunction should limit their strength training and concentrate more on moderate endurance exercise (Sheldahl et al. 1983; MacDougall et al. 1985). Hagberg and Seals (1986) noted that aerobic training resulted in an 8-mmHg reduction in both systolic and diastolic blood pressure in elderly hypertensive subjects. Baroreceptorreflex function Baroreceptorsensitivity decreaseswith age (Gribbin et al. 1971; Pickering et al. 1972). Therefore, rapid adjustment of the cerebral circulation to changes in posture may be impaired in the elderly. Adrenergic blocking agents should be carefully titrated, and blood pressure should be checked in the supine, sitting and standing positions. Regular endurance training does not seem to rectify the gradual deterioration in orthostatic blood pressure regulation with age. Carroll et al. (i995), however, found an improved tolerance of postural changes in elderly men and women who had experienced presyncopal symptoms during head-up tilt prior to endurance training.

Changes in blood pressure Systolic blood pressure usually rises with advancing age (Kannel1976;Amery et al. 1978).Longitudinal data from the Framingham study (Kannel1976;

Renal function Glomerular filtration rate (GFR) and renal plasma flow are well maintained through the fifth decade of



life. Even so, a linear decrease in GFR and renal plasma fiow after the age of 20 years leads to a Ioss of GFR amounting to 4 m1.min-l per decade of GFR, and a loss of renal plasma flow of 35ml.min-' per decade of renal plasma flow (Slack & Wilson 1976). Redistribution of cardiac output during exercise results in an acute yet reversible reduction in GFR and renal plasma flow. There is a need to investigate whether these changes become superimposed on the alterations associated with ageing, adversely affecting renal function. A defect in renal concentrating ability and sluggish renal conservation of sodium intake make elderly patients more liable to dehydration (Papper 1973; Epstein & Hollenberg 1976). Therefore, diuretic agents should be used cautiously, and elderly participants in endurance events should be encouraged to drink plenty of fluids. Hyponatraemia and an oversecretion of antidiuretic hormone further compromise normal salt, water and electrolytehomeostasisin the elderly,a problem that can be compounded by overzealous administration of diuretics.

Renin-angiotensin-aldosterone system Plasma renin activity and plasma aldosterone concentrations decrease with age in normotensive subjects, and values are even lower in elderly individuals with hypertension (Hayduck et al. 1973; Amery et al. 1978; Ogihara et al. 1979). Sympathetic nervous system deterioration with ageing is due, in part, to a decrease in P-receptor reactivity; on the other hand, plasma catecholamine levels are elevated. This is reflected in a gradual decrease of renin-angiotensin-aldosterone activity. As a result, patients have high normal or slightly elevated resting serum potassium concentrations. This tendency is clinically augmented by the administration of potassium-sparing diuretics, P-adrenergic blocking drugs, angiotensin-converting enzyme inhibitors and non-steroidal anti-inflammatory drugs. The hyperkalaemia may be further exacerbated if the patient is an insulin-dependent diabetic with a degree of renal insufficiency. Serum potassium increases as a result of vigorous

endurance exercise. The elderly have some protection against a lethal hyperkalaemiabecause skeletal muscle mass, the major source of intracellularpotassium, is reduced. After endurance training, exerciseinduced increases in potassium are not as large as in the untrained (Braith et al. 1990). Carroll et al. (1994) found that increases in plasma volume and total blood volume following endurance training in men and women 60-82 years old were not associated with changes in resting levels of adrenocorticotrophic hormone, vasopressin, aldosterone, norepinephrine, epinephrine, sodium, potassium or protein. Hepatic function Senescence affects hepatic function, with a decrease in the production of albumin, alteration in its molecular structure or changes in receptor affinity. This affects many drugs that are bound to albumin and it also decreases phase I (oxidation, methylation, hydroxylation) pathways of drug biotransformation (Lowenthal 1990). Exercise, acutely and reversibly, decreases hepatic blood flow, and it is therefore possible that changes in liver function with age and exercise exaggerate certain pharmacodynamic effects.Panton et al. (1995). however, found no effect of aerobic training on propranolol pharmacokineticsin healthy men and women 60-80 years of age. Musculoskeletal changes Manifestations of disease are at times difficult to distinguish from age-related physiological changes (Cummings et al. 1985; Lane et al. 1986). A decrease in muscle mass relative to total body mass starts in the fifth decade of life, and it becomes marked in the seventh decade. This change leads to decreases in muscle strength, muscular endurance, muscle mass and the number of muscle fibres. There is also a selective reduction in type I1 (fast-twitch) skeletal muscle relative to type I (slow-twitch) muscle. Enzymes that regulate glycolytic energy metabolism are reduced more than those enzymes involved in oxidative metabolism. The diaphragm and


cardiac muscle do not seem to incur metabolic changes with age. Hyaline cartilage on the articular surface of various joints generally shows degenerative changes with age. Clinically, this is the fundamental alteration in degenerative osteoarthritis (Lane et a / . 1986). Bone loss is also a hallmark of ageing (Cummings et a / . 1985; Heidrich & Thompson 1987).The rate of bone loss is highly individual, and is greatly augmented in postmenopausal women. A decrease in bone mass (osteoporosis)can reduce body stature as well as predispose an individual to spontaneous fractures. Dynamic weight-bearing exercise slows the decrement in bone mass. Older women are more prone to osteoporosis than older men; this may reflect hormonal differences affecting bone (Lane et al. 1986).

Exercise in preventive geriatrics Health in older people is best measured in terms of function, mental status, mobility, continence and a range of activities of daily living. Primary preventive strategies, including proper nutrition (Wheeler et al. 1993)~can forestall the onset of disease. Whether exercise can prevent the development of atherosclerosis, delay the occurrence of clinical CAD or prevent the evolution of hypertension is at present debatable. But moderate endurance exercise (leisure-time activity or physical training) significantly decreases cardiovascular mortality (Paffenbarger et al. 1986;Leon et al. 1987;Blair et al. 1989; US Department of Health and Human Services 1996). Risk factors associated with CAD are still relevant for the elderly, and should be taken into consideration when planning a preventive regimen (Kannelet al. 1987;Mazzeo et al. 1998).Secondary prevention is aimed at the early diagnosis and treatment of subclinical disease. Endurance exercise can alter the contributions of stress, a sedentary lifestyle, obesity and diabetes to the development of CAD (Kannelet a/. 1987; US Department of Health and Human Services 1996). Tertiary prevention focuses on maintaining or improving functional status after the onset of symptomatic disease; the latter con-


tribution is particularly useful in the elderly (Williams 1984).

Special concerns related to medical clearance for exercise Exercise for the healthy elderly person needs to be addressed in the same manner as that for a younger individual. The US position is that a physician should perform a comprehensive history, physical and mental status examination, basic laboratory studies and a dynamic graded exercise test. Clearance for graded exercise testing and the absolute and relative contraindicationsto exercise are generally similar for elderly and younger participants (Table 38.1). However, there are some special concerns for the elderly individual (Table 38.2). The graded exercise test must include careful attention to changes in cardiac rhythm and changes in blood pressure indicative of ischaemia. Abnormalities in patient response and /or symptomatology are not necessarily signs of disease. Careful

Table 38.1 Contraindications to exercise testing in 3 5 4 4 year-olds. Recent acute myocardial infarction Unstable angina pectoris Uncontrolled hypertension Uncontrolled arrhythmia Symptomatic left ventricular dysfunction Acute myocarditis Acute pericarditis Thrombophlebitis and/or recent pulmonary embolus Tertiary heart block Psychotic mental illness

Table 38.2 Contraindications to exercise testing or training unique to the elderly population. ~


Dementia Frailty Global cerebrovascular accident with no evidence of reversibility Multiple pressure sores Idiopathic gait disturbances and falls Urinary incontinence




observation during recovery from the graded exercise test is critical, since dysrhythmias and sudden changes of blood pressure may occur during this phase. Older patients may need a short, active, walking recovery period after both testing and training sessions in order to decrease venous pooling and to attenuate abrupt increases in intravascular volume that would occur if they were placed promptly supine. Once the formal test recovery period has been completed, the patient should be observed while upright for at least an additional 5min, and the blood pressure should be checked before normal activity is resumed.

Effects of endurance training in the elderly Even though endurance training has a favourable effect on blood pressure (Hagberg 1990; Fagard & Tipton 1994). glucose tolerance (Holloszy et al. 1986; Durstine & Haskell i994), concentrations of HDL cholesterol (Wood et al. 1983; Haskell 19861, cardiovascular mortality (Paffenbarger et al. 1986; Leon et al. 1987; Blair et 01.1989;Sherman et al. 1994; LaCroix et al. 1996), bone density (Smith et al. 1981; Chow et al. 1987; Drinkwater 1993) and other physical and health-related factors, this section focuses on the effects of endurance training on aerobic power and body composition (body mass, percentage fat and fat-free mass). The importance of resistance training and its effect on strength and fat-free mass are also discussed. The important question is no longer whether elderly participants can improve function with exercise, but to what extent training-induced adaptations can improve their fitness and wellbeing. Also, how do their training results compare with the responses of middle-aged and younger participants? Aerobic power (Vo2,,,=)

Vo,,,, decreases with age (Robinson 1938; Dehn & Bruce 1972; Buskirk & Hodgson 1987; Rowel1 & Tipton 1993). This decline can be attributed to a decrease in maximal cardiac output and arteriovenous 0, difference (Ogawa et al. 1992; Stratton et al. 1994; Fleg ef al. 1995). Heath et al. (1981) reported a

5-15% reduction in vo2max for each decade after the age of 30 years. Longitudinal studies on average participants (Kasch & Wallace 1976; Kasch et al. 1985; Astrand & Rodahl1986) and athletes (Pollock et al. 1987,1997;Kohrt et al. 1991) have shown that an active lifestyle (chronic endurance training) significantly attenuates this decline. When such training is maintained, there may be little or no decline in VoZmax over 10-20 years of follow-up evaluations. Thus, it has been concluded that the decline in Pozmax is less than 5% per decade for active individuals (Buskirk& Hodgson 1987). Early studies showed moderate to no improvement in ~ o Z mwith a x endurance training in persons over 60 years of age (Benestad 1965; deVries 1970) (Table 38.3). This led many to suggest that elderly participants did not adapt to endurance training to the same extent as middle-aged and younger subjects. However, the short duration of the Benestad (1965) study and the relatively low intensity of training used by deVries (1970) may have limited the potential for improvements. More recent studies confirm that changes in aerobic power are minimal following light-intensity training (Seals et al. 1984; Hagberg et al. 1989). Recent reviews (Pollock & Wilmore 1990; American College of Sports Medicine (ACSM) 1998; Mazzeo et al. 1998) have shown that aerobic power is increased by i5-30% in most populations following 3-12 months of endurance training. The ACSMs position stand (1998) on The recommended quantity

and quality of exercise for developing and maintaining cardiorespirato y and muscular fitness and flexibility in healthy adults is shown in Table 38.4. Intensity and duration of training are interrelated. Lower-intensity exercise must be pursued for a longer duration in order to elicit results that are comparable to those found with higher-intensity training. Within this framework, the total amount of energy expended appears to be the important factor (ACSM recommends 1050-1260 kJ (250-300 kcal) per exercise session for a 70-kg person). Thus, activities with an intensity similar to moderate walking require a training duration of 40-5omin and 3 0 jogging/running requires 2 ~ ~min. Table 38.3 shows the effects of endurance training on Vozmaxin the elderly. Even though several



Table 38.3 Effect of exercise training on improvement of Vojolmax in the elderly. Mean age (years)



Sidney & Shephard

14 62 8 64 8 65 12 71 100 63

Training (weeks)

Intensity (% H K a X )

Frequency (daysweek-')

Duration (min)

VoZmax (%)


(1978) Cunningham





80 80

zoo/ loo mmHg), headache, bradycardia, flushing, unusual sweating and nasal congestion. EFFECTS OF EXERCISE T R A I N I N G

Arm exercise training using arm ergometry wheelchair ergometry, wheelchair treadmill exercise, free wheeling, swimming and wheelchair sports (e.g. wheelchair basketball, quadriplegic rugby) can all increase arm musculature strength and endurance, improving peak aerobic power by 10-zo%, and enhancing the sense of well-being (Figoni 1997). MEDICATIONS/MANAGEMENT

Management of persons with SCI is complex because of the following complications.

Skin. The risk of pressure sores and abrasions, especially in the areas of the ischial tuberosities, sacrum and coccyx, can be reduced by the use of seat cushions, and avoidance of sitting for long periods without pressure relief. Bone. Persons with SCI have an increased risk of fractures secondary to osteoporosis.Therefore, care must be taken in making transfers from wheelchairs or exercise equipment. Stabilization. Seat-belts or strappings are recommended for those with significant loss of trunk control/balance. Hand-grip. The hands of those with weak or absent grip strength (e.g. quadriplegia) should be secured to ergometer handles with elastic bandages or gloves fitted with Velcro straps.


Bladder. Emptying of the bladder or leg bag before exercise is recommended to avoid bladder distension or overfilling of the bag during activity.Bladder distension may induce autonomic hyperreflexia in persons with lesions above T6. Bowels. A regular bowel maintenance programme will avoid autonomic dysreflexicsymptoms. Hypotension. If the resting blood pressure is 41"C, cooling should commence immediately after the rectal temperature has been measured. Another obvious exception to this rule is cardiac arrest, which occurs uncommonly, but with an unambiguous diagnosis. One reason why treatment is often initiated expeditiously is that the rate of admission to the medical facility can be extremely high. For example, close to 50% of the 14000 competitors in the 90-km Comrades Marathon complete the race during its final hour. If 4% of those subjects collapse (Table 40.2), the average rate of admission during that period will exceed four patients per minute. Admissions are likely to be even faster in the last iomin of the race, when the rate of finishing accelerates further. Another reason why treatment is often initiated without a diagnosis is because of the dogma that dehydration is the sole important cause of athletic collapse. Physicians who hold this belief assume that all collapsed athletes are severely dehydrated



Table 40.2 Percentage of starters treated for 'collapse' after races of different lengths. Type of athletic event Running (21km) Running (42km) Ultratriathlon Cycling Surf-ski paddle marathon (244km) Cross-country skiing

Casualties (% of race starters) 1-5 2-20


5 0.9


Table 40.3 Guidelines for determining the severity of the collapsed athlete's condition. Non-severe



Immediateassessment Conscious Alert Rectal temperature < 4 0 T Systolicblood pressure > ioommHg Heart rate < 100beatsmin-' Specialized assessment Blood glucose 4-10 mmol.l-' Serum sodium 135-148 mmol.l-' Body weight loss 0-5%

and therefore require immediate intravenous fluid. But it is possible to manage high rates of admission to the medical facility only if selected patients who require urgent, sophisticated management receive such treatment. If all collapsed athletes are treated identically, without a triage based on the nature and severity of the condition, it is very difficult to provide sufficient medical staff to cope with the high rates of admission expected when less welltrained individuals run in the heat. Thus, we need a rapid system of triage. The athlete can then be referred to the correct area of the medical facility for immediate and appropriate treatment. Criteria for determining the severity of collapse are described in Table 40.3. The initial assessment is based on the athlete's level of consciousness, and knowledge of where in the race the athlete collapsed. Patients who are seriously ill show alterations in their level of consciousness and almost always collapse before completion of the race, as discussed subsequently.

Unconscious or altered mental state Confused, disorientated, aggressive Rectal temperature > 40°C Systolicblood pressure < ioommHg Heart rate > 100beatsmin-' Blood glucose < 4 or > iommol.l-' Serum sodium < 135 or > 148mmol.l-' Body weight loss > 10% Body weight gain > 2%

Additional helpful information is provided by measurement of rectal temperature, blood pressure and heart rate. In longer races (>25 km) when hypoglycaemia is more likely, a glycometer should be provided. In mass events of much longer duration (>4 h), including ultramarathons and ultratriathlons, equipment for measuring the serum sodium concentration must be available so that potentially lethal exercise-related hyponatraemia can be diagnosed expeditiously. Intravenous fluid therapy should only be considered after a serum sodium concentration > 135mm0l.l-l has been demonstrated.

Diagnostic steps for the optimum management of collapsed athletes who are unconscious If the collapsed athlete is unconscious, the initial differential diagnosis lies between a medical condition not necessarily related to exercise, for example, cardiac arrest, grand ma1 epilepsy, subarachnoid



haemorrhage or diabetic coma, and an exerciserelated disorder, especially heatstroke, hyponatraemia or severe hypoglycaemia. The latter is an uncommon cause of exercise-related coma in nondiabetic subjects.The emphasis in this chapter is not on the diagnosis of medical conditions unrelated to exercise, as the differentiation of these conditions does not usually present a problem to experienced clinicians. The critical issue in the vast majority of cases of collapse is rather the rapid differentiation of the serious from the benign, with the expeditious initiation of correct treatment for the serious conditions. If the patient is unconscious, the crucial initial measurement is rectal temperature, followed by heart rate and blood pressure. If the rectal temperature is >4i°C, the diagnosis is heatstroke, and the patient must be cooled immediately. Patients with heatstroke are also hypotensive and have a tachycardia. If the rectal temperature is 36omin). Over all of these events, the potential power of the muscles depends particularly on fatigue-resistant slow-twitch fibres (STF). Successful road cyclists have a high proportion of STF (7095%).To sustain bicycle exercise for several hours, a motor stereotype is required. This stereotype is developed by prolonged training and is characterized by the dominant recruitment of STF. A stable motor stereotype considerably restricts motor readjustments. The motor variability only increases if FTF are again included in the motor programme by short-term exercise bouts. If cycling training is combined with training to augment explosive power or to maintain and enhance strength, the STF will hypertrophy, increasing cross-sectional area to about 70008000 pm2. Endurance training improves the blood supply of the muscles, because capillarization is increased. E N E R G E T I C B A S I S OF P E R F O R M A N C E

The glycogen stores in the muscles and liver are only sufficient for intensive efforts lasting 90i2omin. In long-term endurance I11 exercise, additional food and fluid intake is necessary during exercise.After I h, an intake of 40-5og carbohydrate is needed. Endurance training increases the triacylglycerol (TG) content of the muscles in road cyclists. A TG content of io0-35og serves as a stable fat reserve. Long-term endurance-trained athletes store more fat in the STF, in droplets located near the mitochondria (Hoppeler 1986). After 3 days of prolonged cycling exercise (4.5h.day'), the TG content of the muscles declines significantly (Brouns et al. 1989). About 50% of the FFA oxidized during exercise are derived from local energy stores (Paul & Holmes 1975).During prolonged exercise, FFA from adipose tissue may account for up to 60% of total energy



Table 58.7 Urea, free fatty acids (FFA) and betahydroxybutyrate (BHB)after cycling competitions. Distance (km) 40*





Urea (mmol.1-')







7.0t 2.2

0.70t 0.12

50 t 20





f 0.25

210 i 30


6 6 9

32 27

7.8i 1.3 9.8k 2.0 8.8t 1.4

1.25 t 0.29 1.50 0.30

450 i 80 -


11.0f 3.0

1.72f 0.60

640 i 520

300 540



needs (Hultman & Sjoholm 1983). Fat metabolism spares muscle glycogen. In cycling training lasting several hours, the availability of carbohydrates is always limited. At first the muscle breaks down amino acids for hepatic gluconeogenesis (Wahren et al. 1971). Knowing that i g of amino acid yields an average of 0.65g of glucose (Poortmans 1988),protein catabolism could account for more than 10%of energy requirements during prolonged exercise, when muscle glycogen is low (Lemon & Mullin 1980).A serum urea concentration of about 7mmol.l-l reveals elevated protein catabolism. The longer the duration of exercise, the greater the increase in serum urea (Table 58.7). The concentration of ketone bodies also rises, because the decreased availability of carbohydrate augments fat metabolism (see Table 58.7). T H E C A R D I O V A S C U L A R SYSTEM

In cycling exercise of several hours' duration, the heart rate lies between 140 and 170beats.min-'. The increase in core temperature caused by the active muscles is of great importance with regard to the increase in heart rate. Due to increasing dehydration, the transport of heat to the body surface is impeded. During dehydration, the blood volume is reduced proportionally less than the loss of body water. The wind protects the body from overheating during cycling. With increasing muscle fatigue, the heart rate rises further. In long-term endurance exercise, only about 70% of Vozmaxis utilized. This means, in road cycling, that an athlete with a body mass of 72kg and a vo2max of 78ml.kg-'.min-' will

utilize approximately 54 ml oxygen.kg-'.min-' at a speed of 37kmh-'.

Assessment of functional capacity Laboratory tests

The most important device for laboratory testing of a cyclist is the cycle ergometer. In most laboratories, the test exercise starts at a power output between 90 and 120W. It is then increased by steps of 3-50 W. Individual steps may last for 2-5min. One test widely used in Germany is described in Fig. 58.7; it may be performed as an incremental test. Important data recorded during the test include heart rate, oxygen intake, pulmonary ventilation and blood lactate concentration. Significant parameters for the assessment of performance capacity include the vozmax, the work rate at a lactate concentration of 2mmol.l-' and the percentage of Vozmaxdeveloped at a lactate concentration of 2mmol.l-'. MAXIMAL


Elite cyclists achieve a $'oZmax of 7580 ml.kg-'.min-', but several years of performanceoriented training are necessary to achieve such high values. A hereditary predisposition to excellence in endurance-based sports also has considerable influence. Depending on the content of the training programme, the Pozmaxmay vary by 8izml~kg-'~min-'over the training year. Only in an ideal case does a cyclist achieve his or her individual




Fig. 58.7 An incremental ergometer test for cyclists.

best vohx value at the time of a world championship. If the proportion of intensive training at the aerobic-anaerobic transition is increased, the vo2mx will drop again (Fig.58.8). One reliable indicator is the power output (W) that can be sustained at a lactate concentration of 2mmol~l-'(PL2).Former calculations,based on concentrations of 3 or 4mmol.P (PL3 or PL4), are too high for road cycling. The determination of PL2 allows a better differentiation of aerobic power than the use of vo2m, alone (Neumann & Schuler 1994). The PL2 is representative of the economy in endurance or strength-endurance training. With an increase in aerobic capacity, the lactateperformance graph (aerobic-anaerobic threshold) shifts to the right (Fig. 58.9). Determination of the maximum lactate concentration at the end of effort gives information on the ability to mobilize anaerobic metabolism. Although track cyclists reach blood lactate values of 10-14mmol.l-~ in laboratory tests, road cyclists reach values of only 6-iommol.l-' lactate. In road cyclists, training reduces the level of anaerobic enzymes (see Table 58.6). The endurance training of cyclists is performed at about 70-80% of Vo, or a blood lactate concentration of less than 2rnmol.l-'.

Field tests An incremental test may be performed under field

conditions. Distances may vary between 3 and 5 km.

The velocities set may increase from 70%, 80%, 85% and 90% up to 100%of individual maximal performance. Between these steps a break of zmin is required to measure the blood lactate concentration. Lactate is measured imin after each bout of effort. As in all progressive tests, four stages are considered a minimum, and five stages are a desirable optimum. FOLLOW-UP



To evaluate the optimal intensity and volume of exercise, fitness level and the degree of recovery, such parameters as heart rate, lactate, serum urea and creatine kinase (CK) are suggested. TRAINING INTENSITY

Depending on the type of event, adaptation to cycling is facilitated by performing training in a combination of aerobic, aerobic-anaerobic and anaerobic metabolic states. The data necessary to control the intensity of exercise are listed in Table 58.8. The heart rate, in particular, is an appropriate parameter for individual differentiation of intensity during aerobic exercise (lactate < 2mm01.1-'). The dominant part of training is performed at the level of basic endurance (see Table 58.8); 70-80% of training (for professionals 30000-35 000 kmsyear-') is performed at this aerobic level. The heart rate is a reliable parameter to control



Oxygen intake
















Power (W)

120 100


















Power (W)

1210 864-

Fig. 58.8 Longitudinal s-tudyof a female cyclist showing Vo,, heart rate and performance at the aerobic-anaerobic transition.






Table 58.8 Follow-up of elite cyclists during the training process.

Basic endurance Distance Speed (km.h-') Pedal frequency (pedalling ratemin-') Energy exchange Measurement of actual

100-25okm 27-32 80-100


Basic endurance and intensity

60-iookm 33-37 95-105 Aerobic-anaerobic


30-5okm 37-40

Short-term endurance intervals

200-1000m 42-50





adaptation in field tests Lactate (mmol.l-') Heart rate (beatsmin-')



4 7




'7 180-200

868 10










$ -2









0 150






















Power (W)

Fig. 58.9 Age-related increase in aerobic capacity in cycling. The lactateperformance graph (aerobic-anaerobic threshold) shifts to the right.

intensity in cycling. 'Polar' heart rate monitors allow permanent measurements of heart rate during exercise and presentation of data as a graph (Fig. 58.10). Because of external influences (wind, profile of the road course, road surface) speed gives an uncertain indication of the intensity of exertion during cycling. P R O T E I N CATABOLISM

Measurements of serum urea can indicate an elevated protein metabolism. Depending on the individual's fitness level and the duration of exercise, the concentration of serum urea is increased at subsequent rest. Training may induce resting serum urea levels of 6-8 mmol.1-'. If the resting serum urea reaches iomrnol.l-' on two successivedays, there is a danger the athlete is overreachingand the training volume must be reduced. A high rate of protein

catabolism impedes the process of adaptation. Immediately after long-term endurance exercise, serum urea concentration may rise by up to 15mmol.1-I (haematocrit 0.43); see Table 58.7. A recovery period of approximately 15h causes a decline in serum urea of 2--3mm0l.l-~. A good method to evaluate the intensity of cycling, especially the effect of heavy training, is to measure the activity of CK. Heavy-intervaltraining can push CK levels to 3-10pmold.l-~.If the level of CK exeeds ic-15 p m o l d - I , the rate of exercise must be reduced or the recovery period prolonged. THE I N F L U E N C E O F R E C O V E R Y

Replenishment of energy stores, especially the glycogen in muscle and liver, is of central significance in cycling training and competition. In prolonged daily training on the road (>18okm) or in



Fig. 58.10 Heart rate and lactate in endurance training of cycling capability. PR, pedalling rate.

tour races, the glycogen stores cannot be replen26 MJ.day-' (5go0-6200kcaEday-') during the Tour ished within 24 h if the athlete remains on a normal de France. The highest energy intake was 32.7 diet. For cyclists the percentage of carbohydrate in MJ.day-' (7780kcal.day-'). The energy intake while their food should be 55-60%,the share of fat 2 ~ ~ 2 5 % cycling was 4 ~ 5 0 % of total daily intake during and of protein 15-18%. Chronic consumption of a the event. high carbohydrate diet facilitates a greater training If environmental temperatures are high, the capacity, whereas chronic consumption of a moderathlete's fluid requirements may reach i o l.day-', ate carbohydrate diet may produce suboptimal with 61 being ingested during a race. Road cycling cycling training and performance capabilities has high requirements of both energy and fluid (Costill & Miller 1980; Costill et al. 1981; Sherman compared with other sports. If the energy consumpet al. 1989,1991; Coyle 1991; Wright et al. 1991; Lug0 tion during normal training does not surpass et al. 1993). ioMJ.day-' (about 4800 kcaI.day-'), recovery may It is reasonable for cyclists to consume a diet that be ensured by consumption of a high carbohydrate contains 8-log carbohydrate.kg body mass-'.day-'. diet. Any higher energy consumption requires an Because liver stores are limited (100-120g), additional intake of glucose concentrates, glucose the blood glucose concentration will decline, and fluids, vitamins and minerals (Table 58.9).One-third fatigue will occur without carbohydrate suppleof carbohydrate requirements may be met from mentation. carbohydrate-rich liquids. The polysaccharides Significant glycogen sparing, as well as superprevent stomach disorders or diarrhoea during compensation within 24 h of recovery, was observed exercise. The amount of carbohydrate needed after consumption of a high maltodextrin/low frucduring cycling is 40-60 g of glucose for each hour of tose beverage (Brouns et al. 1989).If catabolism preexercise. In practice, cyclists consume both liquid dominates, body mass will decrease. Saris et al. and solid forms of carbohydrate during cycling. (1989) found a beverage energy intake of 25Carbohydrates that are ingested without fluid






Table 58.9 Daily intake of energy, protein, carbohydrate, fat and micronutrients from food and energy-containing food supplements, and the percentage intake during the Tour de France (from Saris et al. 1989). Cyclists (n = 5)

Mean daily intake (fs.d.)

Energy (MJ) Protein (g) Carbohydrate, simple (g) Carbohydrate, complex (g) Fat (g) Calcium (mg) Iron, haem (mg) Iron, non-haem (mg) Vitamin B, (mg) Vitamin B, (mg) Vitamin B, (mg) Vitamin C (mg) Water (1)

24.3 5.3 217 f 47 463 159 386 100 '47 f 39 3044 f 1000 5.3 f 1.6 24.9 k 9.4 2.4 2 0.7 5.0 k 1.6 2.4 f 0.7 158 f 146 6.7 f 2.0

* * *

Intake during race (%) 49 35 61 55 39 60 1

55 44 61 46 29 61

*Mean body mass was 69.2 kg and 68.9kg, before and after the race respectively.

are not digested as quickly. The blood glucose begins to decline after about 2h of training exercise. Carbohydrate ingestion must begin before there is a significant decline in the body's carbohydrate reserves. If only 20g of glucose.h-' are taken, a marked gluconeogenesis and ketogenesis may develop and hypoglycaemic reactions may occur. The majority of published studies have reported that pre-exercise carbohydrate feeding improves cycling performance capabilities (Gleeson et al. 1986; Neuffer et al. 1987; Sherman et al. 1989, 1991; Wright et al. 1991). Between 2 and 5 g of liquid carbohydrate9kg body mass-' was consumed between 1

and 4h before exercise. Pre-exercise carbohydrate feeding did not improve performance, but it increased the rate of carbohydrate oxidation and impeded the mobilization of FFA (Essig et al. 1980; Sasaki et al. 1987; Sherman 1991). In the postexercise recovery phase, carbohydrate ingestion (1-1.5 g k g body mass-') stimulates glycogen synthesis. When carbohydrate is consumed immediately after exercise and at 2-h intervals thereafter, the rate of muscle glycogen synthesis is 6rnmol.kg-'.h-' (Blom et al. 1987; Ivy et al. 1988a, b; Reed et al. 1989).Carbohydrate ingestion should begin immediately after glycogen-depleting endurance exercise.

References Astrand, E O . & Rodahl, K. (1986) Textbook of WorkPhysiology. McGraw-Hill Book Company, New York. Blom, P.C.S., Hostmark, A.T., Vaage, O., Kardel, K.R. & Maehlum, S. (1987)Effect of different postexercise sugar diets on the rate of glycogen synthesis. Medicine and Science in Sports and Exercise 19, 491-496. Brouns, F., Saris, W.H.M., Beckes, E. et al. (1989)Metabolicchanges induced by sustained exhaustive cycling and diet manipulation. International Journal of Sports Medicine 10,S49-S62. Costill, D.L. &Miller,J.M. (1980)Nutrition

for endurance sport: carbohydrate and fluid balance. International Journal of Sports Medicine I, 2-14. Costill, D.L.,Sherman, W.M.,Fink, W.J., Maresh, C., Whitten, M. &Miller,J.M. (1981)The role of dietary carbohydrates in muscle glycogen resynthesis after strenuous running. American Journal of Clinical Nutrition 34,1831-1836. Coyle, E.F. (1991) Timing and method of increased carbohydrate intake to cope with heavy training, competition and recovery. Journal of Sports Science 9 (SUppl.),29-52. Essig, D., Costill, D.L. &van Handel, P.J.

(1980)Effects of caffeine ingestion on utilization of muscle glycogen and lipid during leg ergometer cycling. International Journal of Sports Medicine 1, 86-90, Gleeson, M., Maughan, R.J. & Greenhaff, P.L. (1986)Comparison of the effects of preexercise feedings of glucose, glycerol and placebo on endurance and fuel homeostasis in man. European Journal of Applied Physiology 55,65-76. Hagberg, J. & McCole, S. (1996)Energy expenditure during cycling.In: Burke, E.R. (ed.)High-Tech Cycling, pp. 167-184. Human Kinetics, Champaign, IL. Hoppeler, H. (1986)Exercise-induced


ultrastructural changes in skeletal muscle. International Journal of Sports Medicine 7,187-204. Hultman, E. & Sjoholm, H. (1983)Substrate availability In: Knuttgen, H., Vogel, J.A. & Poortmans, J. (eds) Biochemistryof Exprcise, pp. 6375. Human Kinetics, Champaign, IL. Ivy, J.L.,Katz, A.L., Cutler, C.L., Sherman, W.M. & Coyle, E.F. (1988a) Muscle glycogen synthesis after exercise: effect to time of carbohydrate ingestion. Journal of Applied Physiology 64,148+1485. Ivy, J.L., Lee, M.C., Brozinick, J.T.&Reed, M.J. (1988b)Muscle glycogen storage after different amounts of carbohydrate ingestion. Journal of Applied Physiology 65,2018-2023. Lemon, P.W.R. & Mullin, J. (1980)Effect of initial muscle glycogen levels on protein catabolism during exercise. Journal of Applied Physiology 48,624-629. Lugo,M.J., Sherman, W.M., Wimer,G.S. & Garleb, K. (1993)Metabolicresponses when different forms of carbohydrate energy are consumed during cycling. International Journal of Sport Nutrition 3, 398-407, Medbe., J.I. & Tabata, I. (1989)Relative importance of aerobic and anaerobic energy release during short-lasting exhaustive bicycle exercise.Journal of Applied Physiology 67,1881-1886. Neuffer, P.D.,Costill,D.L., Flynn, M.G., Kirwan, J.P.,Mitchell, J.B. & Houmard, J. (1987)Improvements in exercise perfor-

mance: effects of carbohydrate feedings and diet. Journal of Applied Physiology 63, 983-988. Neumann, G. & Schuler, K.-P. (1994) SportmedizinischeFunktionsdiagnostik. J.A. Barth, Leipzig. Neumann, G., Pf&xer, A. & Berbalk, A. (1998) Optimales Ausdauertraining. Meyer & Meyer, Aachen. Paul, P. & Holmes, W.L. (1975) Free fatty acid and glucose metabolism during increased energy expenditure and after training. Medicine and Science in Sports and Exercise 7,176-184. Poortmans, J.R.(1988) Protein metabolism. In: Poortmans, J.R. (ed.) Principles of Exercise Biochemistry. Med Sport Sci, Vol. 27, pp. 164-193. Karger, Basel. Reed, M.J.,Brozinick, J.T., Lee, M.C. &Ivy, J.L. (1989)Muscle glycogen storage postexercise: Effect of mode of carbohydrate administration. Journal of Applied Physiology 66,720-726. Sahlin, K. (1986)Metabolicchanges limiting muscle performance. In: Saltin, B. (ed) Biochemistryof Exercise VI,pp. 232343. Human Kinetics, Champaign, IL. Saris, W.H.M., van Erp-Baart, M.A., Brouns, F., Westerterp,K.R. & ten Hoor, F. (1989)Study on food uptake and energy expenditure during extreme sustained exercise: the Tour de France. International Journal of Sports Medicine 10, s25-s31. Sasaki, H., Maeda, J., Usui, S. & Ishiko, T. (1987)Effect of sucrose and caffeine


ingestion on performance of prolonged strenuous running. International Journal of Sports Medicine 8,261-265. Sherman, W.M. (1991) Carbohydrate feedings before and after exercise. In: Lamb, D.R. &Williams, M.H. (eds)Perspectives in Exercise Science and Sports Medicine: Ergogenics, pp. 1-34. Brown & Benchmark, Indianapolis. Sherman, W.M., Brodowicz, G., Wright, D.A.,Allen, W.K.,Simonsen, J.C. & Dernbach, A.R. (1989)Effects of 4-hour preexercisecarbohydrate feedings on cycling performance. Medicine and Science in Sports and Exercise 21,598-604. Sherman, W.M.,Peden, M.C. &Wright, D.A. (1991)Carbohydrate feedings I hour before exercise improve cycling performance. American [ournal of Clinical Nutrition 54,86&870. Swain, D.P. (1994)The influence of body mass in endurance bicycling. Medicine and Science in Sports and Exercise 26, 58-63. Wahren, J., Ahlborg, G., Fehling, P. & Jorfeld, L. (1971)Glucose metabolism during exercise in man. In: Pernow, B. & Saltin, 8.(eds)Muscle Metabolism during Exercise, pp. 17y203. Plenum Press, New York. Wright, D.A., Sherman, W.M. & Dernbach, A.R. (1991)Carbohydrate feedings before, during, or in combination improve endurance performance. Journal of Applied Physiology 71, 1082-1088.

Chapter 59 The Triathlon GORDON G . SLEIVERT

A triathlon event requires the uninterrupted and sequential completion of swimming, cycling and running events. There are two major classifications of triathlon: the 'Olympic' distance and the ultra-endurance or 'Ironman' triathlon. The Olympic triathlon usually comprises a 1.5-km swim, a 40-km cycle and lo-km run, whereas the Ironman triathlon requires competitors to complete nearly 4km of swimming, about 180km of cycling and (usually) 42.2km of running (a full marathon). Completion times are generally in the range of 2-4 h for the short-course event and 8-14h for ultraendurance triathlons. This chapter reviews the demands of training and competition for these two classifications of triathlon and discusses the factors that impact on or are related to triathlon performance.

Demands of the triathlon The demands of the triathlon differ from other endurance events, because of the sequential performance of three different modes of exercise, using different muscle groups and differing amounts of muscle mass in different postures and markedly different environments. Although each phase of the triathlon relies on aerobic rephosphorylation of ATP, the percentage of vo2max that can be sustained and the challenge of maintaining cardiovascular and thermoregulatory homeostasis while exercising at a maximal sustainable pace differ between exercise modes. These differences are accentuated in the triathlon, because of the sequential nature of the swim-cycle-run event.


Thermoregulation Kreider et al. (1988a) were the first to investigate the thermoregulatory responses to triathlon competition. They studied nine male triathletes who performed a simulated short-course triathlon, comparing their physiological responses to a control cycle and run. The water temperature was maintained at 23"C, and the air temperature during the cycling and run segments was maintained at 29°C. Postswim, the core temperature averaged 37.8"C; values continued to rise throughout the triathlon cycle, and rose more steeply during the run, to average approximately 39.6"C by the end of the triathlon. In the light of this final core temperature, it is not surprising that five out of the nine triathletes who were studied experienced heat complications. It therefore appears that thermoregulatory homeostasis can be a major challenge for competing triathletes. The run phase probably provides the biggest heat challenge, since a large muscle mass is actively producing heat, and the convective and conductive cooling, available in cycling and swimming, respectively, are much reduced. Although water is an excellent heat sink, many triathletes wear a wetsuit to increase their buoyancy and decrease hydrodynamic drag (Toussaint et al. 1989). This may improve swimming performance (Parsons & Day 1986),but it also has the potential to impair performance in subsequent triathlon segments, since the insulative effects of neoprene potentiate exercise-induced hyperthermia. Several studies have examined whether a wetsuit adversely affects thermal homeostasis. Trappe et al. (1995)


studied the thermoregulatory responses of nine competitive triathletes and/or swimmers who were swimming at water temperatures of 20.1, 22.7 and 25.6"C with and without full-body 3-4-mm-thick wetsuits. The subjects swam for 3omin, had a 3-min transition and then rode a cycle ergometer for 15min. There were large individual variations in the core temperature response. On average, the core temperature rose similarly whether or not a wetsuit was worn at all three water temperatures. The wetsuit maintained skin temperature of the trunk 3-4°C warmer than when the subjects were in the swimsuit condition, and at the two cooler water temperatures several swimmers demonstrated a drop in core temperature when wearing only a swimsuit. This drop was attenuated or prevented when wearing a wetsuit. At the warm water temperature of 25.6"C, the wetsuit did not cause greater hyperthermia than a swimsuit alone. In fact, the core temperature rose to a greater extent in the swimsuit versus the wetsuit condition. This is a surprising finding; the researchers suggested that it could be due to a large peripheral vasoconstrictor response in the swimsuit condition, decreasing the core to skin temperature gradient to a greater extent than when a wetsuit was worn. This would impair heat loss and accelerate the rise in core temperature. Cycling in an air temperature of 21°C after the swim caused a transient drop in body temperature; this is probably explained by warm blood being circulated through a cold periphery (Webb 1986). Thus, the swim essentially acts as a precooling manoeuvre, and precooling has previously been shown to enhance endurance performance (Lee & Haymes 1995; Booth et al. 1997).It is possible that the thermoregulatory advantages of cooling down during a swim confer transient benefits later, in the other segments of the triathlon, and the swimsuit condition might achieve a greater precooling effect. Alternatively, the performance gains from using a wetsuit may be more worthwhile, since the swimmers covered a 188-m greater distance (a 9.8% improvement) and also had longer stroke distances when wearing a wetsuit versus a swimsuit. Another recent study by the same research group has more completely examined the influence of a wetsuit on body heat storage during the triathlon.


Kerr et al. (1998) studied five well-trained male triathletes who randomly completed two simulated triathlons (comprisinga 30-min swim, a 40-km cycle ride and a lo-km run). The only difference between the two triathlons was that in one subjects wore a 3-4-mm-thick neoprene wetsuit that covered the torso and legs during the swim. The water temperature averaged 25.4"C; environmental conditions for the cycle and run were hot, and maintained at 31.9 o.i°C and 65% relative humidity. Although the skin temperature was warmer during the wetsuit swim, by 15min into the cycling segment there were no differences between the swimsuit and wetsuit conditions in skin, core or mean body temperatures. Therefore, even in relatively warm water and a hot air environment, a wetsuit worn during swimming does not compromise thermoregulation in the latter phases of the triathlon. However, the swims undertaken in this study were controlled to occur at identical paces and the metabolic cost of swimming in the wetsuit appeared to be less than when wearing the swimsuit. It is likely that, in actual competition, the triathlete would swim faster in the wetsuit condition and therefore more heat would be stored. This distinction could be particularly relevant for triathletes with higher body fat percentages who do not dissipate heat easily. Individual differences in body composition must be considered when deciding whether to wear a wetsuit or not.


Dehydration Kreider et al. (1988a) monitored dehydration and fluid consumption during a simulated triathlon. Subjects ingested 56% and 72% more water during triathlon cycling and running, respectively, than in control runs or cycles. Despite the greater water intake, the triathletes had dehydrated by 3% of body mass at the end of the triathlon and a half of this dehydration occurred during the running segment of the event. Consequently, stroke volume decreased and heart rate increased during both the cycling and running segments to a significantly greater extent than was seen during control cycling and running. However, the cardiac output was significantly lower than control only during the triathlon cycle. This could reflect the lower mean



cycling power output that occurred in the triathlon. Similar information was reported by Farber et al. ( q g i ) ,who studied an Ironman triathlon event over 2 years; they observed that dehydration occurred progressively throughout the event, despite allowing competitors free access to food and fluid. The swim occurred in a water temperature of 21-22OC and dehydration averaged 0.9% of pretriathlon body mass by the end of the 2.4-mile (3.85-km) swim. The land temperature was between 19 and 26°C and the relative humidity was between 50 and 96%. Triathletes dehydrated by a further 0.6% of body mass over the 112-mile (180-km) cycling segment and by yet another 2.1% of body mass during the 42.5-h run.By the end of the triathlon, the competitors had lost a total of 3.6% of body mass. These patterns of dehydration reflect the difficulty of hydrating the competitor adequately during all phases of the event. Little hydration probably occurs during the swim, whereas cycling may be the easiest phase in which to consume fluid. The rate of dehydration was greatest during the running phase, reflecting the whole-body nature of this exercise mode driving sweat rate; moreover, triathletes perhaps find it difficult to consume adequate volumes of fluid when running, due to the gastric discomfort that may be associated with impact exercise and a full stomach. When triathlons are held in hotter climates, the extent of dehydration would probably be markedly greater and the consequences of dehydration more severe. Conversely,there have been documented cases of triathletes consuming too much fluid during a race, and becoming hyponatraemic (see Chapter 40). Most recently, Speedy et al. (1999) reported the results of a large prospective study that examined changes in body mass and plasma sodium concentrations in those completing the Ironman race. They found that 18%(58) of race finishers were clinically hyponatraemic (serum sodium < 135mmol.l-'), but only 31% were symptomatic and sought medical care. A small percentage of the hyponatraemic athletes had severe hyponatraemia (serum sodium < 130mmol-l-~).Three-quarters of these individuals either maintained or gained body mass over the triathlon, suggesting that a primary aetiology of hyponatraemia may be an excessive fluid consump-

tion, rather than a large salt loss through excessive sweating. This prospective study also reported that female triathletes were at a higher risk of hyponatraemia, possibly because they sweat less and are more likely to maintain body mass during the race. Acute effects of sequential exercise The sequential completion of swimming, cycling and running stages presents the triathlete with unique demands when compared to endurance specialist sports. For example, many triathletes experience difficulty in the early stages of the run after the cycle-run transition, but the reason for this is unknown. Quigley and Richards (1996) studied 11 competitive biathletes and triathletes in order to determine whether previous exercise disrupted running mechanics; they found that running mechanics were unchanged after either previous running or cycling. This finding was replicated in a more recent study of seven male competitive triathletes who performed a 10-km run either with or without 40km of previous cycling (Hue et al. 1998). One study has, however, reported greater forward trunk lean and decreases in stride length (7%)after previous swimming and cycling.These biomechanical changes were attributed primarily to local muscle fatigue, but no single kinematic variable could account fully for the decrease in running economy observed in the triathlon run compared to the control run (Hausswirth et al. 1997). These studies suggest therefore that the feeling of awkwardness experienced in running immediately after cycling may be due to changes in a combination of motor control, physiological and biomechanical factors. For example, triathletes entrain their breathing rate to the rhythm of exercise, and this has a small effect on ventilatory efficiency (Bonsignore et al. 1998).Since cycling cadence generally occurs at 1.5-2.0Hz and running cadence is slower at 1.01.25Hz, the entrainment of breathing and ventilatory efficiency may be disrupted in the early stages of a run after cycling. It is possible that with regular transition training (BRICK training), which involves two or more modes within a single session, triathletes may develop strategies to entrain their breathing quickly with stride rate, and ventilatory


efficiency may be improved. This remains to be confirmed. Economy may change throughout the course of an event. Kreider et al. (1988a) observed that compared to a control run, triathlon running at an identical pace was performed at a higher core temperature, with a significantly lower stroke volume and mean arterial pressure. The triathlon run required a significantly larger oxygen consumption, ventilation and heart rate, a finding replicated in several recent studies (Guezennec et al. 1996; Hausswirth et al. 1996,1997; Hue et al. 1998).Besides biomechanical factors, other changes known to occur over the course of a triathlon have been suggested as decreasing the economy of running after previous cycling and swimming. Possibilities include progressive muscle damage, glycogen depletion and a resulting increase in fat metabolism, and thermal stress and dehydration leading to increased cardiac and ventilatory work (Kreider et al. 1988a; Farber et al. 1991; Guezennec et al. 1996; Hausswirth et al. 1996,1997).With these problems in mind, it has been suggested that detrimental changes in economy can be minimized by proper pacing strategies, utilizing a progressively increasing intensity of effort as the race progresses (Kreider et al. 1988b; OToole & Douglas 1995). De Vito et al. (1995) examined the impact of residual fatigue from one exercise mode on the performance of another by measuring the treadmill Voaax in a rested state and after completion of the first two segments of a triathlon (1.5km swimming, 32km cycling). They found that the Vo2max decreased from 69 to 64 rnl.kg-'.min-'. The oxygen consumption at the running ventilatory threshold (v,)was also a smaller percentage of Vo2max(74.3 versus 84.6%) after completion of the partial triathlon, indicating that the ability to sustain a high percentage of voaax in running is impaired after completing the swimming and cycling sections of a triathlon. In addition, the heart rate at the V , was lower after previous exercise, which has implications for setting training and competition pace. Regular exposure to sequential exercise in training as a means of simulating the physiological responses experienced in a triathlon may be important in this respect.


Triathlon training The triathlete must train regularly in the three exercise modes of swimming, cycling and running. The reported volumes and intensities of training in each mode are diverse, depending upon the competitive level of the triathlete and the type of triathlon for which training is being undertaken. Training and performance An early study of 65 Olympic distance triathletes showed strong systematic relationships between training practices and triathlon performance (Zinkgrafet al. 1986).These triathletes averaged 4-5 workouts in each exercise mode per week, and the specificity of their training was evident, since the training distance for each exercise mode was correlated most strongly with performance in the matching phase of the triathlon. Additionally, the fastest triathletes of the sample studied had completed the greatest number of triathlons, trained for more months prior to the race, had longer single workouts and engaged in higher training volumes. OToole (1989) was one of the first to report on training practices of Ironman triathletes. She reported data on 323 Hawaii Ironman participants. In general, these triathletes prepared themselves seriously for at least 8 months before the event, training approximately 21 h.week-'. Swim training took place on average 3.5h.week-', bicycle training 12h.week-' and run training about 6 h.week-'. Swimming was spread over 3-5 days.week-', cycling 4-5 days.week-' and running 4-6 daysweek-'. This necessitated multiple workouts each day. Approximately 46% of the swim training was interval based, whereas 80% of the cycle and run training was continuous in nature. When relating training practices to finishing times, it appeared that bicycle and run training volumes were most important to a fast finish time, and that 11 km of swimming, 320km of cycling and 65km of running per week were the minimum volumes required for any triathlete to finish in a faster time than 10.5h. Hendy and Boyer (1995) used a questionnaire to collect information on training behaviour from 203




Ironman competitors and 421 competitors in an Olympic distance triathlon. As previously reported, the training behaviour was diverse, but those competitors training for the Ironman had greater average training volumes (10, 290, 57 km.week-') than the Olympic distance competitors (8, 198, @krn.week-') in swimming, cycling and running, respectively.In contrast to the previous studies that had observed training volume to be most strongly correlated with triathlon performance, Hendy and Boyer (1995) reported that training intensity in the same exercise mode was the best predictor of swimming and running performance for both Olympic and Ironman triathlons, reinforcing the importance of training specificity. Cycling performance over either the Olympic or the Ironman distance could not be predicted very well from training data. The researchers suggested that this could be because cycling is the longest of the triathlon stages, and it offers a longer time for external factors to influence performance. Alternatively, the quality of the bicycle can have a large impact on performance, and now that drafting is allowed during the cycling stage, this will further attenuate the strength of any relationship between cycling training and triathlon cycle performance.

Training and injuries It seems logical that with the high training volumes reported for triathletes, susceptibility to overuse injuries would be high. OToole et al. (198913) reported training and injury statistics in a group of 95 Ironman competitors. There was wide variability in triathlete training practices, but on average the sample trained 210, 684 and 35omin.week-' in swimming, cycling and running, respectively, spending 3-5 days.week-' in each exercise mode. A massive 90.3% of these competitors had had at least one injury during the previous year. The most common site of injury was the back, although many triathletes (72%)reported multiple injury sites that included the lower limbs. Surprisingly, no training variables were related to injury. Ireland and Micheli (1987) reported on the training practices and injury patterns of 168 recreational and competitive triathletes who had previously


completed a mean of six triathlons. These triathletes trained an average of i~h.week-',but the range was large (5-60h). Similar to the findings of OToole (1989), most training time was spent on the bicycle (7.5h.week-', 44%), followed by running (6h.week-', 35%) and swimming (3.5 h.week-', 21%).At least 66%of the triathletes studied had sustained at least one injury; the lower extremity was involved in 85% of these injuries, most of which were due to overuse. Running training accounted for the bulk of the overuse injuries (78%),but no training variables were related to either the occurrence or the number of injuries. A more recent study of 155 British triathletes whose normal competitive distance ranged from a sprint to a full Ironman event reported relatively low training volumes for sprint triathletes of 7h.week-', the corresponding figures for an 8-week period being ioh.week-' for half and full Ironman competitors (Korkia et al. 1994).For both the sprint and the ultra-endurance competitors, about half the training time was spent cycling, with the remaining training time split equally between running and swimming. Thirtyseven per cent of the sample sustained an injury over the 8 weeks of training that were studied, with 41% of injuries being diagnosed as overuse and 86% of the injuries occurring in the lower limb. Sixty-five per cent of the injuries occurred while running. Similar to previous studies, however, there was no association between the extent of training practices and injury. Several other studies have shown weak associationsbetween training practices and injury. Williams et al. (1988) surveyed 332 triathletes competing in a variety of events ranging from Olympic to Ironman distance triathlons. The mean training volumes were 7, 157 and 47 kmweek-' in swimming, cycling and running exercise modes, respectively. Fifty per cent of this sample reported injuries, and 20% of these injuries were of sufficient severityto cause cessation of training or withdrawal from an event. The principal sites of injury were the knee (22%), lower back (17%) and foot or ankle (14%). The majority of injuries were thought to arise from run training (53%),although there was no significant correlation between the run training volume and the likelihood of injury. Significant but weak correlations were obtained between the


weekly training distances in cycling and the number of injuries, and between the number of years involved in triathlons and the number of injuries. Taken together, these training variables only accounted for 4% of the variance in occurrence of injuries. Manninen and Kallinen (1996) surveyed 92 Japanese triathletes retrospectively. This sample trained on average 14.6heweek-', spending 29, 38 and 33% of their triathlon training time in swimming, cycling and running, respectively; the majority (79%) of their training was performed at or below the anaerobic threshold. Seventy-two per cent of the triathletes sustained at least one trainingrelated musculoskeletal injury in the previous year, with most of the injuries occurring in the lower limbs, primarily the knees. Similar to previous studies, running was the most common perceived cause of the lower limb injury. Thirty-twoper cent of the triathletes surveyed had also experienced lower back pain in the previous year, and there was some indication that the average weekly training load was associated with the incidence of lower back pain. Neither cycling position nor the use of triathlon aerobars was associated with back pain, but nevertheless the authors suggested that cycling may cause most of the lower back pain in triathletes, since there was an almost significant difference in average weekly cycling time ( P = 0.065) between those triathletes with and those free of lower back pain. This agrees with the findings of Williams et al. (1988) that a high cycling volume may relate to injury risk. Vleck and Garbutt (1998)studied the training and injury characteristics of 12 elite, 17 developmental and 87 male British club triathletes, using a 5-year retrospective questionnaire. The elite (15.6h) and developmental (13.1h) triathletes trained more hours per week than the club-leveltriathletes (5.3h). For example, the elite group spent 5.6, 6.3 and 3.7 h.week-' swimming, cycling and running, respectively, compared to the 2.3, 4.4 and 2.4 h.week-' average time that the club triathletes spent in training in the same exercise modes. Despite differences in training behaviour, the prevalence of injuries did not differ between ability groups. Between 56 and 75% of the triathletes suffered an overuse injury over the time studied, and the


number of injured sites ranged from 1.9 to 2.9, with lower extremity injuries accounting for 43-48% of the total number of overuse injuries. The most common sites of injury were the knees and lower back, although multiple sites of injury were common. Additionally, each group identified run training as responsible for the greatest fraction of injuries. When the groups were combined, the number of overuse injuries sustained was significantly related to a variety of indices of training volume and intensity. Injuries in one discipline, for example running, were correlated not only with the training volume in that discipline but also with the training volume in other disciplines. As Vleck and Garbutt (1998) suggest, this may reflect simply that those with high training volumes in one mode are likely to have high training volumes in other modes, or it may indicate that the recovery interval between disciplines is an important injury risk factor. It can be concluded from these studies that the high volume of training required to excel in the triathlon predisposes these athletes to overuse injuries. In particular, lower limb injuries appear to be related to run training volume and back injuries may be related to cycle training volume. However, the interaction effect of training in three exercise modes on the incidence of injuries is not well understood, since training variables do not generally relate strongly to injury. As first suggested by Williams e f al. (19881, it may not be training volume per se that leads to injury in triathletes, but rather rapid increases in training volume. Further prospective studies of this issue are required.

Characteristics of triathletes and their relationship to performance Physical characteristics Elite male triathletes (OToole et al. 1987; Horrell 1989; Travill ef al. 1994; Bunc ef al. 1996; Vafier et al. 1996; Hoogeveen & Schep 1997; Vleck & Garbutt 1998) are similar in height to specialist cyclists (Burke et al. 1977; Neumann 1992; Coyle e f al. 19881, but tend to be taller than specialist runners (Pollack 1977; Conley & Krahenbuhl1980;Tittel & Wutsherk 1992) and shorter than specialist distance swimmers



(Holm& et al. 1974; Tittel & Wutsherk 1992; Travill et al. 1994) (Fig.59.ia). There seems to be little difference in height between Ironman and Olympic triathlon competitors. Female Ironman triathletes (OToole et al. 1987) tend to be taller than their Olympic triathlete counterparts (Leake & Carter 1991; Laurenson et al. 1993); both groups of triathletes are taller than elite female endurance runners (Wilmore & Brown 1974; Tittel & Wutsherk i992), but similar in height to elite cyclists (Astrand & Rodahl1986; Neumann 1992)and swimmers (Tittel & Wutsherk 1992;Travill et al. 1994) (Fig.59.ib). Taller triathletes may have an advantage over

shorter triathletes, since longer limbs offer greater leverage. Long limbs allow a greater running stride and a longer swimming stroke, with lower stride and stroke frequencies for a given velocity. Longer stride lengths are more economical than a high stride frequency,as demonstrated by oxygen uptake and blood lactate measurements (Tittel & Wutsherk 1992). Conversely, an excessive height may be a disadvantage. Increased height is associated with an increased body surface area, and the greater the surface area, the greater resistance opposing movement of the athlete (Neumann 1992; Tittel & Wutsherk 1992). Air resistance is the major component

Fig. 59.1 Weighted mean height values for male (a) and female (b) elite Olympic and Ironman triathletes compared to that of elite 1500/800-m swimmers, road cyclists and distance runners. Mean height values for each population were generated by taking a mean of the means weighted against the sample size of athletes used in each study referenced in the text, using the equation: X = Api (ni.xi)/N where: X i s the mean of the means, Api is the sum of sample size weighted means, ni is the sample number in each study, xi is the mean value for each study and N is the sum of ni for all studies.


of resistance to movement during level cycling (Neumann 1992; Chapter 581, and it is also a significant form of resistance during running (Astrand & Rodahl1986). Elite male triathletes (OToole et al. 1987; Horrell 1989; Travill et al. 1994; Bunc et al. 1996; Vallier et al. 1996; Hoogeveen & Schep 1997; Vleck & Garbutt 1998) have a similar body mass to elite cyclists (Burke et al. 1977; Coyle et al. 1988; Neumann i992), but weigh less than swimmers (Holm& et al. 1974; Tittel & Wutsherk 1992; Travill et al. 1994) and more than runners (Pollack 1977; Conley & Krahenbuhl 1980; Tittel & Wutsherk 1992) (Fig. 59.2a). Surpris-

Fig. 59.2 Weighted mean mass values for male (a) and female (b) elite and average (all triathletes) endurance and ultra-endurance triathletes compared to that of elite 1500/soO-m swimmers, road cyclists and distance runners. Weighted mean values were generated as detailed in Fig. 59.1.


ingly, elite ultra-endurance male triathletes have a larger body mass than their Olympic distance counterparts. Similar patterns are evident in female triathletes (Fig. 59.2b), with the elite Ironman females (OToole et al. 1987) weighing more than their Olympic triathlete counterparts (Leake & Carter 1991; Laurenson et al. 1993). cyclists (Astrand & Rodahl 1986; Neumann 1992) and runners (Wilmore & Brown 1974; Tittel & Wutsherk i992), but having similar weights to elite swimmers (Tittel & Wutsherk 1992; Travill et al. 1994). The body composition may influence performance in swimming, cycling and running differen-



tially. In swimming, extra body fat may improve buoyancy, thus helping to reduce hydrodynamic drag (Gullstrand 1992; Chapter 55). In contrast to swimming, where hydrodynamic drag is the greatest force to overcome (Gullstrand 1992; Tittel & Wutsherk i992), gravity is the major force to overcome during running. As a result, excess weight is detrimental to running performance (Deitrick 1991; Houtkooper & Going 1994). However, excess weight may not be detrimental to weight-supported cycling. In cyclists, the increase of frontal surface area with an increase in body mass is offset by an increased absolute power output, as long as the extra mass is muscle (Neumann 1992). None the less, the influence of body mass on cycling performance will depend somewhat on the topography of the cycling course. A hilly route will substantially increase the effect of gravity on the cyclist (Neumann i992), which may disadvantage the heavy triathlete (Deitrick 1991). Elite male endurance and ultra-endurance triathletes typically carry between 6 and 11%body fat (Holly et al. 1986; Travill et al. 1994; De Vito et al. 1995)~whereas elite female triathletes have 1218% body fat (OToole et al. 1987; Dengel et al. 1989; Schneider & Pollack 1991). Deitrick (1991) found that 'heavy-weight' triathletes (90.9kg) compared to 'typical' triathletes (66.6 kg) were taller, had a higher body fat content, a lower running economy and a lower vojmax, shorter treadmill performance times in an incremental run to exhaustion and a lower power/ weight ratio on the bicycle ergometer. The heavier triathletes also trained less than their typical counterparts. Thus excess weight, particularly an excess of fat, is probably not beneficial to triathlon performance. The buoyancy advantages that fat can offer in the swimming phase can be largely offset by the use of a wetsuit, thereby eliminating the possible advantage that fatter individuals may have while swimming. Thus, it would appear that successful triathletes should be characterized by a blend of the physical traits observed in specialist endurance swimmers, cyclists and runners. This does not imply that all successful triathletes will have the same shape and size, but it does indicate that an individual's physi-

cal attributes can help to predict in which exercise mode a triathlete is most likely to be successful, or in which mode they have the potential to improve. Similarly, triathletes with different physical attributes may excel on one type of course (e.g. flat) but not be suited to another (e.g.hills), or they may excel in one exercise mode at the expense of the other two. Physiological characteristics A E R O B I C P O W E R (POzmax)

High levels of aerobic power generally characterize successfulendurance specialists in swimming (Holmer ef al. 1974; Gullstrand i992), cycling (Burke et al. 1977; Stromme et al. 1977; Burke 1980; Astrand & Rodahl 1986) and running (Wilmore & Brown 1974; Pollack 1977; Davies & Thompson 1979; Shephard i992), and the same is true for triathletes (Holly et al. 1986; OToole et al. 1987; Millard-Stafford et al. 1991; Schneider & Pollack 1991; Laurenson et al. 1993; De Vito et al. 1995; OToole & Douglas 1995; Vallier ef al. 1996; Miura et al. 1997; Kerr et al. 1998). Elite triathletes generally have slightly lower weight-adjusted vozmaxvalues than single-sport endurance specialists in their respective exercise modalities (Fig. 59.3a-c). The mean Po2max values for treadmill running in elite runners (Costill et al. 1973; Wilmore & Brown 1974; Pollack 1977; Davies & Thompson 1979; Conley & Krahenbuhl 1980; Shephard 1992) are on average 8-23% higher than the corresponding values for triathletes (OToole et al. 1987; De Vito et al. 1995; OToole & Douglas 1995). Similarly, VoZmaxvalues in elite single-sport athletes are i5--23% greater in cyclists (Stromme et al. 1977; Burke 1980; Coyle et al. 1988)and 18-20% greater in swimmers (Holm& et al. 1974) than most of the values reported for triathletes (Holly et al. 1986; Dengel et al. 1989; Douglas 1989; Toussaint 1990; Deitrick 1991; Millard-Stafford et al. 1991; Schneider & Pollack 1991; Sleivert & Wenger 1993; OToole & Douglas 1995). The lower values in triathletes may be partially attributable to the carrying of the extra muscle mass required in one exercise mode, e.g. swimming, which is not required in the other exercise modes, e.g. cycling or running. This could decrease the 002max in any given mode of



exercise. That vozmax values are lower in triathlete than in endurance specialists may also be due to differences in training volumes, since the triathlete necessarily spreads training between three exercise modes (OToole et al. 1989a). The greater values generally obtained by single-sport specialists reinforce the concept of a specificity of training response. Some studies, however, have shown improvements in both cycling and running after training in only one exercise mode, with the magnitude of Vo,, improvements being largest for the exercise mode adopted during training (Boutcher et al. 1989; Hoffman et al. 1993). Conversely, the addition of 6 weeks of increased cycling training resulted in an increase of running performance of similar magnitude to that achieved by the addition of extra run training in well-trained male distance runners (Flynn et al. 1998). It therefore appears that training in one exercise mode may cross over and influence performance in another exercise mode, even in well-trained athletes, although the bulk of evidence still suggests that specificity of training should remain a central premise in any triathlete training programme. Relatively few data exist, but it appears that elite values than subelite triathletes have greater vo2max and recreational triathletes. For example, treadmill voZmaxvalues of 70-85 ml.kg-'.min-' have been reported for elite male triathletes (Holly et al. 1986; OToole et al. 1987; De Vito et al. 1995; OToole & Douglas 1995). whereas lower-level triathletes have voZmax values of between 55 and 67ml.kg-'.min-' (Zinkgraf et al. 1986; Kreider et al. 1988b; Douglas 1989; Delistraty et al. 1990; Sleivert & Wenger 1993; Miura et al. 1997; Rowbottom et al. 1997; Zhou et al. 1997).Similarly, elite and recreational female triatha x of between 54 and letes have treadmill ~ o Z mvalues 73 ml-kg-'.min-' (Schneider & Pollack 1991; Laurenson et al. 1993) and 44-65 ml.kg-'.min-7 (Laurenson et al. 1993; Sleivert & Wenger 1993; Bunc et al. 1996), respectively. These results suggest a relationship bemeen ~ o Z mand a x triathlon performance. When triathletes of mixed abilities in short-course triathlons, swimming, cycling and running performances have been reported to be related to event-specific $'02maxin some cases. For example, in a mixed gender sample, Butts et al.


Fig. 59.3 Weighted mean values for elite male and female Olympic and Ironman triathletes compared to (a) elite distance swimmers, (b)elite road cyclists and (c)elite distance runners. Weighted mean values were generated as detailed in Fig. 59.1.



(1991) found the swim time to correlate with the absolute (1.min-') tethered swimming Pobx (r = -0.49), the cycling time to correlate with both the absolute ( r = -0.57) and the relative (ml.kg-'.min-') Pozmax ( r = -0.78), and the running time to correlate with the relative Pohax (Y = -0.84). These relationships must be interpreted with care, since a mixed gender sample may have elevated these correlations by increasing the range of both Pozmax and performance scores. Sleivert and Wenger (1993) reported gender-specific correlations. They found that the swimming time was related to the relative tethered swim in both females (r = -0.93) and males (r = +.48), but the cycling time was not related to the cycle in either gender, and the running time was related to the treadmill Pohax in females ( r = -0.88) but not in males. The small sample of females in this study (n = 7) exhibited greater variance in abilities than the males ( n = is), which is likely to have inflated the observed correlations for the female sample. Another recent study of a very heterogeneous sample of triathletes (e.g. running Poamax values ranging from 54 to 82 ml.kg-'.min-') reported significant correlations between the run time in an Olympic distance triathlon and the relative treadmill Pozma, (r = -0.73); however, there was no relationship between the cycling Pozmax and the cycling performance, despite the fact that the absolute cycling Poha was correlated with the overall triathlon time (r = -0.72) (Zhouet al. 1997).In a more homogeneous group of 17 male competitive triathletes, Miura et al. (1997) reported that the exercise mode-specific Pobx was significantly related to performance in swimming (r = -0.65)~cycling (r = -0.82) and running (r = -0.73) phases of an Olympic distance triathlon; moreover, each Pozm measure was correlated with the overall triathlon completion time ( r = -0.62 to -0.89). In recreational triathletes of low average fitness, Loftin et al. (1988) reported significant relationships between cycling and running VoZmaand cycling and running performance in the triathlon ( r = -0.56 and -0.58, respectively),but no relationship between the arm crank Pohax and swimming performance. It therefore appears that Pohax is important to performance over the Olympic distance, but the relationship is moderate and often not statistically significant. In triathletes of mixed abilities, the Pozmax is a valid predictor of

performance, and lower-level triathletes should emphasize training to develop this attribute in each exercise mode. The Pozmax has a less clear relationship to performance in events longer than the Olympic distance triathlon. Dengel et al. (1989) reported weak correlations between the event-specific Pohax and halfIronman triathlon performance in male subjects, with only the cycle ergometer V Obeing ~ related to cycling time ( r = -0.70). In another group of halfIronman triathletes of varying abilities, Kohrt et al. (1987) reported that the event-specific Pozmax was related to performance in cycling and running (r = -0.68 and -0.78, respectively), but not to performance in swimming. At the Ironman distance, one study reported no relationship between the eventspecific and triathlon performance (OToole et al. 1987).This may be because of the lower relative intensity of Ironman events; nutrition, fluid and electrolyte balance and psychological factors are likely to become major determinants of success in these ultra-endurance events (OToole & Douglas 1995). One study observed that cumulative fatigue experienced over the course of a triathlon event did not appear to decrease the magnitude of the relationship between Pohaw and triathlon performance. As previously mentioned, De Vito et al. (1995) measured treadmill Pozmax both in a rested state and after completion of the first two segments of a triathlon (1.5-km swim, 32-km bike). They found that the Pozmadecreased from 69 to 64 ml.kg-'.min-' at the second assessment. Surprisingly, the Pozmax measured from basal conditions was a better predictor of running performance in the triathlon (r = -0.86) than the data collected in the fatigued state (r = -0.77). Whether this holds true for ultradistance triathlons remains to be determined. FRACTIONAL

U T I L I Z A T I O N O F POZmax

Performance in the triathlon has been significantly related to the ability of the triathlete to exercise at a low percentage of vohaxfor any given submaximal work rate (Dengel et al. 1989). This ability is influenced by a combination of factors, including aerobic power, economy of movement and anaerobic threshold (AnT).


The ability to exercise at a high fraction of Pozmax is largely influenced by An,, expressed as either ventilatory threshold (V,) or lactate threshold (L,). A non-linear increase in either respiratory minute ventilation or blood lactate concentration when plotted against Po2or velocity is commonly used to determine A,, (Thoden 1991; Chapter 22). Endurance time at an exercise intensity above A,, is reduced due to metabolic acidosis and accelerated glycogen depletion (MacDougall et a/. 1977). Therefore, the successful endurance athlete is often characterized by an ability to perform high amounts of work at or just below A,, (Costill e t a / . 1973; Tanaka e t a / . 1984). In Olympic triathletes, V , has been reported at 72-75% of swimming Vo2max,63-85% of cycling and 7491% of running Pozmax (Schneider & Pollack 1991; Sleivert & Wenger 1993; De Vito et a/. 1995; Bunc et a/. 1996; Zhou et a/. 1997). Likewise, L, has occurred at 72-88% of cycling vo2max and 8c-85% of treadmill Pozmax (Kohrt et a / . 1989).These percentages are similar to or slightly lower than those reported in endurance specialists (Withers et a / . 1981; Sjodin et a/. 1985; Simon et a / . 1986). It has been suggested that the amount of muscle mass involved in a movement partially determines the percentage of Pohax at which All, occurs. This may be because the average metabolic rate per unit of contracting muscle is greater in exercise modes where less muscle mass is recruited (Koyal et al. 1976; Schneider & Pollack 1991). The training history may alter this relationship. Kohrt et a/. (1989) reported that over the course of a triathlon season, the cycling L, increased by 6%, and the running L, by lo%, without improvements in Pozmax. Similarly, Rowbottom et a/. (1997) reported that over 9 months of training, the running velocity at L, in a group of well-trained male triathletes improved from 15.6 to 16.6km.h-’, with no Withers et a/. (1981)found cyclists change in vo2max. could use larger fractions of than runners when tested on a cycle ergometer, whereas runners had a higher fractional utilization on a treadmill. Hoffman ef a/. (1993) reported that with run training, V , improved on the treadmill but not the cycle ergometer; however, cycle ergometer training improved V , in both cycling and treadmill running. Others also have reported improvements of L, in


cycling through run training (Boutcher e t a / . 1989). The data therefore indicate that training may improve V , and L, measures specifically, allowing triathletes to compete at higher percentages of VoZmax;the findings also provide some support for the benefits of cross-training. Sleivert and Wenger (1993) reported that the running velocity at V , was related to the run time in both females ( r =-0.88) and males (~=-0.73), and the resistance pulled at V , during tethered swimming was related to the swimming time (Y = -0.81) for females in a short-course triathlon. The overall triathlon time was related to the velocity at the running V , in both genders ( r = -0.78). The sample of recreational triathletes used in this study was heterogeneous in terms of performance ability, particularly in the female triathletes, and this may have inflated the magnitude of the correlations. Nevertheless, V , measures have also been related to performance in a small group ( n = 6) of well-trained male triathletes (De Vito et a/. 1995). In the study of De Vito et a/. (1995). the Po2 at the running V , was measured both starting from resting conditions and after completion of a partial triathlon (1.5km of swimming, 32km of cycling). After completion of the partial triathlon, the V , occurred at a lower percentage of Pohax (74.3 versus 84.6%), demonstrating that the ability to sustain a high percentage of Pozmax in running is impaired after the swimming and cycling sections of a triathlon. In addition, the heart rate at V , was lower after previous exercise, a finding which has implications for setting training and competition pace. De Vito’s group also found that vo2 at the running V , was related to running performance in an Olympic triathlon ( r = -0.79), and this relationship was even stronger when V , was tested after completion of the partial triathlon (r = -0.85). The L, has also been related to performance in running and cycling during a half-Ironman event ( r = -0.73 and -0.72, respectively) (Kohrt et a/. 1989). Zhou et a / . (1997) have similarly reported that the work rate at V , for both cycling (Y = -0.79) and running ( r = -0.68) was significantly correlated to the overall Olympic triathlon performance; the work rate at the cycling V , was not related to cycling performance, but the speed at the running V , was correlated with



running performance in the triathlon (r = -0.85). Thus, the ability to perform high rates of work at or below V , or L,, and to minimize muscle acidosis, are probably important determinants of success in short-course triathlons. The one study that has reported no relationship between V , and triathlon performance examined a homogeneous group of triathletes who were competing in a long-course triathlon (OToole et al. 1988). It may be that other factors, such as energy reserves, fluid and electrolyte balance and economy of movement are more important in ultra-endurance triathlons (OToole & Douglas 1995). E C O N O M Y OF M O V E M E N T

Economy has been defined by numerous researchers as the oxygen cost of exercising at a standard, predetermined velocity (Daniels et a / . 1977; Farrell ef al. 1979; Morgan et a/. 1995). An economic triathlete uses less oxygen than her or his less economic peers at a standard velocity, and theoretically such an individual is able to move faster or to conserve energy for the later stages of an event. Economy has been shown to account for the large variation in lo-km race performance times of highly experienced runners with similar values (Conley & Krahenbuhl 1980). Other studies have shown significant relationships between economy and cycling (Coyle et a / . 1988) and swimming (Montpetitet a/. 1988)performance. Economy is important to performance in triathletes. Laurenson et a/. (1993) reported that elite female triathletes were significantly more economical than club-level triathletes during treadmill running at 15km.h-' (respectiveoxygen costs of 51.2 versus 53.8ml.kg-'.rnin-'). The elite females also exercised at a lower percentage of their vozmax (78.2 versus 89.2%)and had lower lactate and heart rate values at submaximal running velocities. The percentage of Pozmax at 15 kmeh-' was a significant predictor of Olympic-distance triathlon performance. Dengel et al. (1989) also reported that the po2values at submaximal speeds of running, cycling and swimming were strong predictors of corresponding performance times in a half-Ironman triathlon, the strongest predictors being the ability to use a low

percentage of at a given submaximal work rate in each exercise mode (r = 0.91,0.78 and 0.87 for swimming, cycling and running performance times, respectively). OToole et al. (1989a) also reported that the percentage of Pozmax used during submaxima1 cycling was significantly related to the cycle finish time in an Ironman-distance triathlon. Most recently, Miura et al. (1997) measured the economy of 17 competitive male triathletes during a simulated triathlon comprising flume swimming, cycle ergometry and treadmill running (60% in each exercise mode, for fixed durations of 30.75 and 45 min, respectively).The economy index (%Vo2max) was taken during the last minute of each stage, since it is known that the oxygen cost will drift higher during prolonged exercise, as demonstrated in numerous triathlon studies (Kreider et a / . 1988a; Guezennec et a/. 1996; Hausswirth et al. 1996, 1997; Hue et a/. 1998). This study found significant relationships between the percentage of $'02mxused during the swimming (r = 0.55), cycling (r = 0.61) and running ( r = 0.55) stages and performance in the corresponding phases of an Olympic triathlon. The swimming economy was not related to the overall triathlon performance, but the cycling and running economies were reasonable predictors of triathlon performance (r = 0.60 and 0.77, respectively). The index of economy used in this study reflects the ability to maintain a stable percentage of over the course of a triathlon; therefore, it probably reflects the degree of cardiovascular and thermal stability that the triathletes were able to maintain. This might explain the lack of correlation between economy in swimming, the first event of the triathlon, and overall performance. The fact that the relationship between economy and overall performance strengthened on moving from cycling to the running mode, the latter phases of the triathlon, lends some support to the importance of minimizing cardiovascular drift during sequential endurance exercise. Although the economy of movement in swimming did not predict overall triathlon performance in the study of Miura e t a / . (1997). it may still be an important determinant of success in the swimming phase of the triathlon, where a large emphasis is placed on technique. Toussaint (1990) compared


propulsion efficiency (the energy used to overcome drag/ total energy used) between elite swim specialists and elite triathletes. At an equal power output, the two groups did not differ in gross efficiency, stroke frequency or work per stroke, but the elite swimmers covered a greater distance per stroke (1.23 versus 0.92m) and had a greater mean swimming velocity (1.17 versus o.95m.s-'). The elite swimmers used a higher proportion of their power output to overcome drag, and expended less power in moving the water backwards. The overall mean propulsion efficiency for swimmers was 61%, but it was only 44% for the triathletes. It was concluded that the triathletes should focus their attention on improving swimming technique, rather than on improving their ability to generate power. The distance covered per stroke may be a simple criterion that triathletes can use to evaluate their swimming skill. A number of extrinsic factors may influence exercise economy. The use of a wetsuit in the swimming section can reduce drag by up to 14% (Toussaint et al. 1989).Cycling economy can be affected by factors such as seat position, crank length, body position and shoe-pedal interface (Cavanagh & Kram 1985; Gregor & Wheeler 1994).A triathlete's cycling performance is also affected by the quality of the bicycle, including the design of its wheels, tyres and handlebars (Faria 1992).


Conclusions The triathlon significantly challenges human capacity for thermoregulatory and cardiovascular homeostasis. This is particularly evident in the latter stages of the event, when hyperthermia, dehydration, a reduced Vozrnax and a poor economy of movement are all observed. Successful triathletes are able to minimize homeostatic disturbances over the course of the event, probably largely as a result of high volumes of training in swimming, cycling and running. Unfortunately, these necessarily large volumes of training predispose the triathlete to overuse injuries, with the knees and lower back being the most common sites of injury. Triathletes develop physical and physiological characteristics that are a blend of those seen in endurance swimming, cycling and running specialists, largely through specific training, but probably partially through cross-training. Elite triathletes have high VoZrnaxvalues in swimming, cycling and running, and are able to exercise at high fractions of vo2rnax in each exercise mode, due to well-developed anaerobic thresholds and economy of movement. More research is required on acute interaction effects arising from sequential exercise in swimming, cycling and running, and there is also need for further information on the influence of different training interventions on triathlon performance.

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Introduction Canoeing was invented out of necessity, but has since become a popular form of sport and pleasure activity.Canoes were the first objectsbuilt for travelling on rivers and lakes. Three characteristics differentiate the canoe from most other types of watercraft: 1 the participant(s),seated or on their knees, look in the direction in which they are heading; 2 the propelling element is a paddle without a fixed support on the boat, held freely in the hands of the paddler; and 3 the canoe is a craft with a pointed stem and stern. These particular characteristics permit a great mobility and manageability. Some small rowing boats built by canoe makers in Canada have also adopted this design. A report written by some Russian hunters indicates that around 1745, Europeans already knew about the use of this particular type of boat by Inuits from Greenland.About 100 years later, the Scot John McGregor designed and built a canoe similar to the kayak. Even if he was founder of the sport, he always preferred to stress the recreational aspect of canoeing rather than competitive racing. In 1866 he founded the first canoe club which, in 1873, became the Royal Canoe Club. In April 1867, the first canoe race was held on the River Thames, over a distance of 1.6km (I mile).By 1900, the kayak had been adopted by the majority of European countries. The first treatise on paddling dates back to this year. It was written by the Norwegian Nansen. The pioneer period ended in 1936,at the Olympic Games


in Berlin, when canoeing became an Olympic speciality. At present, the sport is regulated by the ICF (International Canoe Federation) and by various national federations. Canoeing has developed as a sport with two main specializations:speed canoeing (in calm water) and whitewater canoeing (in rough water). Other specialities include polo canoeing, sail canoeing and marathon canoeing. Contestants in speed canoeing follow parallel courses in calm water. The classic races cover distances of 500 and iooom. The following types of craft are used: kayaks (Ki, K2, Kq, according to the number of crew members) and Canadian canoes (Ci, Cz) (Fig.60.1). Whitewater canoeing (an Olympic speciality from 1992) involves slalom events on a river with falls, on which has been installed a race course with obligatory 'gates' (doors) to be passed by either stem or stern. The craft used are the kayak (Ki) and the Canadian canoe (Ci, C2); the latter has a different design to the high-speed canoe; whitewater canoes are less rapid, but more stable. The materials from which paddles and canoes are made, and their shapes, have evolved over time. The paddles, in particular, have undergone a dramatic change, from wood to synthetic material such as kevlar and carbon, and from a flat blade to the most recent wing-shaped type.

Biomechanics Kayak technique The following description is valid both for speed


Kayak 1


and opposing rotation of the trunk, so that the traction arm, remaining extended, receives and transmits to the paddle the power resulting from the above-mentioned thrust. In the second phase, the rotation of the trunk and the thrust of the leg continue, while the rotation of the traction arm begins until the forearm reaches a minimum angle of 90". The active arm completes the extension at the same time. 3 Extraction. After passage through the water, made with a rapid outward rotation of the traction arm, the extraction phase begins. This is also called the return phase. 4 Aerophase. In this phase, the paddle cycle ends and the next one begins. As in extraction, the aerophase is made by the traction arm, which completes the outward rotation. The rotation and upward movement permit the paddle to achieve the semirotation necessary to change sides.

Kayak 2


Canoe 1

Canadian technique Canoe 2


Fig. 60.1 Various types of kayak and Canadian canoe.

canoeing in calm water with any number of crew members, and for whitewater canoeing in rough water. To make the technique more easily understood, four fundamental phases can be distinguished. I Position of attack, or beginning of the paddling cycle. The trunk is in a position of maximum rotation; the attacking shoulder is stretched forward, and the corresponding arm is extended and horizontal. The active shoulder moves backward behind the head; the arm and the forearm are flexed at about 90". The pelvis rotates forwards on the attack side and the corresponding leg flexes at around 130". 2 Passage in the water. The first phase is dominated by pushing of the leg corresponding to the traction

Here again we can distinguish four phases in the paddling cycle. I Position of attack. Both arms are extended: the trunk is in a position of maximum rotation and flexion; and the forward leg maintains the angle of the basic position. The angle formed between the paddle and the water surface in the phase of attack is about 65". 2 Phase of traction. From the position of attack, while maintaining extension of the arms, an opposing rotation and extension of the trunk is effected until returning to the basic position. The active arm makes a downward pressure on the paddle, trying to keep this pressure perpendicular. The uppermost arm, by moving the wrist, makes the paddle rotate outwards until the extraction phase. 3 Phase of extraction. In this phase, the extracting fist is at the level of the hip and the semiflexed arm moves rapidly outwards. 4 Aerophase. In this phase, the athlete passes from the basic position to the position of attack, keeping the arms extended and achieving a torsion of the body, with the trunk flexed. Figure 60.2 shows the forces applied during the paddling cycle as registered by means of a

Fig. 60.2 (a) Force exerted during kayak paddling, as registered with a dynamometric paddle. (b)Force developed during Canadian canoe paddling, as registered with a dynamometric paddle.FM, maximal force; GF, angle of force; TC, paddling time; TE, effective time; TFm, time to reach maximal force.


dynamometric paddle (Perri et al. 1990) both in the kayak canoe (Fig. 60.2a) and in the Canadian canoe (Fig. 60.2b).

Anthropometry Height Hirata (1977) has demonstrated from a study of Olympic winners that the ideal paddler is generally 0.02-0.08m taller than the average person. He has also shown that there is a height difference of about 0.03-0.05m between the best kayakers and the best canoeists, the former being the taller.

Body mass According to Sidney and Shephard (19731, junior competitors are relatively light. On the other hand, senior competitors carry a substantial excess mass (an average of 5.8 kg in men and 9.5 kg in women). This influences their performance. The correlation between lean body mass and overall ability is 0.72. In support of this view, Hirata (1977) showed that the gold medal winners in the Montreal Olympics were 3-iokg heavier than the average contestant.

Muscle fibres Canoeists have an unusual body composition; the deltoid muscles contain 63% slow-twitch fibres, as compared with 44% in a student population (Gollnick et al. 1972; Tesch & Karlsson 1985). The 'ideal' composition would be 50%, 65% and 70% of slowtwitch fibres for distances of 500,iooo and ioooom, respectively (Shephard 1987).


Muscle force Canoeists show large peak isometric forces for hand-grip, elbow flexion and knee extension. The coefficients of correlation between such measurements and overall performance are, however, quite low: 0.58 for knee extension, 0.29 for hand-grip and 0.11 for elbow flexion (Sidney & Shephard 1973). However, some researchers have not found particularly high values in the muscular regions of the trunk, especially in extension. In this region the peak muscle force is only 29% higher than in untrained students (Cermaket al. 1975). We studied force-velocity curves for the upper limbs, using an isokinetic ergometer at an angular velocity similar to that of the stroke frequency during competition. The canoeists reached their maximum power at about 7or.p.m. (Table 60.1). Studies completed by Armand (1983) and Vandewalle et al. (1983) have demonstrated that the force-velocity relationship plotted with data obtained on an arm ergometer gives higher figures for canoeists than for athletes practising other sport disciplines (Table 60.2).

Anaerobic metabolism The literature gives conflicting data as far as blood lactate is concerned, with results perhaps depending on the type of test and ergometer used and on the motivation of the subjects. Cermak et al. (1975) observed peak blood lactate concentrations as high as 18.4mmol~l-'in men and 16.8rnmol.l-' in women canoeists. Tesch and Lindberg (1984) reported values of 5 mmol.l-' (males) and 6 mmol.l-' (females). Dal Monte (1983) observed a final concentration of 14mmolP in a test that simulated

Table 60.1 Average isokinetic data: the canoeists reached their maximum power at about 70 strokesmin-'.

Junior kayak (male) Senior kayak (male) Senior kayak (female)

Maximum velocity (r.p.m.)

Maximum force (N)

Maximum power (W)

No. of subjects

70 70

514 674 393

705 928 471

4 7 5




Table 60.2 Forcevelocity relationship for various types of athlete, using an arm ergometer. Reference


Vandewalle et al. (1983)

Canoe/ kayak men women Handball (men) Boxing (men) Tennis (men) Sedentary (men)

Armand (1983)

Senior kayak (male) Junior kayak (male) Senior canoe (male) Junior canoe (male) Senior canoe/kayak (female) Junior canoe/kayak (female)

Maximum velocity (r.p.m.)

Maximum force (N)

Maximum power (W)

948 549 768 768 662 578

243 218 230 240

237 222

226 216 233 213 211

1045 698 916 642 583



Table 60.3 'Fractionated laboratory test, simulating the distances covered by Olympic kayak canoes in 500- and moo-m races. Time of work (4 m i d

Mechanical work (kJ)

Mechanical power (W)

Oxygen intake during test (l,min-' )

Total test (0-4 min) I min (0-1 min) I1 min (1-2min) 111min (2-3 min) IV min (3-4 min)




26.26 21.80 -

437 363 366 401

1.82 4.36 4.40 4.45

Blood lactate mmol.l-'*


6.70 8.00 8.12 8.44

6.70 1.3 0.12


*Lactateconcentration: differencebetween maximal blood lactate value and resting value. t Difference between peak blood lactate concentration and peak value the minute before.

competition. In a laboratory test simulating the duration and energy outputs anticipated in races over 500 and i m o m in speed-racing kayak canoes and a kayak ergometer ('Modest' kayak ergometer), Colli et al. (1990) obtained blood lactate measurements of 12.7mm0l.l-~ and 11.7mmol.l-', respectively. Table 60.3 presents laboratory data in tests simulating these same distances. Notice that the blood lactate concentration reached a high level after the first minute and then maintained a constant value for the rest of the test. We may conclude that there is

no accumulation of blood lactate even if the metabolic intensity far exceeds the anaerobic threshold and is close to Pohax. This indicates that the measurement of blood lactate concentration alone could give misleading information about anaerobic glycolytic activity. In 500- and 1000-m competitions of highly specialized athletes, we obtained values of 16.0 (s.d. f 0.70) mmol.1-' and 13.5 (s.d. & 0.47) mmol.P, respectively (Colliet al. 1990). Heller et al. (1984) compared test data on two groups of top-level canoeists. The first group (n = 14) were evaluated on the cycle ergometer and sub-


sequently on the paddle ergometer, and the second group ( n = 10) were tested on the treadmill and paddle ergometer. Respective lactate values of 8.6mmol.1-’ and 8.8 mmol.1-’ were not significantly different for the first group; values for the second group were 13.2 and 12.5mmol.l-I ( P < 0.1). These figures suggest that notable muscular and metabolic adjustments occur in canoeists, so that when using the specific ergometer, and thereby activating a relatively small muscular mass, the lactate value remains similar to that obtained on the treadmill or cycle ergometer. We have also carried out studies on whitewater canoeists, both during slalom performance and during specific tests, in order to study their maximal lactate capacity (DAngelo et 01. 1987).The ‘figure of eight’ distance (Fig. 60.3) had to be completed as many times as possible in I min, and the distance covered was calculated according to the landmarks between the two gates. When that slalom had ended, we found a mean blood lactate concentration of 7.0 (s.d. 0.51)mmol.l-’, whereas during specific tests in water we found a maximum of 13.2 (s.d. i.ii)mmol.l-’. Field studies on Canadian canoeists have indicated values similar to those for kayakers. The only trend to a difference was between the two racing distances, i.e. 500 and iooom, with respective blood lactate values of 14.9 (s.d. 0.78)mrnol~l-~ and 13.0 (s.d. _t o.g5)mmol.l-’



(not significantly different) (Colli et al. 1990, personal communication). When the anaerobic capacity was evaluated by measurement of oxygen deficit, we (Faina et al. 1997) found a positive (r = 0.55). but not statistically significant, correlation between the time limit at the minimum exercise intensity capable of inducing the and the accumulamaximal oxygen intake (I$’oZmax) tion oxygen deficit (AOD). These data suggest that, in kayakers, during an effort at the I~oZmax, which is close to the intensity adopted in actual competition, endurance seems to be influenced heavily by the anaerobic capacity.

Anaerobic threshold Cerretelli et al. (1979)and Tesch and Lindberg (1984) have noted a high anaerobic threshold in paddlers. Possible factors include rapid oxygen kinetics at the onset of exercise, a high capillary density in the shoulder muscles, and a high oxidative power (Gollnick et al. 1972)or a low lactate dehydrogenase activity. Bunc et al. (1981)examined anaerobic thresholds, using various ergometric tests. They found that when paddlers were tested on the treadmill, they had a threshold at 79% of ~ o j m awhereas x, the value on the kayak ergometer was around 86% of $‘02max (Tesch et al. 1976). Colli et al. (1990) measured the

10 m

1 Fig. 60.3 Specific test for whitewater canoeing: plan of the course.





Table 60.4 Power at 4-mM blood lactate concentration measured on the kayak ergometer in the five fastest Italian paddlers. Power (W) 268 500-m kayak (male) 1000-m kayak (male) 356 500-m kayak (female) 225 260 500-m canoe (male) 1000-mcanoe (male) 299

Heart rate %co2max (beatsmin-') 79 86 88 77.5 87.3

anaerobic threshold by an incremental test on the kayak ergometer (the power at a blood lactate concentration of 4mM); values for the best Italian canoeists, divided according to their specialities, are shown in Table 60.4. When Dal Monte's kayak ergometer was used on members of the Italian national kayak team, an anaerobic threshold 82% (s.d. 6.3%) of was obtained (Paselli et al. 1986). The heart rate at the anaerobic threshold also reaches high values. During an incremental test on the treadmill, with a constant slope of 5% and speed increments of ikmh-'.min-', Bunc et al. (1981) found a heart rate of 177 beatsmin-' in top Hungarian male canoeists who had a maximum heart rate averaging 192 beatssmin-'. Corresponding values for women were 182 and 195 beatsmin-', respectively.


Aerobic metabolism Various tests and ergometers have been used to study the aerobic metabolism of canoeists and kayakers. Data have frequently been obtained using the treadmill. Sidney and Shephard (1973)reported values of 3.81.min-' in junior males, 4-5 Lmin-' in senior males and 2.81.min-' in women whitewater paddlers. Vaccaro et al. (1984)recorded a mean value of 4.71.min-' in whitewater canoeists from the US national team. Horvath and Finney (1969)reported a mean of 3.8lmin-' in male contestants. Many authors (Cermak et al. 1975; Vrijens et al. 1975; Tesch et al. 1976; Dransart 1977; Rusko et al. 1978),using a variety of leg ergometers, have obtained mean values for male competitors ranging from 5.3 to 5.6

178 179 181 180 177

No. of subjects I

I 1

1 1

Lmin-'. Data referring to winners are larger: Tesch and Lindberg (1984)reported a po2max of 4.91.min-' in Swedish junior males, 5.01.min-' in senior males and 5.41.min-I in a male world-champion. Dransart (1977) presented exceptional data, 5.6 1.min-' (85ml.kg-'.min-') in a French male competitor. However, the canoeist provides a classic example of a fundamental feature of living beings: adaptability. The athlete continuously modifies her or his morphofunctional characteristics in relation to the specific requirements of the sport. The canoeist develops the upper part of the body, thus opposing the evolutionary law which privileges the upright position of humans and thus the usual morphofunctional difference between upper and lower limbs. Therefore, in order to obtain valid and specific information on the functional qualities of a canoeist as well as on his or her training status, ergometers that can simulate paddling should be used. If such apparatus is not available, an upper limb ergometer can be used. In canoeists and kayakers, the difference in Pohax between a test carried out with the lower limbs and one carried out with a specific ergometer is very small (the same is not true for athletes in other sport disciplines). Dal Monte and Leonardi (1975) found a difference (in rnl.kg-'.min-') of only 7.3% in favour of the results obtained by the cycle ergometer test. Likewise, Heller et al. (1983) obtained a value of 4.451.min-' with the cycle ergometer versus 4.16 l.min-' with the kayak ergometer. Differences are slightly larger if comparison is made with the results of treadmill tests: in the above-mentioned study, Heller et al. obtained a value of 4.871.min-' with the treadmill, compared with 4.01 1.min-' with



the kayak ergometer. It is generally agreed that when sedentary people exercise on an upper limb ergometer, they reach only about 70% of the maximal oxygen intake attained during running, but canoeists attain much higher values on a specific ergometer (Table60.5). Faina et al. (1988, personal communication) tested eight good-level kayakers and found a vo2max of 54.4 ml.kg-'.min-' on the kayak ergometer and of 53.3 ml.kg-'.min-' on the cycle ergometer. In contrast, a group of eight cyclists showed a of 68.7ml.kg-'.rnin-' on a cycle ergometer and of 46.8ml.kg-'.min-' on an upper limb ergometer. Dal Monte (1975) noted that a highly specialized athlete was even able to reach a higher Pohax on a kayak

ergometer than on a cycle ergometer. However, this last observation is not universally true; in fact, this is not the case with medium-level athletes or young athletes (Colliet al. 1990). The efficiency of paddling seems to be quite an important limiting factor too. In a laboratory simulation of speed-canoe races over distances of iooom and 300m, and in non-specific tests, Colli et al. (1990) found that the amount of energy released aerobically (vo2)and anaerobically (lactate) was the same, both in high-level Olympic canoeists and in national-level canoeists, but the mechanical power produced was higher in the high-level competitors (Tables60.6-60.8). These data could indicate that the latter group developed more specific coordinative,

Table 60.5 Percentage of leg paddlers. From Shephard (1987).

Table 60.7 Comparison between top-level and good-level

developed by

athletes in two kayak ergometer tests simulating distances of 1000 and 3oom. % leg GoZmax

Reference Vrijens et al. (1975) Paddlers Controls Cermak et al. (1975) Male paddlers Female paddlers Dransart (1977) Tesch & Lindberg (1984) Paddlers Vaccaro et al. (1984)

89 81 95 100

77 87 89


Top level

Good level

i m m W.kg-' J.paddle-'.kg-' r.p.m.

3.66 f 19 2.129 i 3.6 102.7 ? 3.6

3.37 0.34 2.016 i 0.12 100 ? 1.0

0.05 0.05 n.s.

300 m W.kg-' J.paddle-'.kg-' r.p.m.

5.01 i 0.24 2.360 i 0.15 127.0 7

4.62 f 0.57 2.310 + 0.10 119 f 10

0.05 n.s. 0.05



Values are mean f s.d.; n.s., not significant; r.p.m., revolutions per min.

Table 60.6 Comparison between top-level and good-level athletes using non-specific tests. The performance of top-level athletes in running, traction and pushing with weights did not differ from that of good-level athletes.

Swimming loom ( s ) swimming 3oom (s) Running izoom (s) Tractionson bench (rep.50kg-I.6os-l) Push on bench (rep50kg-'.6os-') Tractionson bar (rep.60s-l) ~~~

Top level

Good level


Student's t test

77 ? 8 284 f 38 247 ? 27 40.4 f 5

90 ? 15 327 f 56 231 ? 8 40.4 f 6.8

0.05 0.05 n.s. n.s.


34.6 9.8




43.8 f 6.8





? 12


Values are mean ? s.d.; ns., not significant;rep, repetitions.


1.51 0.02



technical and muscular adaptations that can be detected either by means of specific tests that reproduce the race situation or on the field.

Cardiovascular system Echocardiography has produced some interesting data on the heart volumes and ventricular mass of

Table 60.8 Comparison between metabolic parameters in top-level and good-level athletes during kayak ergometer tests simulating the distance of i o m m (duration qmin). The only statistically significant differenceis in mechanical efficiency. Top level Oxygen consumption (mLkg-*) c-i min 1-2 min 2-3 min 3-4 min Efficiency (%) Values are mean

Good level


21 f 4


51 4 53 4 53.5 + 5



53 + 3 14.6 f 0.74

* *

13.4* 0.51


n.s. n.s. ns. n.s.


* s.d.; n.s., not significant.

canoeists and kayakers. Values are similar to those of athletes who practice middle-distance running events (Table 60.9). Similar results are obtained when data are related to body surface area (Fig. 60.4) (Pelliccia et al. 1991). Sidney and Shephard (1973) noted that the resting heart rate of their sample of whitewater canoeists was relatively high: they reported values of 71 beatsmin-' in young male competitors. The systolic blood pressure is relatively high in this class of athletes, around i35mmHg. Armand (1983) attributes this to a high stroke volume and to a blockage of the peripheral circulation by the thoracic ribcage during paddling. The lung volumes are not particularly remarkable and within the average range for body size. However, Sidney and Shephard (1973) found a relatively high correlation between lung volumes and performance (0.64 for the absolute vital capacity and 0.69 for the percentage according to age and height standards).

Conclusions The aforementioned differences in level of

Table 60.9 Left ventricular end-diastolic volume and left ventricular mass (mean value f s.d.) in aerobic sports. From Pelliccia et al. (1991).

Males Cross-country skiing Walking Marathon Long-distance running Middle-distance running Canoeing Rowing Cycling Control Females Cross-country skiing Marathon Long-distance running Middle-distance running Cycling

Left ventricular end-diastolic volume (ml)

Left ventricular mass (g)

167 f 14

314 46

121 f 6

162 * 16 151 f 22

163 f 8 162 f 14 168 + 23

164 + 30 118 f 22

111 122

+ 16 + 30

104 f 10 115 121

* 10

+ 12


255 + 20 332 f 42 258 + 12 336 + 28 388 * 52 365 f 55 355 * 80 197 * 36 213 f 31

228 * 19 183 + 18 227 f 22 251 t 19



Fig. 60.4 Ratio of left ventricular (LV) volume to body surface area (BSA)in male athletes (aerobic and anaerobic sports).

7 /

Fig. 60.5 Training monitoring of kayaking. The figure shows the results of six tests completed by a

the lactate/velocity curve and were carried out in the field. The last test was carried out after a period of res-





-10-91 (Basal value) - 4-92

(Aerobic power training)

.......... 12-91 (Organic training)





6-92 (Races)

- - - 2-92 (Aerobic and SE training)


7-92 (after altitude training)



adaptation between junior and senior athletes, as well as between specialized and 'top-level' athletes, emphasize the need for specific training of this group of contestants. For a distance of imom, the limiting factors in both kayak and Canadian canoes seem generally to be the efficacy of aerobic metabolism (both as voZmax and as the ability to oxidize the lactate produced), the capacity to tolerate low pH values, and the ability to maintain a level of mechanical power close to maximum. For a distance of 500m, anaerobic capacity, buffering capacity, oxygen kinetics and a high mechanical power are even more important limiting factors than vo2max. Based on experience acquired from specific adaptation in top-level athletes, training must simulate the race situation continuously and progressively.

This is not the case if muscular dynamics differ from those performed in a race, for example, training by swimming, jogging or lifting weights. Aerobic and anaerobic exercise performed out of the water must adopt precisely simulated movements (specific ergometers) that can involve in the same order the muscles and muscle fibres that are used for propulsion and removal of lactate. On the other hand, it is of paramount importance to use equipment capable of detecting trends in the main physiological parameters directly 'in the field'. This is possible today, thanks to the improvement of field methods to measure lactacidaemia (Fig. 60.5)and the introduction of miniaturized telemetric equipment which can monitor specific physiological parameters (Dal Monte et al. 1989; Faina et al. 1992,1996).

References Armand, J.C.(1983) Surveillance medicale de l'entrainement dune kquipe de canoe kayak de haut niveau de performance. MD thesis, Universite d e Paris Ouest. Bunc, V., Leso, J., Heller, J., Novak, J., Strejkova, B. & Novotnj, V. (1981) Anaerobic threshold by specific and non-specific load. Lekar a TV-Physician and Physical Education 3,35-37. Cermak, J., Kuta, I. & Parizkova,J. (1975) Some predispositions for top performance in speed canoeing and their changes during the whole year training programme. Journal of Sports Medicine and Physical Fitness 15,243-251. Cerretelli, P., Pendergast, D., Paganelli, W.C. & Rennie, D.W. (1979) Effects of specific muscle training on Vo2on response and early blood lactate. Journal ofApplied Physiology 47,761-769. Colli, R., Faccini, P., Schermi,C., Introini, E. & Dal Monte, A. (1990) Della valutazione funzionale all'allenamento del canoista. (Functionalevaluation and training of canoeists.) Scuola dello Sport. Rivista di Cuftura Sportiva 18,26-37. Dal Monte, A. (1975) Metodologiadella valutazione funzionale specifica negli atleti praticanti attivitl sportive di mediae lunga durata. (Methodologyof specific functional evaluation of long and middle distance athletes.) Medicina dello Sport 28,323-353. Dal Monte, A. (1983) Ln Valutazione Funzionale dell'Atleta. (TheFunctional Eualuation ofAthletes.) Ed. Sansoni,Florence.

Dal Monte, A. & Leonardi, L.M. (1975) Sulla specificitl della valutazione h n zionale negli atleti: esperienze sui canoisti. (The specificity of functional evaluation of athletes: data on canoeists.)Medicina dello Sport 28, 213-219. Dal Monte, A. & Leonardi, L.M. (1976) Functional evaluation of kayak paddlers from biomechanicaland physiological viewpoints. In: Komi, P. (ed.) Biomechanics, Vol. VB., pp. 258-267. University Park Press, Baltimore. Dal Monte, A,, Faina, M., Leonardi, L.M., Todaro, A,, Guidi, G. & Petrelli, G. (1989) I1 massimo consumo di ossigeno in telemetria. (Maximal oxygen intake measured by telemetric equipment). Scuola dello Sport. Rivista di Cultura Sportiva 15,35-44. DAngelo, R., Coan, G., Mazzanti, L., Perli, C.P. & Trompetto, M. (1987) Costruzione ed analisi dei test da campo. (Planning and evaluation of field tests.) Canoa Ricerca z, ~ 1 4 . Dransart, G. (1977) Contribution ti lu connaissance du canoe kayak. Thesis, National Institute of Sport and Physical Education,Paris. Faina, M., Marini, C., Sardella, F. et al. (199.2) La scienza ed il controllo dell'allenamento. (Sport science and monitoring of training.) Scuola dello Sport. Rivista di Cultura Sportiva 26,7-14. Faina, M., Pistelli, R., Franzoso, G., Petrelli, G. & Dal Monte, A. (1996) Validity and

reliabilityof a new telemetric portable system with CO, analyser (Kq Cosmed). In: Proceedings of 1st Congress of European Cofkgeof Sports Science (ECSS), Nice, p. 572. Faina, M., Billat, V., Squadrone, R., De Angelis, M., Koralstein,J.P. & Dal Monte, A. (1997) Anaerobiccontribution to the time to exhaustion at the minimal exercise intensity at which maximal oxygen uptake occurs in dlite cyclists, kayakists and swimmers. European Journal ofApplied Physiology 76,1320.

Gollnick, P.D., Armstrong, R.B., Saubert, I.V.C.W.,Piehl,K.&Saltin,B. (1972) Enzyme activity and fiber composition in skeletal muscle of trained and untrained men. Journal ofApplied PhysiolO g Y 33,312-319. Heller, J., Bunc, V. & Kuta, M. (1983) Functional predisposition for top canoe and kayak performance, p. 15 (abstract).Intemational Congress on Sport and Health, Maastricht. Heller, J., Bunc, V., Novak, J. & Kuta, I. (1984) Acomparison of bicycle, paddling and treadmill spiroergometry in top paddlers. In: Lollgen, H. & Mellerowicz, H. (eds)Progressin Ergometry: Quality Control and Test Criteria, pp. 236241. Springer,Berlin. Hirata, K. (1977) Selection of Olympic Champions, Vols 1 & 2 . Karger Publishers, Basel. Horvath, S.M. & Finney, B.R. (1969) Pad-


dling experiments and the question of Polynesian voyaging. American Anthropology p,271-276. Paselli, L., Dal Monte, A,, Faccini, P. & Faina, M. (1986) Fosfati e prestazione fisiche. (Phosphates and performance.) Canoa Ricerca i,3-11. Pelliccia, A., Maron, B.J., Spataro, A,, Proschan, M.A. &Spinto, P. (1991) The upper limit of physiologic cardiac hypertrophy in highly trained elite athletes. New England Journal of Medicine 324,295-301. Perri, O., Dal Santo,A,, Haszik, E. & Toth, A. (1990) La tecnica di pagaiata in kayak e canadese. (Paddling technique in kayaking and canoeing.) Canoa Ricerca 5, 5-15. Rusko, H., Haw, M. & Karvinen, E. (1978) Aerobic performance capacity in ath-

letes. European Journal of Applied Physiology 38,151-159. Shephard, R.J. (1987) Science and medicine of canoeing and kayaking. Sports Medicine4,rg-33. Sidney, K.H. & Shephard, R.J. (1973) Physiological characteristicsand performance of the whitewater paddler. European Journal of Applied Physiology 32,55-70. Tesch, P. & Karlsson, J. (1985) Muscle fiber type and size in trained and untrained muscles of elite athletes. Journal of Applied Physiology 59,1716-1720. Tesch, P. & Lindberg, S. (1984) Blood lactate accumulation during arm exercise in world class kayak paddlers and strength-trained athletes. European Journal of Applied Physiology 52,441445.

Tesch, P., Piehl, K., Wilson, G. & Karlson, J.


(1976) Physiological investigations of Swedish elite canoe competitors. Medicine and Science in Sports 8,214-218. Vaccaro, P., Clarke, D.H., Morris, A.F. & Gray, P.R. (1984) Physiologicalcharacteristics of the world champion whitewater slalom team. In: Bachl, N., Prokop, L. & Suckert, R. (eds) Current Topics in Sports Medicine, pp. 637447. Urban & Schwarzenberg,Vienna. Vandewalle, H., Pers, G. & Monod, H. (1983) Relation force-vitesse lors dexercises cycliques realises avec les membres superieurs.MotricitiHumaine 2,22-25. Vrijens, J., Hoestra, I?, Bouckaert, J. &Van Vytvanck, P. (1975) Effects of training on maximal work capacity and haemodynamics response during arm and leg exercise in a group of paddlers. European Journal ofAppIied Physiology 36,113-119.

Chapter 61 Endurance Aspects of Soccer and Other Field Games THOMAS REILLY

Introduction Field games impose different physiological demands on participants than do individual sports such as running, cycling and swimming, where activity is continuous. Exercise in field games is intermittent, brief recovery periods or pauses intervening between exercise bouts. The intensity and duration of activity vary in an irregular manner. In all field games there is an underlying reliance on aerobic metabolic processes, but the energy provided for the critical actions of match-play may be largely anaerobic. It is nevertheless imprudent to generalize to all field games, despite their common characteristics, since each of the sports has unique aspects. Pitch dimensions vary among games, the largest being for Australian Rules and the Gaelic games (football and hurling), and field hockey having relatively the smallest area for play. The number of players allowed on the field at one time (and the freedom to substitute players) also differs among games. Within those football codes in which use of the hand is permitted, exchange of players is relatively rigid for the rugby games and more fluid for American football. In association football (soccer), use of the hand is prohibited, whereas use of the foot is illegal in hockey, the goalkeeper being excepted in both cases. The professional games (Rugby Union, Rugby League, American football, soccer) are more systematized than are the amateur games (field hockey, Australian Rules, lacrosse and the Gaelic games codes) in terms of training and remuneration of players. There are also mini-football versions of the football games, e.g. seven-a-side for outdoor


play and four- or five-a-side for indoor soccer. The 'Rugby-Sevens' form of Rugby Union had its first world championships in 1993 and was introduced to the Commonwealth Games in Malaysia in 1998. A hybrid version of Australian Rules and Gaelic football, 'Compromise Rules', combines these two codes, so that teams from each subdiscipline can compete against one another. The theme of this chapter is endurance in the context of the major field games. Emphasis is placed first on soccer.It is the leading sport world-wide and has attracted more attention from researchers than any of the other games. The rugby codes are then considered together, followed by the national codes. Special attention is given to field hockey; the other stick-and-ball games (hurling and lacrosse) are evaluated together. For each of the sports discussed, the demands of the game are covered initially. The intensity of exercise and physiological responses to match-play are reviewed. Of the many factors influencing performance in the game, those related to endurance are identified. The fitness characteristics of players provide insights into how individual capabilities match the games' demands. Consideration is also given to training and the problems of preparing for competition in the different games.

The physiological demands of association football (soccer) Activity profiles

The physiological demands of soccer are indicated


by the exercise intensities at which players perform their many activities during match-play. This exercise pattern has implications for the fitness of players and for the designing of appropriate training regimens. The training and competitive schedules of players and their habitual activities determine their daily energy expenditures and hence their nutritional requirements. There are repercussions also for injury prevention and proper rehabilitation following soft tissue injuries. The exercise intensity during competitive soccer can be gauged by the overall distance covered. This index represents a global measure of energy expended, encompassing all the discrete movements of an individual player over a whole game. Activities can be classified according to type (action), intensity (quality), duration (distance) and frequency. Juxtaposing the activity profile on a time base allows average exercise-to-rest ratios to be calculated. These ratios may be used in physiological studies that model the demands of soccer, and they also help in the design of soccer players’ training programmes. Information from these profiles can be augmented by monitoring physiological responses during actual or simulated play. Motion analysis has been conducted on national league players; the various methods of recording




activities were reviewed by Reilly (1994).The most comprehensive system employed to date utilizes six cameras from vantage points high in the stands. Linked to a computer, such monitors enable the intensity of effort to be documented for an entire team during the game. Whatever method is adopted must comply with quality control specifications of validity and reliability. A summary of the overall activity patterns reported in the literature (Table 61.1) indicates that outfield players cover a distance of 8-12 km during a match, movement being more or less continuous. The overall distance covered during a game masks frequent changes in activities; each player completes about 1000 different activities in a typical game, representing a change in either the level or the type of activity every 6 s. Alterations in the pace and direction of movement also incorporate game skills and the tracking of opponents’ movements. The distance covered by outfield players during a match consists of 25% walking, 37% jogging, 20% submaximal cruising, 11% sprinting and 7% moving backwards (Reilly i997a). Within these broad categories are included sideways and diagonal movements. These proportions (Fig. 61.1) are representative of contemporary play in the European top leagues, in international tournaments

Table 61.1 Mean distance covered per soccer game according to various sources. Original sources are in Reilly (1994) and Rienzi et al. (1998). Source and year Czechoslovakia (1967) Sweden (1970) Sweden (1973) England (1974) England (1976) Finland (1980) Japan (1981) Australia (1982) Sweden (1986) Japan (1988) Belgium (1988) Denmark (1991) Japan (1991) Uruguay (1998)

Distance covered (m)

n 1

11 500



9 40 40 7 -

10900 4834 8680 7100 9971 11527 9800 9845 10245 10800 11529 8638

20 10 2

7 14 50 17

Method Undisclosed Cine-film Cine-film Hand notation Tape-recorder TV cameras (two) Trigonometry Video Hand notation Trigonometry (two cameras) Cine-film Video (24 cameras) Trigonometry Video



sion of the ball or without, is crucial, since their success may determine the outcome of the game. Factors affecting intensity of effort

Fig. 61.1 Proportion of various categories of activity during soccer match-play (from Reilly 1996).

and at top-level matches in Japan (Ogushi et al. 1993). Cruising (striding) and sprinting can be combined to represent high-intensity activity in soccer. The ratio of low-intensity to high-intensity exercise is then about 2.2:I in terms of distance covered, but is about 7 : i in terms of time. This proportion denotes a predominantly aerobic outlay of energy. Each outfield player has a short rest pause, averaging only 3 s every 2 min; rest breaks are longer and occur more frequently at lower levels of play, where players are more reluctant to run to support a colleague in possession of the ball. Less than 2%of the total distance covered by top players is with possession of the ball. Actions are mainly ’off the ball’, running to contest possession, supporting team mates, counter running by a marking player, jumping for the ball, tackling an opponent, or playing the ball with one touch only. Whilst the majority of activity during a top-level game is submaximal, high-intensity efforts are extremely important. Players generally have to run with effort (cruise) or sprint every 30s, but on average sprint all-out only once every 90s. The timing of these anaerobic efforts, whether in posses-

The team configuration in contemporary top-level soccer is relatively flexible; nevertheless, the intensity of effort is influenced by a player’s positional role. The greatest distances are covered by midfield players, who act as links between defence and attack (see Reilly 1996). Among English league players, the full-backs have shown the greatest versatility (Fig.61.2).Although they cover more overall distance than the centre-backs, they sprint less. The greatest distances covered in sprinting are by strikers and midfield players. The greatest overall distance covered is found in players who undertake more running at low speeds. This profile denotes an aerobic type of activity for midfield players in particular. A more anaerobic profile is displayed by the centre-back, sweeper or libero. The pace of walking is slower in centre-backs than for any other outfield position (Reilly & Thomas 1976). Centre-backs and strikers jump more frequently than full-backs or midfield players. However, the frequency of once every 5-6min indicates that jump endurance may not be particularly important in soccer. The goalkeeper covers about 4km during a match (Reilly & Thomas 1976). Time spent standing still is much greater than for outfield players. Their activity profile emphasizes anaerobic efforts of brief duration, when the goalkeeper is directly involved in play. The goalkeeper is engaged in play more than any outfield player; nevertheless, this involvement has been reduced by the rule introduced in 1992, which prevents back-passes from defenders. This rule has had only a marginal effect on the activities of outfield players. The endurance training requirements for playing outfield are not necessary for the goalkeeper. The ability to exercise at a high power output depends on the maximal aerobic power (vozrnax), but the upper limit at which continuous exercisecan be maintained is influenced by the so-called ‘anaerobic threshold’ and a high fractional utilization of Vohax. Soccer play calls for an oxygen intake of




Fig. 61.2 Distance covered per game according to positional roles (from Reilly & Thomas 1976).

roughly 75% Pohax (Bangsba 1994a,b), a value which is close to the 'anaerobic threshold of top soccer players. The voZmax of English league players is correlated significantly with the distance covered in a game, underlining the need for aerobic fitness, particularly in midfield players (Reilly 1994). The vo2maw also influences the number of sprints that players attempt (Smaros 1980). Bangsb0 and Lindquist (1992) showed that the distance covered during a game was correlated with performancein a continuous 2.16-km field test, and also with the Pohax and the vo2corresponding to a blood lactate level of 3mM. It seems the intensity of effort in soccer matches depends on physiological indications of aerobic fitness as found in endurance athletes. The style of play may influence a player's energy expenditures. Emphasis on retaining possession of the ball, controlling the pace of the game and delaying attacking moves until opportunities to penetrate defensive line-ups are presented underlines the dependence on speed and timing of movement in such critical phases of the game. Conversely, the direct method of play, as used by the Ireland team in the 1990 World Cup and later by Norway in 1994

and 1998, raises the overall pace of the game. The main elements are fast transfer of the ball from defence to attack to create scoring chances, use of long passes rather than a sequence of short passes, exploitation of defensive errors, harrying opponents into mistakes when they possess the ball, and alternating midfield players to support the strikers when they are on the offensive (Reilly 1996). This style of play has an equalizing effect on the energy expenditure of outfield players, since they are expected to exercise at a high intensity 'off the ball' and throughout all the playing zones of the field. A similar levelling of aerobic fitness demands applies to the 'total football' style, exhibited first by the Netherlands national side in the 1970s and characteristic of current top European club sides. The pace of play in international matches within South America is more rhythmic than in Europe; as a result players cover about 1 km less during a game (Rienzi et al. 1998). Fatigue

Fatigue is defined as a decline in performanceand is manifest as a deterioration in power output towards



the end of a soccer game. Comparisons of exercise intensities between first and second halves of matches have provided evidence for the occurrence of such fatigue. Belgian university players were found on average to cover 444m more in the first than in the second half of a match. Likewise, Bangsb~et al. (1991) reported that the distance covered in the first half was 5% greater than in the second. However, not all players show such a decrement. Reilly and Thomas (1976) noted an inverse relation between aerobic power ( Q O ~ , , , ~ ~and ) the decrement in work rate. Those with the higher values, midfield and full-back players, were the least likely to show fatigue. In contrast, all of the centre-backs and 86% of the strikers covered greater distances in the first half than in the second half. It seems that the impact of a high aerobic fitness level is especially evident in the later parts of a match. The amount of glycogen stored in the leg muscles prematch appears to be an important determinant of resistance to fatigue. Swedish club players with a low glycogen content in the vastus lateralis muscle covered 25% less overall distance than the other players (Saltin 1973). A more marked effect was noted for running speed; those with low muscle glycogen stores prematch covered 50% of the total distance walking and 15%at top speed compared to 27% walking and 24% sprinting for players who started with high muscle glycogen concentrations. Attention to diet and a tapering of training are recommended in the immediate build-up for competition. Benefits would be most evident when drawn matches are extended into 3omin extra time, in 'cup' matches or in the professional 'J' League in Japan, for example. Whilst goals may be scored at any time, an aboveaverage proportion are scored towards the end of a game. In the 1998 World Cup finals, a higher than average scoring rate was evident for the final 15min of play. This cannot be explained simply by a fall in power output of players, since this should be balanced out between the two opposing teams. Deteriorations of performance among defenders may give an advantage to attackers towards the end of a game. Alternatively, the late scores may be linked with 'mental fatigue', lapses in concentration as a

consequence of sustained physical effort and/or a low blood glucose level leading to tactical errors and opening up goal-scoring chances. The phenomenon may be a factor inherent in the game, play becoming more urgent and adventurous towards the end of a match despite a fall in the players' physical capabilities. Goals scored in the 1998 World Cup also had a higher than expected incidence in the first 3 min following half-time: whether this is related to a lack of warm-up or a lapse similar to that assumed to be occurring late in the game is unknown. Clearly, a team that is physiologically and tactically prepared to last 9omin of intense play is likely to be an effective unit. Gleeson et al. (1998) investigated the effects of endurance exercise, designed to simulate the physiological demands of match-play, on leg strength, electromechanical delay and knee laxity. Even though peak torque was preserved following the activity, the authors considered that the risk of ligamentous damage may be increased by a concomitant impairment of electromechanical delay and anterior tibiofemoral displacement. Environmental conditions can impose a limit on the exercise intensity that is maintained throughout a soccer game, and/or hasten the onset of fatigue during a match. Major soccer tournaments are often held in hot conditions with ambient temperatures around 30°C. The intensity of effort is adversely affected when such conditions are combined with high humidity. Performance is influenced both by the rise in core temperature and by dehydration, and sweat production is ineffective in dissipating body heat when the relative humidity approaches 100%.During gomin of continuous exercise, cognitive function, akin to the kind of decision-making required during match-play, is better maintained when fluid is supplied intermittently than in a control condition (Reilly & Lewis 1985). Adequate hydration pre-exercise and during intermissions is important when players have to play in the heat. The opportunity to acclimatize to heat prior to competing in tournaments in hot climates is an essential element of preparing for such events. Acclimatization may be achieved in training camps, a good physiological adaptation being realized within 10-14 days of initial exposure to hot weather. Alter-


natively, regular repeated exposures to heat in an environmental chamber are partially effective. The major consequence of playing in cold conditions is likely to be an increased liability to injury. Icy pitches that lack facilities for underground heating promote risk. Muscle performance deteriorates as muscle temperature falls below optimum; a good warm-up prior to playing in cold weather and the use of appropriate sportswear (more than one layer) to maintain core body temperature and avoid the deterioration in performance synonymous with fatigue are important. Injury is more likely to occur if the warm-up routine is inappropriate (Reilly & Stirling 1993). Therefore, prematch exercises should engage the muscle groups employed during the game, particularly in executing soccer skills.

Physiological responses to match-play The relative metabolic loading during soccer play can be calculated, given direct measurements for both energy expenditure during competition and V O . , ~Analysis ~~. of expired air collected in Douglas bags has indicated energy expenditure rates of 22-44 kJ.min-' and 32.2 kJ.min-' in two studies (see Reilly 1996). These values are probably underestimates, due to the restrictions placed on players by the apparatus and also the low skill levels of the subjects investigated. Seliger (1968a,b) reported values of 54.8 kJ.min-' for energy expenditure and 76I.min-' for minute ventilation in Czech players. The Po, of 35.5 ml.kg-'.rnin-' agrees with figures of 35-38 and 29-30 rnl.kg-'.min-' for Japanese players (Kawakamiet al. 1992).An alternative research strategy is to measure the heart rate during match-play and to juxtapose the observations on heart rate-po, regression lines determined during running on a treadmill. The heart rate itself is a useful indicator of the overall physiological strain. The circulatory strain is relatively high and does not fluctuate greatly during a game. The heart rate is about 77% of the heart rate range (maximal minus resting heart rate) for 66% of the playing time (Rohde & Espersen 1988). For a large part of the remaining time, the heart rate exceeds this level. The heart rate during soccer varies with the exercise intensity and so may differ between playing



positions and between the first and second half of a game. Van Gool et al. (1988)reported mean figures of 155 beats.min-' for a centre-back and a full-back, 170 beats.min-' for a midfield player and 168 and 171 beats.min-' for two forwards. These values were closely related to the distances covered by the corresponding players in a match. Mean values for a Belgian university team were 169 beats.min-' in the first half and 165 beats.min-' in the second half of a friendly match (Van Gool et al. 1988). Again, the physiological responses reflected a drop in energy expenditures during the second half. These trends have been confirmed in matches played by English university teams (Florida-James& Reilly 1995). Several studies have employed heart rate to estimate the relative metabolic loading during matchplay. Generally, the exercise intensity during soccer is about 75% of Pozmax and heart rate averages 170 beats.min-'. Use of heart rate regressions may overestimate the real Poz,but the error is generally small (Bangsb0 i994a). Progressively higher blood lactate levels during matches have been observed on progressing from the fourth to the top division in the Swedish league (Ekblom 1986). Higher blood lactate levels were associated with person-to-person marking roles when compared with zone coverage responsibility (Gerisch et al. 1988).Peak values above 12mM were frequently observed in higher league players (Ekblom 1986).Physical activity cannot be sustained continuously under such conditions which reflect the intermittent consequences of anaerobic metabolism during competition. Whilst other studies of blood lactate concentration have yielded values of 4-6mM during play (Table 61.2),such measures are determined by the activity just prior to blood sam-

Table 61.2 Mean (&s.d.)blood lactate concentrations (mM) during soccer. 1st half

2nd half


5.1 f 1.6 5.6 & 2.0 4.9 4.4 f 1.2

3.9 + 1.6 4.7 2 2.2 3.7 4.5 + 2.1

Rohde & Espersen (1988) Gerisch et al. (1988) Bangsbb et al. (1991) Florida-James & Reilly (1995)



pling. Consequently,higher values are noted at halftime compared to the end of the match. Muscle glycogen appears to be the most important substrate for the exercising muscles during soccer play. Glucose taken up from the blood and lipids mobilized from triglyceride stores become important towards the end of a game. The metabolic responses closely resemble those of endurance runners, for whom the sparing of muscle glycogen stores is important to overall performance. Physiology of game-related activities The total distance covered in a game underrepresents the energy expended, because it does not take account of the extra demands of game skills and match events. These demands include frequent accelerations and decelerations, angular runs, changes of direction, jumps to contest possession, tackles, avoidance of tackles and other multiple aspects of involvement in play. There have been attempts to quantify the additional physiological demands of game skills over and above the physiological cost of locomotion. Reilly and Ball (1984) examined physiological responses to dribbling a soccer ball at four different speeds, each for 5 min. Arebound box on the front of a treadmill returned the ball to the player’s feet after

each touch. The simulation allowed precise control over the player’s activity while expired air, blood lactate and perceived exertion were measured. The energy cost of dribbling, with one touch of the ball every 2-3 full stride cycles, increased linearly with running speed. The added cost of dribbling averaged 5.2kJ.minW1 (Fig.61.3). When dribbling the ball, the player’s stride rate increases and the stride length shortens compared with normal running at the same speed; these changes add to the energy cost. Changing stride length from that freely chosen by the individual increases the Po2 for a given speed (Cavanagh & Williams 1992). The energy cost is further accentuated by changing stride irregularly, or feigning lateral movements whilst possessing the ball in order to outwit an opponent. Stride length must be reduced when dribbling in order to control the ball properly and propel it forward with the right amount of force. The energy cost is also increased by the muscle activity required to kick the ball and the action of synergistic and stabilizing muscles to maintain balance while the ball is being kicked. Blood lactate levels and perceived exertion are elevated as a consequence of dribbling the ball, lactate increasing disproportionately at high speeds (Fig. 61.3). Reilly and Ball (1984) estimated that the lactate inflection point occurred at a speed of

6.0r 5.5 -

78 -





5.0 -



‘E 70 2G 66-







58 54 1.5-, 9


11 12 13 Speed (kmh-’)


I 9





11 12 13 Speed (kmh-’)

I 14

Fig. 61.3 The added physiological cost of dribbling a soccerball at four differentspeeds (fromReilly & Ball 1984).


10.7km.h-' for dribbling but not until 11.7km.h-' in normal running. The metabolic strain of fast dribbling is underestimated unless the additional anaerobic loading is considered. Moving backwards or sideways can account for 16%of the distance covered by players. The percentage is highest in defenders who often must back up quickly under high forward kicks from the opposition's half, or move sideways when jostling for position before making a tackle. The added physiological costs of unorthodox movements have been examined by getting nine soccer players to run on a treadmill at three different speeds whilst running normally, running backwards and running sideways (Reilly & Bowen 1984).The extra energy cost of the unorthodox movements increased disproportionately with the speed of movement.There was no difference in energy expenditure or perceived exertion between running backwards or sideways (Table 61.3). Improving muscular efficiency during these unorthodox modes of movement should benefit the player's performance. Fitness measures As the capability for a high energy expenditure is important in soccer, top players tend to have a high level of aerobic fitness. The significance of aerobic fitness was demonstrated by Apor (1988); the mean vo2max of top Hungarian teams was inversely

Table 61.3 Mean (is.d.) for energy expended and ratings of exertion at three speeds and three directional modes of motion (n = 9). From Reilly and Bowen (1984). Direction of motion Speed (km.h-')


5 7 9

37.0 i 2.6 42.3 f 1.7 50.6 f 4.9



Energy expended (kJ.rnin-') 44.8 i 6.1 53.4 i 3.5 71.4 i 7.0

46.6 f 3.2 56.3 i 6.1 71.0 i 7.5

Perceived exertion (Borg units) 5 7 9

6.7 i 0.1 8.0 f 1.4 10.2 2 2.1

8.6 i 2.0 2.9 14.0 2.0 11.2 f

8.7 f 2.0 11.3 f 3.2 13.8 i 2.5


related to their position in the league. Wisloff et al. (1998) confirmed the relationship between maximal aerobic power and performancein the Norwegian soccer league. The mean voZrnaxof 29 players was 63.7ml.kg-'.min-': the authors concluded that the vo2max should be scaled by a factor of 0.75 when evaluating aerobic power of soccer players, to allow for the influence of body size. Whilst the vo2rnax does not necessarily limit performance in soccer, the high values observed in elite players underline the aerobic contribution to play. This point is further emphasized by the physiological characteristics of muscle samples taken from soccer players. Oxidative enzyme activities in leg muscle biopsies of Danish players taken at the time of full training were characteristic of endurance-trained athletes (Bangsbn & Mizuno 1988). Findings in Finnish and Japanese players were similar. Smaros (1980) reported that glycogen depletion occurred mainly in slow-twitch muscle fibres, reflecting the aerobic regimens of match-play. The fibre type distribution tends to be mixed, and exhibits a wide range within a team (see Bangsbn i994b). Training and habitual activities The dimensions of the training programme -intensity, frequency, duration and mode of exercise-are manipulated by the trainer. The stimuli therefore depend on how the training regimens are organized. A fundamental principle is that training should be specific to game requirements. The training classificationshown in Fig. 61.4 depicts the proportionate allocation of time adopted traditionally in English league soccer (Reilly 1979). The training intensity as reflected by the mean heart rate is indicated in Table 61.4. Players are prepared to endure higher physiological stresses when engaged in actual matches. Field-based drills without the ball are relatively unreliable, so activity patterns from the game should be incorporated into training regimens where possible. There is a need for balance among the integral components of a training programme. Preseason regimens usually emphasize aerobic training stimuli, which may interfere with the development







Table 61.4 Heart rates (*s.d.) and estimated energy expenditure during various components of soccer training. From Reilly (1990). Heart rate (beabmin-') Warm-up Flexibility Running Circuit and weight training Skills practice Drills Games Recovery periods


Energy expended (kJ.min-')

14454 125 f 4

38.9 31.4 58.6 43.1

128 k 5 137 f 4 157 f 7 102 * 3

45.2 53.6 68.6 22.6

120 2 112 f 3

Fig. 61.4 Distribution of time in training according to its components.

of muscle strength (Reilly & Thomas 1977). During the competitive season, the aerobic fitness tends to remain stable. Muscle strength is depressed at the start of the playing season, and at this time, players may be more vulnerable to injury. Players with greater muscle strength at the start of a season are more likely to remain injury free throughout the season (Reilly & Thomas 1980). Typically, soccer players compete each weekend. This schedule permits a gradual build-up to a peak training load in midweek, and a tapering off in preparation for match-play (Fig. 61.5). This pattern

of conditioning safeguards the player against overtraining and a reduction of prematch muscle glycogen levels (Reilly & Thomas 1979). This regimen cannot be employed when players have a hectic competitive schedule, including extra matches midweek. Under such circumstances, only certain components of physiological training can be included between matches and the matches themselves provide the major physiological stimuli. Emphasis should be placed on accelerating recovery following each game so that players are prepared fully for the subsequent game. Priorities are warmdown after the game, restoration of fluid and energy losses soon afterwards and appropriate modification of training on the next day. Variations in energy expenditure over the week have implications for the way footballers organize their diets. The dietary practices of soccer players tend to be imperfect,in terms of both overall energy intake and the distribution of macronutrients (Piearce 1993).Recommendations for soccer players are 1 ~ 4 2 % protein, 25% fat and 65-70% carbohydrate, compared to respective percentages of 12,42 and 46 in the normal population. Manipulating the nutritional intake of players enhances both performance in training (Miles et al. 1992) and resynthesis of muscle glycogen following competition (see Reilly 1990). Top soccer teams experience phases during the season when recovery between successive matches is short, for instance when cup and league matches are played in the same week. The high frequency of full-scale competitive engagements may compro-





Fig. 61.5 Distribution of average energy expended in training within a professional soccer team according to the day of the week (from Reilly &Thomas 1979).

mise the immune system. The immune system may be depressed following strenuous exercise, but usually returns to resting values within 20 h. Rebelo et al. (1998) failed to provide evidence of any immune system impairment in soccer players during a season of intense training and competition. Nevertheless, following matches during the highfrequency phase of the competitive season, players should take steps to restore fluids and energy following a match and to speed recovery before the next engagement.

The physiology of rugby football Historical introduction Rugby Union had been nurtured in the grammar schools of England. The Union split off from the professional game of Rugby League in 1895 (following the breakaway of the Northern Union 2 years earlier), with league players coming mainly from a working-class background in northern England. The divide was complete until 1995, when Rugby Union became professional. Rugby Union is played in more countries than is Rugby League. The first World Cup competition was held in Australia and New Zealand in 1987; subsequent championships were located in Great Britain and France (1991), South Africa (1995)and Wales (1999).New Zealand, Australia, South Africa and Australia again were

victorious in the first four tournaments, the inauguration of which marked the escalation of scientific approaches towards preparing teams. The demands of Rugby League and Rugby Union have been reviewed elsewhere (Brewer & Davis 1995; Reilly i997b). The focus here is primarily on Rugby Union, with observations on endurance aspects of Rugby League where appropriate. The physiological demands are outlined first; then fitness and training aspects of the game are considered. Many factors determine the physiological load on individual players. Each positional role in rugby football has its unique demands, and there is less homogeneity among these roles than in soccer. The type and frequency of training also vary with the level of play. Game performance relies on tactical awareness, interplay of individuals in tactical moves, competence of players in catching, passing, kicking and tackling, and skills specific to playing position. Rugby Union and Rugby League both require an amalgam of fast reactions, speed, agility, muscular strength and anaerobic and aerobic power, although combined in a complex manner. Nevertheless, an attempt can be made to assess rugby games from a physiological perspective and to match this assessment of physiological responses to match-play with fitness profiles of the players. The increase in women’s participation in football games is reflected in the growing popularity of women’s Rugby Union football. The first World



Cup for women’s national teams was held in Wales during April 1991. Researchers have given little attention to the women‘s game, except for some anthropometricreports (Sedlocket al. 1988;Kirby & Reilly 1993). Consequently, this part of the review focuses on research reported for men’s Rugby Union football. Activity patterns in Rugby Union football A Rugby Union game lasts 80 min plus time added by the referee, but it typically has only 25-3omin of actual play. On average, it contains 140 sequences of action. Altogether, 32% of sequences are 0-5s in duration, 24% are 5-10s, 29% 10-2os, 10%are sequences 20-30 s long and only 5% are longer than 30s. These figures imply an emphasis on anaerobic metabolism during the intense periods of play (56% < 10-s duration) (see Reilly 199713). The total distance covered in a match may be divided according to the different exercise intensities demanded by discrete activities and it can be complemented by establishing ratios of exercise to rest durations. The overall distance covered in amateur Rugby Union is 5.5km for forwards and 3.8km for backs, with values ranging to a maximum of 9.6 km (Reid & Williams 1974). These distances are relatively modest compared with 6lite soccer play, even after allowing for the iomin shorter duration of Rugby Union play. Morton (1978) reported that Rugby Union play comprised 37% walking, 29% jogging and 34% striding/sprinting. Contemporary topclass play emphasizes support of the player with the ball, or seeking to regain it, and this has increased the energy expenditure required of the backs. Australian centre-backs and half-backs (5530m) and wingers and full-backs (575om) covered more ground than props and locks (4400m) and back-row (4080m) players over 70min of under-19 matches (Deutsch et al. 1998). Rugby Union players spend more time in ’game-related activities’ than players in other football codes, with scrums, rucks and mauls engaging groups of forwards together for protracted periods. About 85% of players’ time is spent in low-intensity activity (Dochertyet al. 1988). Players have to resume formations in order for play to continue following a quick switch of play to the

other half of the field. The remaining 15% of the player’s time is taken up by intense exercise, 6% being related to running and 9% to tackling, pushing and competing for the ball. The demands imposed by the game differ from the demands players impose on themselves. Consequently, McLean (i992), in his analysis of the ’Five-Nations Championship’, concentrated on the game (when the ball was in play) rather than on individual players’ energy expenditures.The analysis was based on video recordings of all matches in the championship.On average, the ball was in play for 29min each game. The exercise/rest ratio ranged from 1: I to 1 : 1.9. These ratios were consistent from match to match, and were later employed in prescribing training and designing field-based tests (McLean 1993).In 63%of cases, the rest exceeded in length the preceding sequence of play; in 37% of cases the rest was shorter than the exercise bout it followed. The exercise periods were mainly in the range 11-25 s, the overall average being 19s. The time during five matches at the 1987 Rugby World Cup was divided between q m i n (31%)of play and 55 min (69%)of stoppages. The mean time for single actions was 7.3s for forwards and 6.5 s for three-quarters; time for stoppages averaged 33 s. During any one match, there were 181 pieces of action, 96 stoppages and 30 scrummages. Altogether, 70% of playing sequences were 4-10s in duration and 75% of stoppages lasted between 5 and 40s. Recovery from periods of fast intense play was often incomplete (Menchenelli et al. igg2a). Special endurance capabilities were recommended to speed recovery after intense passages of play. Docherty et al. (1988) reported a mean (ks.d.1 blood lactate of 2.8 (*1.6) mh4 in players at the end of Canadian university matches, reflecting the moderate intensity of exercise at this standard. McLean (1993) tested players in top Scottish clubs, repeated measurements being made during natural breaks in the game (injuries, penalty kicks and so on). Values ranged from 5.8 to 9.8mM, indicating that competitive rugby can entail appreciable lactate production. Roughly similar values (range 6-12mM) were reported for top Italian and Argentinian sides (Menchenelliet al. iggzb). Values in the blood considerablyunderestimate concentrationsin the active


muscles (Chapters 3 and 22). Deutsch et al. (1998) showed that the mean blood lactate (4.8-7.2mM) did not differ between positional roles: they concluded that there was a need for 'lactate tolerance' training to improve hydrogen ion buffering and facilitate lactate removal following high-intensity efforts. Further, the distances covered (4.2-5.6 km in 70min) and the intermittent nature of match-play indicated a need for sound aerobic conditioning to minimize fatigue in both backs and forwards. The energy expenditure in competitiverugby was first evaluated by Yamaoka (19651, who calculated an 11-fold average increase of metabolism. Forwards expended more energy (2510-3350 kJ) than backs (1840-2930kJ). Assuming an average vokax of 4.5 Lmin-', this expenditure would correspond to an energy expenditure about 52% of Qozmax. The exercise intensity in contemporary professional Rugby Union may be greater than these findings (particularly among the backs), owing to the faster current pace of play, but it is still below the intensity in soccer (estimated 75% vo2max). Muscle glycogen stores are not exhausted at the end of a rugby match, confirming that the overall energy expenditure is low compared to that observed in soccer. Carbohydrate loading increases carbohydrate utilization during play, but it does not offer the ergogenic benefits seen in endurance athletes. Nevertheless, carbohydrate loading may be advantageous during tournaments, when a number of matches have to be played within a short time. Many teams in the late 1990s have used creatine loading regimens to prepare their players for competition. Whilst creatine loading has proved beneficial in reloading creatine phosphate stores within muscle, its value lies chiefly in preventing a decline in performance during a sequence of highintensity sprints. Its ergogenic effects in a game context are unproven. Factors affecting work rate As the traditional European Rugby Union season spans the winter months, matches may frequently take place in temperatures that are too cold for thermal comfort. Warm-up is especially important in cold conditions, in order to raise body tempera-



ture for the more strenuous activities to follow, either in training or in competition.Players attribute about 18% of injuries to inadequate warm-up. To reduce injury risk, the warm-up regimen should include flexibility exercises with actions similar to those employed in the game (Reilly & Stirling 1993). Reilly & Hardiker (1981) reported a greater incidence of injury shortly after half-time than at other points in the game. This was attributed to players getting cold while standing outdoors during the half-time break. Environmentaltemperatures during the competitive Rugby Union season are generally much warmer in the southern than in the northern hemisphere. Rugby matches-in Australia and the Southern African countries, in particular-may be played in conditions that precipitate heat stress. Players competing in air temperatures of 24-25 "C had rectal temperatures of 39.4"C at the end of a game (Doncaster 1972).Temperatureswere elevated equally in backs and forwards, but the forwards sweated more, being larger in body size. Rehydration at half-time should follow guidelines designed for soccer players (Maughan & Leiper 1994). More attention should also be given to the fabric of team clothing in conditions where hyperthermia is a risk. Altitude challenges the oxygen transport system due to the reduction in alveolar oxygen tension. This is likely to affect aerobic performance, Pozmax decliningby 15%at an altitude of 2280 m (Astrand & Rodahl 1986).Teams competing in South Africa in the 1995Rugby Union World Championships had to consider altitude training as a part of their preparation. The physiological adaptations to sojourns at altitude, notably increased red blood cell production stimulated by renal secretion of erythropoietin, have also been employed in attempts to improve aerobic performance at sea-level. Whilst altitude training has been used by some endurance athletes since the early i97os, its systematic use in Rugby Union has been limited largely to French teams (Bishon 1993). During the 1995 World Cup tournament, the South African team applied patches to the bridge of the nose with the aims of decreasing nasal resistance and increasing respiratory minute volume (PJ. The practice was adopted by British players in the



subsequent Five-Nations Championship and it spread also to soccer, Rugby League and Gaelic football players. Whilst such patches may have marginal benefits when playing at altitude, they have no physiologicaljustificationwhen players are competing at sea-level. Similarly, the benefit of the provision of pure oxygen to speed recovery in Rugby Union or Rugby League, as in American football, is unsupported by any evidence (Winter et al. 1989). Fitness characteristics of players ANTHROPOMETRY

Physical characteristics vary widely among rugby players, depending on the positional role, the level of play and the range of skills required by the game. As styles of play are altered to maintain or gain a competitive edge over opponents, so too may the players chosen to implement the game plan vary in their physical characteristics. The most striking comparison of the anthropometric characteristics of Rugby Union players is between backs and forwards. On average the forwards are 0.2111 taller. The shape and body composition of both Rugby Union and Rugby League players favour strength and muscular power rather than endurance capability. Body mass is an important factor in Rugby Union, particularly in tackling or breaking tackles. It also bestows an advantage in scrummaging, since forwards find it hard to shove a heavy opposing pack backwards. It is preferable to have this weight as lean body mass rather than as adipose tissue since the latter would constitute an extra load for the muscles to lift repeatedly against gravity in locomotion and in jumping. Forwards can enhance mobility by trimming adipose tissue levels; this indirectly improves their endurance capabilities. The heaviest of the Rugby Union club players studied by Rigg and Reilly (1988) were the second-row forwards (101 7 kg); the lightest were the half-backs, with 24 kg less body mass. Wing-backs were traditionally light, their major requirement being sprinting ability. A recent trend has seen the use of threequarter line players large in body size and so able to contribute to the other aspects of the game that


demand a high power output. Nevertheless, the need to recover quickly from short-term efforts and to reproduce high-intensity bouts after only a brief pause requires a high anaerobic endurance capability. MUSCLE STRENGTH A N D E N D U R A N C E

Muscle strength is employed in a host of activities during Rugby Union match-play, especially in view of the contact nature of the sport. This feature is even more evident in Rugby League. Muscle strength is required of forwards in all aspects of scrummaging in Rugby Union; force is applied isometrically in the first instance, and is coordinated in a sustained team push. It is also required in rucks and mauls, in ripping the ball from opponents and by all players in tackling and breaking tackles. In many of these contexts, muscle endurance is also required. In view of the many ways in which forces are exerted during a game, muscle strength has been measured by various methods. Tests of 'muscular fitness' have incorporated both strength and endurance factors. Performance in press-ups (either the number completed at a set rhythm before exhaustion, or the number achieved in a given time) discriminated between first-class and second-classRugby Union club players; among forwards, values were best in front-row players (Rigg & Reilly 1988).The 'push-ups' used in assessing the US national squad players (Maud 1983)consisted of extending the elbows, with the hands leaving the ground and being clapped together, the criterion being the number of 'clap' push-ups achieved in 45s. The backs (35 f 6.8) were better performers than the forwards (31.7 f: 8.1). This superiority was evident also in sit-ups and squat thrusts over the same time frame of 45 s. Carlson et al. (1994) used a motor performance test battery along with kinanthropometric variables to 'profile' US national rugby players. The performance variables that best distinguished between backs and forwards were the repeated jump in place (as many as possible in 45 s), push-ups and vertical jump. These variables contributed 76% to correct classification, the backs having the better performances on all tests.


Laboratory and performance tests have measured anaerobic endurance in terms of jumping ability, power output on a treadmill and on a cycle ergometer, repeated short sprints, shuttle runs and maximal accumulated oxygen deficit (MAOD).The ability to sustain maximal power output has been measured in 'anaerobic capacity' tests. Maud (1983)measured power output by means of a 40-s cycle ergometer test, reporting higher anaerobic power and anaerobic capacity in the forwards than in the backs. Rigg and Reilly (1988) observed a similar trend in measurements of peak power and mean power over 30s. The absolute power output was higher in the forwards than in the backs, but this apparent superiority was reversed when data were corrected for body mass. Cheetham et al. (1988) measured the power output of Rugby Union forwards during a 30-s test on a non-motorized treadmill. Results were compared with those previously observed for backs. The forwards performed worse than the backs, mainly due to a greater fatigue in the forwards during the test. The forwards with the highest peak power outputs also fatigued most and had the largest elevations in blood lactate concentrations. The MAOD test was used by Holmyard and Hazeldine (1993)as a measure of anaerobic capacity. Values improved systematically during the 1990 Five-Nations Championship, but had dropped by September prior to a build-up for the 1991 World Championships. At the start of the next home nations international competition, performance was significantlybetter in the backs compared to the forwards. Mean values of 7oml.kg-' were still below the target of 78ml.kg-' set for a 'good' level of anaerobic endurance fitness, 88 ml.kg-' being the target for an elite standard. Muscle fibre characteristics provide information about the dominance of aerobic and anaerobic predispositions. A predominance of slow-twitch fibres is characteristic of endurance athletes. Jardine et al. (1988) reported that university rugby players had 55% fast-twitch fibres in the vastus lateralis muscle, similar to middle-distance runners. This proportion is indicative of the mixture of metabolic attributes associated with competitive Rugby Union play. Rugby League players are likely to have more fast-



twitch fibres and place even greater emphasis on speed and strength training than Rugby Union teams. FIELD TESTS

Distances of 15m and 30 m have been employed in field tests for rugby players, on the basis that these represent typical all-out efforts during a game. A sequence of sprint tests with brief recovery periods (6-30 s) may be employed to measure the ability to repeat all-out sprints. The ability to continue reproducing such sprints places rugby in an endurance context. McLean (1992) developed a shuttle run test, the task being to maintain shuttle running at 85% V O ~ , The , ~ ~recovery . period of 30 s was determined according to average exercise/rest ratios in the game. Backs in the national Scottish team could maintain the required velocity for 9 shuttles on average, performances by the forwards being as low as 5 shuttles at various times during the season. The 20-m shuttle run has been adopted as a field test to estimate Vobax. A number of players can be tested simultaneously and the test incorporates some agility in turning that is related to the rugby games. Observations on players using this test are included in the results for vo2max to be considered later. McLean (1993) designed a functional field test for use with the Scotland national Rugby Union team. It included slalom runs across a football field over a well-marked course. Fifteen points were marked by flags, round or past which the player ran. Games skills were incorporated, including passing the ball, driving a tackle dummy over 2 m backwards, diving to win the ball on the ground and so on. The test took about 30s for forwards to perform, the backs being about 2 s faster. Whilst field tests have face validity, they have to be interpreted cautiously. Results are difficult to express in physiological terms once skills have been added to the demands of locomotion. There may also be influences from environmental conditions and ground surface conditions. Crucially, results depend entirely on the motivation of players to produce maximal efforts.





Maximal oxygen intake values have been reported for various Rugby Union teams (see Table 61.5).Values generally increase with the standard of play. They are higher for backs than for forwards, even though the latter cover more distance in the game. Maximal oxygen intake may not be so important in a game which makes proportionately more demands on the anaerobic system, but it can provide the basis for sustained and repeated anaerobic efforts and recovery from them. Consequently, Pobax values tend to be well below the standards accepted for top soccer players, the exception being the Italian players studied by Menchenelli et al. (1992b). The 'anaerobic threshold (Chapter 22) may be determined as a breakpoint in the linear relationship between running velocity and VE or blood lactate. Alternatively, the exercise intensity corresponding to a fixed lactate concentration (such as 4 mM) may be used as a reference. Douge (1988) reported that the running speed corresponding to the 'anaerobic threshold was lower in Rugby Union players than in Australian Rules or soccer players. In the latter group, the breakpoint is usually observed at about 75% VoZmax.

The average (*s.d.) maximal heart rates of US Rugby Union club players were 182 (*9) beatemin-' and 189 beatsmin-' for forwards and backs, respectively, both groups being within the normal population range (Maud 1983). The corresponding values were 174.6 (k25.6) l-min-' and 176.1 (k16.0) 1.min-'. Values for university players of 110(k16.6) 1.min-l (Williams et al. 1973) were closer to normal population values, reflecting the smaller body size of university players compared to their club counterparts. The poor endurance-run performances of these players compared to professional soccer players suggest that aerobic fitness was neglected in their training. The university forwards studied by Jardine et al. (1988) demonstrated higher pEmxvalues than the backs (133.1 + 13.8 and 110.8 21.6l.min-', respectively). This difference could be due to the greater body size of the forwards (body height 1.88 k 0.08m, body mass 98.0 k 8.7kg) compared to the latter (1.81 0.05 and 75.4 5.8, respectively). The maximal heart rates of these players (188 7 and 193 5 for forwards and backs, respectively) were close to those of US club players. These figures highlight the unexceptional nature of the heart rate response to maximal exercise in rugby players.







Table 61.5 Mean values for maximal oxygen intake (cohax)of Rugby Union players reported in the literature. Source

Level of play

Williams et al. (1973) Maud (1983)

University College forwards US club backs US club forwards Japan college half-backs Japan college three-quarters Japan college forwards England squad Italy club players Scotland squad Wales squad: backs Wales squad: forwards Wales squad seniors Wales squad: under-14s South Africa university backs South Africa university forwards

Ueno et al. (1988)

* Holmyard & Hazeldine (1993) Menchenelliet al. (1992b) * McLean (1993) Tong & Mayes (1995) Mayes & Nuttall (1995) Jardine et al. (1988) ~~


*Indicates value estimated from shuttle run test.

46.3 59.5 54.1 55.8 (k6.7) 54.5 b6.4) 54.7 (*7.2) 58.4 (*3.3) 61.9 (k7.1) 52.0 59.1 (i2.8) 54.3 (f3.1) 55.6 (k3.8) 55.2 (k4.5) 55.8 b 4 . d 52.0 (k4.8)

17 38

44 18 18

23 18 21

37 42 14 15



Rugby Union was traditionally a sport where a scientific approach towards training was eschewed and the lifestyle of players was rarely such as to enhance athletic performance. Rugby League players, on the other hand, have a longer history of systematic training for competitive play. Even since introduction of the Rugby Union World Cup, the fitness levels of international players demonstrate seasonal variations. Players alternate systematic training with pronounced detraining in the offseason. Rugby players have traditionally been negligent with regard to diet and nutrition. Nine rugby players were among the group whose dietary habits were studied by Piearce (1993).Protein intake was above the guidelines recommended for athletes and alcohol intake was above the maximum amount (5% of total energy intake) recommended for the general population. Many players did not consume any carbohydrate in the first 2 h following exercise, a factor which would delay their recovery. Alcohol consumption was traditionally embedded in the postmatch socializing of Rugby Union players. Many players also drank alcohol on the night before playing. OBrien (1992)reported a ‘hangover’effect of alcohol. Players consumed their normal quota on a typical night out and were tested at noon the next day, following a 6-h sleep and a standard breakfast. Whilst anaerobic performance was unaffected, there was an 11.4% decrement in aerobic performance. Clearly, players need to be educated about the adverse effects of drinking the night before playing. Rugby Union demands mobility, agility, muscular strength and muscular power. These vary with positional role and the level of competition. Anthropometric characteristics are more variable between playing positions than between competitive level, and such characteristics may determine the specialization of players in particular roles. Rugby League players tend to be more homogeneous, since scrums and line-outs form only a minor part of the game and the intermissions between exercise bouts are invariably short. Anaerobic parameters play a more dominant role in game-related performance in both rugby codes than in soccer. Nevertheless, aerobic


capacities provide relevant background fitness status and help sustain work rates to the end of matches. A systematic approach to training and competing has been adopted within Rugby Union in recent years, in turn altering the attitudes and lifestyles of players at an Bite level. Those aspiring to play at the highest level in either rugby code must now adopt a scientific approach to training and preparing for competition.

American football Background to the game American football is the largest spectator sport in the US and its major spectacle, the Super Bowl, is watched live on TV worldwide. Games consist of four quarters. Although each lasts only 15min of actual play, the game itself may be spread over 3-4h. The frequent interchange of offensive and defensive line-ups on the field of play as possession of the ball changes hands means that players are only intermittently involved directly in play. When play is in progress, the action is intense. Consequently, the game makes high and prolonged demands on speed, anaerobic power and muscular strength rather than on aerobic power. Each team has a 45-man squad, consistingof three quarter-backs, five running backs, four wide receivers, two tight ends, eight offensive linemen, seven defensive linemen, seven linebackers, four defensive backs, one kicker and one punter, plus three others. The offence contains linemen (tackles, guards and ends) and centres; the defence has secondary lines (safety, guards), linebackers (outside, middle) and linemen (ends and tackles).A typical 3-4-4 defensive unit will have a tackle and two ends, four linebackers and four defensive backs. As the game is a physical contact sport, tackling and blocking are important skills. The game is unique among the football codes in the amount of protective clothing worn by players. The clothing should not interfere with running, execution of other game skills or heat loss when playing in hot conditions.



Demands of the game Periods of play (usually < 30 s) are generally intense before players gain respite at each 'down' or change of possession. As players regularly have intervals off the field of play, they are not required to make multiple repeated sprints, as in soccer or Australian Rules football. Nevertheless, they must maintain attention for the entire game, since at any time they could be called into action. The main demands seem to be on alactic anaerobic power, with some demands on anaerobic power and capacity. It is unlikely that blood lactate reaches very high levels, or that there is pronounced hypoxia within the active muscles. The current use of oxygen for recovery when players reach the sideline is unnecessary and has little to recommend it (Winter et al. 1989). Demands placed on aerobic metabolism are relatively light, the average rate of energy expenditure being 37.7kJ (9 kcal).min-' (Brooks & Fahey 1984). Characteristics of players American footballers on average tend to be taller and leaner than participants in the other football codes. The contemporary game at top level calls for larger players than in the previous generation, and the physiques predispose towards muscular strength and power output rather than endurance. An excess of adipose tissue predisposes against endurance as well as mobility in sprinting. Studies on US college players (Burke et al. 1980) show a mean body fat of 13%for 20 backs and 21.8% for 33 linemen. Defensive backs have less body fat than offensive, 7.3 and 11.5%. respectively. In four separate studies (reviewed by Reilly 1990)~comparative mean values were 6.7-11.5% for defensive backs and 11.5-13.8% for offensive backs. The defensive backs rely more on agility and speed of movement, whilst the extra weight helps the offensive backs to maintain momentum after impacts. The overall values are lower than in normal populations of comparable age, but are higher than values reported for endurance athletes. Professional footballers have below-average vital capacities, the mean being 94.3% of values predicted


from a standard nomogram. Wilmore and Haskell (1972) found no consistent relationship between height or body mass and vital capacity or total lung volume. Vital capacity values for defensive backs (83% of predicted vital capacity) were especially poor. These results contrast with an earlier study of 16 collegiate footballers (Novak et al. 1969), where players were smaller, but averaged a 1-1 larger vital capacity than the professionals. The average maximal heart rate of the professional American footballers studied by Wilmore and Haskell (1972) was 185 beats.min-'. Values varied from 179 (offensive backs and receivers) to 198 beats.min-' in defensive backs. The pEjEmax values similarly varied from an average of 149.3 for three linebackers to 189.61.min-' for four offensive linemen and tight ends. The values of American footballers are quite modest, average values being highest in defensive backs (54.5ml.kg-'.min-') and lowest in defensive linemen (43.5ml.kg-l.min-'). Since defensive linemen carry a greater proportion of body mass as fat than other players, expressing Vozmax per kg lean body mass brought values for the defensive linemen closer to those for defensive and offensive backs and wide receivers (Wilmore & Haskell.1972). Nevertheless, figures were still well below those observed for linebackers and offensive linemen. Although the defensive backs had the largest aerobic power, their values were below expectations in endurance sports, reflecting the pronounced anaerobic metabolic load in playing the game. This was corroborated by Gettman et al. (19871, whose professional players had an average pozmax of 49.2 ml.kg-'.min-'. A strenuous 14-week conditioning programme improved this value by only 6%. Training Training for American football emphasizes the development of strength and muscle power, in accordance with the demands of the game. Consequently, the vast majority of teams are well equipped with weight-training facilities, including isokinetic and multistation apparatus. Free weights are still widely used in training specific muscle groups, and many coaches prefer such training to


aerobic, circuit weight-training. Specific dynamic practices include use of tackle dummies, where game skills can be improved against fabricated resistance. Despite being recommended to continue fitness training in the off-season, many players return to preseason practices overweight. Frequently, they lack the stamina for long training sessions at this time. In the past, the use of sweat-suits in a misguided attempt to shed unwanted weight quickly led to fatalities from hyperthermia. The footballer clad in the usual protective clothing and exercising in the heat has difficulty in evaporating sweat. This can cause a dangerous elevation of body temperature and slow dehydration of the player. Use of a mesh jersey allows more effective evaporative and convective cooling of the body. Aerobic fitness also helps thermal homeostasis. The risks of heat injury are now recognized by trainers and a high priority is given to replacement of body fluids during practices.

Australian Rules and Gaelic football Introductionto the games Australian Rules matches are held in a large oval field, with 18 players on each team. The game consists of four quarters, each of 25-min duration. The ball is moved quickly from end to end with the purpose of scoring, thereby promoting a flowing style of game. Six points are awarded when the ball crosses between two central uprights, and one point if it goes between the two side uprights. As the game is continually in motion, all players need good running ability, agility in avoiding tackles, catching and kicking skills and tactical sense. The Gaelic football field is approximately qom longer than a soccer pitch, with 15 players on each side. Goalposts at each end have a crossbar, a goal (equal to 3 points) being scored beneath it, and a point if the ball crosses above the bar and between the posts. The ball is round like a soccer ball, in contrast to the oval shape of the Australian Rules ball. Apart from the shape of the ball and the scoring system, the two games are close relatives, having many skills in common. These include high catch-


ing, long-distance kicking for accuracy, passing and moving the ball downfield. Players from the two codes quickly adapt to the 'Compromise Rules' game which has been played at international level (Ireland versus Australia) since the 1960s. Gaelic football consists of two 30-min halves. Time is increased to 70min in intercounty championship games. The normal energy reserves of the body should sustain intense match-play more easily in this than in the Australian Rules game, because of its shorter duration. The extent to which glycogen stores are deployed in competition depends on the work-rate profiles and patterns of activity in each of these football codes. Demands of the games The movement patterns of Australian Rules players are in general similar to those observed in soccer. Players cover over 10 km per game (27% walking, 53% jogging and zo% striding or sprinting); 30% of sprints are 40m. Players sprint more than 40m only a few times per game. The activity profiles differ according to position. The rover, ruckman and centreline players have to cope with sustained efforts whilst the half-back flanker and backpocket player have comparatively short bursts of activity. The distance covered in a game by a half-back flanker was 77% that of a rover (Pyke & Smith 1975), roughly the difference between the work rate of a centre-back and a midfield player in soccer. As in Australian Rules, Gaelic footballers need to accelerate to receive or intercept a pass, or leap to catch a high ball. The ball is seldom out of play for long, so players have few respites during a match. The toe-to-hand method of travelling with the ball means that many forwards cover more distance in possession than do Australian Rules or soccer players. Nevertheless, the distance covered in possession of the ball is a mere 2% of the overall distance covered in a Gaelic football match and only 4min is occupied with high-intensity activity likely to place demands on anaerobic metabolism (Keane et al. 1993).





The overall distance covered in intercounty Gaelic football was calculated to be 8594 (*sad.= 1056) m (Keane et al. 1993). Walking and jogging accounted for two-thirds of the total distance. The greatest distances were covered by centrefield players (9131 977m), followed by backs (8523 1175 m) and forwards (8490 f 673m). Gaelic footballers demonstrate higher average speeds of movement (133m - m i d ) than those reported for Australian soccer players (124mmin-': Withers et al. 1982) and Australian Rules players (106m.min-': Douge 1988).The shorter durations of Gaelic football matches mean that fatigue due to depleted muscle glycogen stores is unlikely. The energy expenditures of the Gaelic football goalkeeper are relatively light, but physiological demands are well distributed among the other players. These consist of three full-backs, three halfbacks, two midfield players, three half-forwards and three full forwards. In the Australian Rules game the highest work rate is accomplished by the 'rovers'. McKenna et al. (1988)reported that walking took 44% of rovers' match time, jogging 40%, highintensity runs 5% and game-related activity 2.5%, and for less than 9%of the time were they stationary. The mean duration of a high-intensity run was 2.7 (* 0.7)s, the maximum being 10.4s, and one such run occurred every 73s on average. The overall physiological strain on players in these two football codes is represented by the irregular superimposition of changes of pace and anaerobic efforts on a background of light to moderate aerobic activity. The activity patterns denote a call on aerobic metabolism and on intramuscular phosphagens. Anaerobic breakdown of glycogen is implicated in the longer sprints. Pohl et al. (1981) observed that the anion gap increased and blood bicarbonate levels decreased during Australian Rules football, changes compatible with a mild metabolic acidosis. An Australian Rules football game is likely to reduce muscle glycogen stores to low levels. The activity patterns and distance covered are broadly similar to those of soccer players, whose thigh muscle glycogen depots are nearly depleted by fulltime (Saltin 1973).On the day following a match, the are below normal peak values for vo2 and





(McKenna et al. 19881, an observation compatible with reduced muscle glycogen. A diet rich in carbohydrate is thus recommended to aid recovery from exercise-relateddecrements in aerobic power. Indices of cardiorespiratory strain during Australian Rules matches confirm a relatively high aerobic load. The mean heart rate during play (161 beats.min-') is comparableto observationson soccer players (Douge 1988).The heart rates of club Gaelic footballershave been measured as 157 10and 164 10beatssmin-' for first and second halves, respectively Blood lactates measured at the end of each half are 4.3 1.0 and 3.4 1.6mM, respectively (Rorida-James & Reilly 1995). The overall relative loading is estimated at 72% vohax. 'Rovers' in Australian Rules seem to have higher heart rates than other players during games. Pyke and Smith (1975) reported values of between 170 and 185beats.min-' (mean 178 beatsemin-I); it is unlikely that in any Gaelic football outfield player operates at this high level.





Characteristics of players Australian Rules players tend to be large. Mean height and body mass were 1.83m and 80kg, respectively (see review by Douge 19881, with ranges of 1.76-1.93 m for height and 79-93 kg for body mass. Interindividual variability was attributed to the demands of specific positional roles. Tallness is an advantage in contesting aerial possession of the ball and catching is an important skill in the game. Not surprisingly, there is a gradation in body size with the level of competition, top professional players being the tallest and heaviest, players in amateur clubs being the smallest and lightest and those in low-level professional clubs having intermediate values. The sprinting performance of Australian Rules players compares poorly with that of top American football players. Pyke and Smith (1975) reported 40yard (36.6-m) times averaging 5.25s for Perth (Western Australia) players. The corresponding time for Dallas Cowboy professionals was 0.35s faster, although they were 23 kg heavier than the Australian Rules players. This reflects the emphasis on anaerobic power in the American game, com-


pared with the more aerobic nature of the Australian code. The inference of a moderately high aerobic demand in the Australian Rules game is supported by observations on Pohu. The 64 rnl.kg-'.min-' average for elite players (Douge 1988) is much higher than corresponding values for rugby and American football. Most positional roles demand a high aerobic power, the 'rovers' having the highest aerobic requirements. of Gaelic footballers depends on the The level of competition. University players had average values of 47mLkg-'.rnin-' (Kirgan & Reilly ig93);whilst a more successful club team had values of 52.6 (*4) ml.kg'.min-'. Successfulcounty teams had mean values of 56 (Keane et al. 1997) and 58.6ml.kg-'min-' (Watson 1995; Reilly & Doran, 1999) as they prepared for the All-Ireland finals. Outfield players tended to be homogeneous with respect to Vo2max. Similar inferences can be made from the data on the physical working capacity of Gaelic footballers. Watson (1977) found that power output at a heart rate of 170 beatsmin-I (PWC,,) was higher in successful than in less successful county teams, even when data were adjusted for the larger body size of the successful players. Values were highest close to provincial or All-Ireland championship finals, suggesting the impact of training for such events. Training The training among top sides is much more systematic for Australian Rules than for Gaelic football. It usually involves 4-5 sessions a week, with 1-2 rest days. Besides, players engage in one and sometimes two matches per week. The traditional conditioning programme emphasized aerobic exercise. Jones and Laussen (1988) introduced a more comprehensive programme which incorporated strength training. Running drills were also designed to resemble activity patterns in the game. The programme adopted by the Fitzroy FC team also utilized a game skill combatrunning circuit: this was intended to develop the agility and acceleration related to competitive play. The conditioning drills included, for example,


blocks of short sprints, repeated every 20s with 2-min rests between sets. During the playing season, the training load tends to be distributed unevenly over the week. The most arduous sessions are on Tuesday evening: from then on, training is tapered in preparation for Saturday's competition. Training is resumed on Sunday, but tends to be light in order to recover from the effects of the previous day's contest. This cyclical organization resembles soccer practices, ensuring that players start their match physiologically recovered from training sessions during the week. Gaelic football is still an amateur game, and this is reflected in training programmes. Highly organized training is concentrated mainly in the championship season, May to September. League and friendly matches provide the main training stimulus in the remainder of the year. Teams eliminated in the first round of championship matches may not attain high fitness standards. Watson (1977) found the highest PWC,,o among players preparing for provincial and All-Ireland finals. The same trend was reported for All-Ireland champions in the mid1990s (Keaneet al. 1997).

Field hockey Historical background The game of field hockey is thought to have evolved from prehistoric human's delight in stick-and-ball games. Its origins as a semiorganized activity have been traced to Asia, about 2 0 0 0 B C . A form of the game was played by the Egyptians 4000 years ago, and later by Ancient Greeks. The Romans developed the game, passing it on to the European nations that they conquered. Thus, German (Kolbe), Dutch (het kolven-a forerunner of ice hockey) and French (hocquet-meaning shepherds crook) versions evolved. The true ancestor of field hockey is thought to be Irish hurling, the original Gaelic term 'iom6n' meaning a vigorous forward drive (see Reilly & Borrie 1992). Field hockey is played on a pitch 9om long and 55m wide. Teams are composed of 11 players, including a goalkeeper. Unlike other stick-and-ball



games (hurling, lacrosse, bandy and shinty), the ball is played with the stick on the ground and the use of the hand in catching is prohibited. Amatch is played over two 35-min halves, with a 5-10-min interval. The game requires a wide repertoire of skills and physical and psychomotor attributes. Two areas of technical development have affected physiological requirements: the hockey stick and the playing surface. Field hockey is similar to most field-invasive games, with one unique feature. The rules governing use of the stick and its design preclude any lefthanded sticks, since the player may use only the flat side of the stick. The easiest position from which to exercise game skills is with the ball out to the right of the body. The effectiveness of this body-ball position determines the pattern of play when two opposing players confront each other. An attacker will try to take the ball around the left side of the defender, the defender's weakest tackling area, whereas the defender tries to force the attacker to pass down his/her right side, the strongest tackling area. Playing right-sided dictates that the right wing is the main channel of attack. Hockey therefore has an in-built asymmetry in terms of individual and team play. This should raise the physiological demands, as players must pay attention to body position in relation to both ball and opponent. Maintenance of correct positioning increases the work rate when playing, and in particular when defending. Energy expenditures in field hockey Fox (1984) included hockey with lacrosse and soccer among sports with a 30% aerobic, 70% anaerobic contribution to energy expenditure. Sharkey (1986) classified the game as bordering on the aerobic side (40% anaerobic, 60% aerobic), grouping it with sports of mixed demands that included canoeing, kayaking, lacrosse, motocross and mountaineering. The contemporary game is aerobically more demanding than previously, with frequent though brief anaerobic efforts superimposed on aerobic metabolism. The exercise intensity in hockey can be gauged from motion analysis. Male players at the 1973

World Cup were active for zo.6min (30% of match time) and in that time covered 5.61km, implying an exercise to rest ratio of 2:5 (Wein 1981). Defenders covered less (5.14km) and midfield players more (6.36km) ground. The player covering the greatest distance (on the New Zealand team) had a value of 8.82 km. A task analysis of players' actions suggested differences among outfield players, at least with the conventional game. Overall, hockey players were reported to 'make more light than strenuous movements', 69% compared with 31%. Centre-forwards made the highest number of strenuous movements (36%), whilst defenders and 'halves' functioned with 70% of light movements. The 'heavy' movements call for great muscular effort in hitting the ball strongly, whereas light movements encompass push passing for precision and dribbling (Wein 1981). Of all the activity on the ball, 61% lasted between 0.5 and 2.05, only 5% lasting more than 7s. Clearly, much of the activity of players involves motion 'off the ball'. Energy expenditure estimates approaching 50 kJmin-' in field hockey have categorized the men's game as 'heavy exercise' (Reilly 1981).Boyle et al. (1994) reported mean heart rates of 155 beabmin-' in international players, which yielded an energy expenditure estimation higher than this value. The greatest energy expenditure was among central midfield players, the lowest in the left corner forward. In the women's game, the most strenuous position, centre-midfield, has an associated energy expenditure of approximately 35 kJ.min-' (Skubic & Hodgkins 1967). The figures are based on predictions rather than direct measurements, due to difficulties in monitoring during play. Direct measurements of Indian soldiers during recreational play yielded a value of 36.4 kJ.min-' (8.7kcalmid) (Malhotra et al. 1962). The energy expenditure is probably higher in competitive match-play. Reilly and Seaton (1990) measured energy expenditure, heart rate and perceived exertion in hockey players dribbling a ball on a treadmill at speeds of 8 and 10 km.h-'. Dribbling increased energy expenditure by 15-16kJ.min-' above that observed in normal running. The heart rate was elevated by 23 beatsemin-I, whilst perceived exertion increased


from 'very light' and 'light' to 'somewhat hard' and 'hard at the two speeds examined. The greater additional energy cost in field hockey compared to dribbling in soccer (Reilly & Ball 1984) reflects postural factors and arm and shoulder exercise when using the hockey stick. The physiological costs of accelerating, decelerating and changing the direction of motion add to energetic requirements. As with soccer, the physiological cost of hockey play is underestimated if prediction of Poz and hence energy expenditure is based solely on the distance covered during a game. The playing surface can influence physical and physiological strain. The effective duration of a hockey match played on grass at the second World Cup in Amsterdam was only 53% of the total game time (Wein 1981). Interruptions lasted 8.7s on average, and were about twice as numerous as in soccer at a comparable standard. There were 230 stoppages per match in the 1975 Pre-Olympic Tournament at Montreal. These averaged one every 18s. Adoption of synthetic surfaces at the 1976 Olympic Games and subsequent international tournaments increased playing times and decreased the number of interruptions. This trend was enhanced by rule changes in 1981-2 which speeded up the game and kept the ball in play for longer than before. Playing characteristics are more consistent on synthetic surfaces than on grass. The ball also travels over the surface at a faster pace. Both factors have changed the style of play and affected physiological requirements (Malhotra et al. 1983). Both anaerobic and aerobic demands on players are likely to have increased. It is easier to execute individual skills on a synthetic surface, thereby retaining possession of the ball under pressure. The speed of ball movement and higher individual skills have increased emphasis on a team's ability to play as a cohesive unit. Teams now adhere more closely to the concept of 'total' hockey, players being able to interchange positions during a game without disrupting team balance. Players thus cover greater distances within a game and must have the aerobic fitness to do so. Malhotra et al. (1983) studied physiological demands using a Kofranyi-Michaelis meter during


a field hockey game. Physiological responses were greater on an artificial pitch compared to grass, mean OE being 56.8 versus 46.61.min-' and mean Poz 2.26 versus 1.9il.min-'. The Po2 values correspond to energy expenditures of 46.5 kJ.min-' (11.1kcal.min-') and 39.3 kJ.min-' (9.4kcal.min-') for artificial and grass pitches, respectively. The higher physiological stress on the synthetic pitch was due to faster play and higher running speeds. However, the game was a six-a-side match, played on half a normal-sized pitch, and so is not representative of normal field hockey matches. Positional role

The evolution of playing formations within hockey initially followed the same pattern as in soccer. The classical 2 :3 :5 formation dominated tactical thinking until the mid-i96os, when a sweeper system was introduced in West Germany (Wein 1981). In the mid-i98os, the formations became more varied and dynamic, the most popular systems being I :3 :3 :3, i:3:2:4 and 4:2:4 (Whitaker 1986). Synthetic playing surfaces also altered styles of play, and players now interchange positions frequently during a game. Ready and van der Merwe (1986) examined positional differences in the Canadian Olympic women's squad. Players were classified as defenders, midfield and strikers, corresponding to the backs, halves and forwards of Indian and Australian researchers. It was thought that the Canadian training programme and system of play would even out the fitness demands of outfield positions, but forwards had the highest Pobax (Fig. 61.6), midfield players had the greatest anaerobic capacity as measured in a treadmill run test, and defenders had the lowest peak lactate level and Vozmax. A fitness evaluation of 24 English female hockey players (Reilly & Bretherton 1986) failed to separate players according to positional roles. This applied to kinanthropometric measures, muscular strength and power, aerobic fitness and field tests. However, goalkeepers tended to be high in anaerobic power measures and poor to moderate in aerobic fitness indices.



Fig. 61.6 Maximum oxygen intake in Canadian female hockey players accordingto positional role (from Ready & van der Merwe 1986).

Fitness profiles: women's field hockey MUSCLE PERFORMANCE

Female field hockey players show a high anaerobic power output relative to other games players (Reilly & Secher 1990). Their mean performance on the stair run (955W) is similar to netball players (953W) and superior to endurance athletesorienteers and cross-country skiers. When adjusted for body mass, the performance of the field hockey players was 3.7 W.kg-' greater than that of netball players. A high anaerobic power output facilitates changes of pace and direction during a game. Anaerobic power discriminates successfully between elite and county-level players (Reilly & Bretherton 1986). Elite players are also superior to county players in a range of muscular fitness measures. Principal components analysis of data on 24 female hockey players identified components of anaerobic power and dribbling speed which were significantly correlated (r = 0.694). The 'dribbling speed' component incorporated a 50-yard (45.5-m) sprint and a 60-yard (54.6-m) run over a 'T'-shaped course whilst dribbling a hockey ball around skittles (Reilly & Bretherton 1986). 'Dribbling speed' discriminated between levels of play, indicating the importance of this skill in field hockey. The relation

with run time suggests that sprinting ability contributes to fast dribbling. Reilly and Bretherton (1986) evaluated English elite female players. Their first test was a z-min 'T' run over a 60-yard (54.5-m) course, dribbling a leather ball around skittles. Sports that engage large muscle groups for I min or more may tax Vozmax,so this test implies a high aerobic loading (Astrand & Rodahl 1986). Use of reversed sticks is excluded, and the best of three trials is recorded. Performance is significantly correlated with both aerobic (r = 0.48) and anaerobic (r = 0.60) power, and it differentiates between Clite and county-level players. AEROBIC FACTORS

The mean vozmxof elite female field hockey squads (Table 61.6) ranges from 45 to 59mJkg-'.min-' (Reilly & Secher 1990). This is comparable to values for lacrosse players, but lower than for crosscountry skiers and orienteers. Elite English squad players had predicted vozmx mean values of 46 f 9ml.kg-'.min-', distinguishing them from county players who had mean values of 41 f Gml.kg-'.rnin-' (Reilly & Bretherton 1986). American (Zeldis et al. 1978) international players demonstrated mean values of 52mLkg-'.rnin-', rising to 57ml.kg1.min-' before the 1996 Olympic Games (Sparlinget al. 1998).




Table 61.6 Mean eoZmax of top female and male field hockey players: only figures obtained in a treadmill test are included (from Reilly & Borrie 1992;Boyle et al. 1994; Sparling et ul. 1998). n

Level of play

Females College (US) Provincial (Australia) College and national (US) County (England) National (Wales) National (US) National (Canada)

42.9 50.1 51.7 52.2 54.5 57.1 59.3


6 10 12 10



Males Provincial (Australia) Provincial and national (Australia) National (UK) National (West Germany) National (Ireland) National Senior B and Junior (Spain)

There is a large genetic component to and improvement with training is normally only about 25-30% (Astrand & Rodahl 1986). Nevertheless, such an effect could contribute to the spread of values reported for top players, reflecting the phase of the competitive season and training status. In the year leading up to the Los Angeles Olympics, the Vo,,, of the Canadian Olympic team increased from 52.7 f 6.0 to 55.7 f 4.5 and finally to 59.3 4.1 ml.kg-'.rnin-' just before the tournament (Reilly & van der Merwe, 1986). Higher values during peak training periods may be attributable in part to a loss of fat mass during training. In the year's build-up to the Los Angeles games, the average body fat content of players decreased from 18.9 to 15.7% of body mass. This alone would account for 25% of the reported increases in Vohax. Typically, intensifying the training programme of field hockey players entails superimposing specific drills on the normal regimen. The mean pojmax of Welsh international players was 54 rnl.kg-'.min-' in the early stages of planning for an intercontinental tournament (Reilly ef al. 1985). The squad had a good background of match-play, endurance and general fitness training in the 2 months prior to initial measurements (3 months before the tourna-


9 14

64.1 60.7 62.2 63.5 61.8 59.7


5 9 26

ment). From then on, the training programme was designed to maintain aerobic fitness, but also introduced elements of sprint training. In the month of the competition, the vohax, body fat, ventilatory threshold and anaerobic capacity were all unaltered, whereas flexibility and sprinting speed were significantly enhanced. It was concluded that flexibility and anaerobic power could be improved prior to major tournaments without detrimental effects on aerobic fitness. Cheetham and Williams (1987)noted similar findings in English county players. Six weeks of highintensity training included four or five training sessions per week (two fast runs of 5-9km, two interval sessions of repeated yy,oo-m runs and at least one circuit training session), in addition to normal hockey commitments of one or two skill/tactical sessions and one o r two matches per week. The improvement in vo2max was small, from 50.1 4.1 to 52.2 3.7ml.kg-'.min-'. These values compared with 43.9 f 2.5 and 44.9 f 2.7 ml.kg-'.min-' for club players who were measured at the same times but did not undertake supplementary training. Aerobic rather than anaerobic factors best distinguished between the two levels of play. Peak blood lactate levels measured 5 min after a 30-s






all-out treadmill sprint were similar for the county and club players (15.4 2.2 and 14.9 f 1.7mM, respectively). The predominance of aerobic over anaerobic factors in female field hockey players is further suggested by muscle biopsy studies. Prince et al. (1977) reported that female college players possessed a significantly higher proportion of fast oxidative glycolytic (Type IIb) and slow oxidative (Type I) skeletal muscle fibres than controls. Whether this trend was due to endowment or training could not be established. Pulmonary and cardiac function data have been reported for female field hockey players. The vital capacity was 17.6 and 16% greater than normal values matched for age, gender and body size in elite and county squads, respectively (Reilly & Bretherton 1986). Corresponding values for I-s forced expiratory volume (FEV,,o) were 14 and 13% above expected. The of the Canadian national squad (Ready & van der Menve 1986) peaked just prior to the Olympic tournament at 96.4* 10.71.min-'. The corresponding maximal heart rates were 195 9 beabmin-'. The mean of the Welsh national team (Reilly et al. 1985) was 100.3 19.2l.min-'. The maximal heart rate of English players (combined elite and county) was 192 7 beatsmir-I, close to general population values (Reilly & Bretherton 1986). The 'ventilatory threshold' of Welsh international players was 76.8 f 6.6%of Vozmax(Reillyet al. 1985). This indicates a good training status, comparing favourably with values expected in good distance runners. The power output corresponding to a heart rate of 170 beabmin-' has traditionally been used as a measure of aerobic capability. Values in the English klite squad members averaged 2.3W.kg-', compared to z.oW.kg-' for county players (Reilly & Bretherton 1986). Mean PWC,, values were about 24% greater in the elite squad than in sedentary females (Davies & Daggett 1977). The average for Welsh international players was 2.87 W.kg-', recorded after a good background of match-play and fitness training. It seems that aerobic fitness influences the standard of play in female field







hockey players and so aerobic training should form an essential part of preparation for competition. Fitness profiles: men's field hockey

Reviewing competitors at the 1964 Olympic Games in Tokyo, Hirata (1966) concluded that the physique of male field hockey players was almost the same as that of soccer players. The age of peak performance for ball players was 24-27 years, soccer success being accomplished earliest and hockey latest. Training programmes for Olympic competitors have improved considerably in the intervening three decades, but field hockey is still largely an amateur game; social pressures rather than ageing determine the duration of top players' careers and the fitness levels they reach and maintain. AEROBIC FACTORS

The average voZmax of teams reviewed by Reilly and Secher (1990) ranged from 48 to 65 ml.kg-'.min-'. The lowest figure was a step-test value for the Argentinian team obtained at the Olympic village in Mexico in 1968 (Di Prampero et al. 1970).The figure for top German players (Rost 1987) was estimated from a graphical presentation of results (Table 61.6); findings were comparable with top German tennis players and middle-distance runners, and exceeded values for handball players and ice hockey specialists. It seems that values in excess of 60ml.kg-'.min-' are required in top field hockey players, much as in professional soccer players (Reilly 1996). The heart size of field hockey players approximated that found in soccer players, and exceeded that noted in ice hockey and handball (Rost 1987). Greater heart dimensions were observed in decathletes, who might be expected to have much more arduous training programmes. The QEmax of the Senior B and Junior Internationals in Spain averaged 148.4 io.gbmin-' (Drobnicet al. 1989). These values compare favourably with observations on professional soccer players (Reilly 1996). Apart from a high aerobic power, field hockey requires a capability to accelerate and decelerate



quickly; this is more critical to performance than maximal speed. In an analysis of state-level Australian sportsmen hockey players had a mean relative leg power which compared favourably with state footballers (Witherset al. 1977). Training Data on the most appropriate training regimens for field hockey are sparse. The significant aerobic contribution to energy expenditure is evident in the of both male and female players (Withers et al. 1977; Reilly & Bretherton 1986; Rost 1987; Reilly 1990). Training must therefore develop aerobic power. The increased speed of movement demanded by synthetic surfaces suggests that the majority of aerobic training needs to be done over shorter distances (5-9km) at high pace, or using interval sessions with high-intensity repetitions. Elite hockey players must also possess significant anaerobic power. The game requires frequent acceleration, deceleration and turning movements. A high peak power output from the leg is therefore important to the physiological profile of the elite player. No specific data are available on the effectiveness of sprint training, but it is likely that regimens successfully utilized by soccer players will benefit field hockey players (Reilly & Borrie 1992). Short (30-m) sprints with maximally explosive starts and an exercise/rest ratio of 1:5 improve sprinting speed in male soccer players (Apor 1988). Daily energy expenditure The severity of the training programme in top-level performers is reflected in daily energy expenditures. Grafe (1971) considered an intake of 23 MJ (5600kcal) daily was adequate for male field hockey players. A similar intake was advised for basketball and handball specialists. In view of the relatively moderate training regimens of players at the time, these figures may have overestimated the real requirements. More recent figures give an actual energy intake of 18ikJ.kg-’.day-I for elite male field hockey players. For a 75-kg individual, this amounts to


13.6MJ (3250kcal), below the figure for soccer players (192kJ.kgl.day-’). Values for female players were 145kJ.kg-’.day-’ or 8.7MJ (zo8okcal)for a 60kg individual (Erp-Baart et al. 1989), marginally above the figure for handball players (142 kJ.kg-’.day-’). These values were derived from 4- to 7-day food diaries, an approach that often underestimates energy requirements (Westerterp & Saris 1991). The activity profiles during play do not suggest the likelihood of muscle glycogen depletion. Consequently, glycogen loading is not essential,but it may have some value in serial competitions or after prolonged training sessions. In these instances, a high carbohydrate diet guards against starting subsequent matches with inadequate glycogen reserves. Carbohydrate supplementation has reduced fatigue during intense training of US national players (Kneider et al. 1995). The US women’s team trained 3-4 h a day, 6 days each week in preparation for the 1996 Olympics (Sparling et al. 1998).The percentage body fat was 16-17%; bone mineral density was 13%above agerelated and weight-matched norms. The elevated bone density and nutritional profile contrast with reports of premature bone loss, stress fractures and eating disorders in elite female endurance runners. Physical strain Skill requirements and postural stress are superimposed on the energy expenditures demanded by the game and its pattern of play. This is accentuated when players dribble the ball or move in a semicrouched posture. Spinal flexion is ergonomically unsound for fast locomotion, and it may predispose to back injury. Cannon and James (1984) reported that 8% of patients referred to a back-pain clinic for athletes over a 4-year period were field hockey players. A survey of local male clubs in the Merseyside region showed that 53% of respondents had experienced low back pain (Reilly & Seaton 1990). Compressive loading of the intervertebral discs during play and practices causes players to lose height. Water is extruded from the disc when the compressive load exceeds the interstitial osmotic



pressure. The result is a decrease in total body length which can be demonstrated by highresolution stadiometry (Troup et al. 1985).Dribbling a hockey ball on a motor-driven treadmill for 7min at a speed of 8.5km.h-’ induced a shrinkage of 0.4rnm.min-’ (Reilly & Seaton 1990)~about four times that observed in running and almost twice that found in circuit weight training (Leatt et al. 1986). Training of back strength and flexibility (Garbutt et al. 1990) may reduce the risk of back injury in field hockey players. Procedures for unloading the spine, notably gravity inversion and Fowler’s posture, adopted before and after exercise or during intermissions, may also help (Leatt et al. 1985).

Hurling and lacrosse Introduction Hurling is the national game in Ireland; the pitch has the same dimensions as for Gaelic football. The female version of the game (camogie) has similar rules to the men’s game. Teams are 15-a-side. Positional roles are relatively rigid, and marking of players is usually adopted. Traditional hurling sticks are made of ash, but in recent years synthetic versions of the ’caman’ have been accepted. Typically, a long puck of the ball could propel it over loom, and it is usual for players to score directly with a shot 70m from goal. The implement used in lacrosse is very different from the caman, allowing the player to catch and cradle the ball. The game originated among North American Indians and has traditionally been popular among females. It has a wider following than hurling (or the Scottish version known as shinty), particularly in Canada, the US and the UK. There are 10 players per side in lacrosse. The pitch is loom shorter than in hurling. Matches are 60min in duration. Demands of the games The physiological demands of hurling probably resemble those of Gaelic football. The play may

change quickly from end to end, in view of the large distances the ball can be hit. Players cover distance with the ball by carrying it or tapping it with the base of the hurling stick, but they are tracked by markers. The game demands a substantial amount of upper body effort as well as leg exercise associated with contesting possession and playing the leather ball or sliotar. There is a small but not appreciable effect of carrying the caman, entailing an elevation in heart rate of 3 beats.min-’ (Fenton 1996). The pattern of play in lacrosse is broadly similar to that in hurling. Lacrosse players have more freedom to roam, since fewer players are on the pitch. Good running abilities are important for play. As in other field games, the majority of the total distance travelled is taken up with movement away from play, in order to become available for a pass or afford an outlet for a player under pressure whilst in possession. The camin is responsible for the majority of injuries in shinty (the Scottish form of hurling). The whole body is vulnerable (MacLean 1989). In hurling and camogie injuries are largely to the hand and to the face (Crowley & Condon 1989). Eye injuries have been highlighted in lacrosse (Livingston & Forbes 1996).Protective measures are clearly important in all stick-and-ball games. Fitness In both sports, players require a good aerobic fitness to withstand the endurance demands of competitive matches. Fitness programmes should incorporate anaerobic components, in view of the need for repeated short sprints. There is also considerable shoulder-blocking body contact, especially in the men’s games. Neither sport is on the Olympic games calendar, but both provide a convenient reference for comparisons with field hockey; hurling, in particular, also bears comparisons with Gaelic football. The Vo2maxof 10 intercounty hurlers was measured at 56.8 (*5.0)ml.kg-’min-* (Fenton 1996). Watson (1977) studied fitness over a competitive season of hurling. The training programmes of successful players increased physical capabilities


(PWC,,). It was concluded that endurance contributes to performance in both Gaelic football and hurling.

Conclusions Field games incorporate bouts of high-intensity exercise superimposed on lower-intensity aerobic activity. Methods of quantifying physiological loading include motion analysis, estimated oo2, heart rate and blood lactate measurements. The highest relative loading among football games is in soccer (about 75% l k ~ ~ followed ~ ~ )by,Australian Rules, Gaelic football, Rugby Union and Rugby League. American football emphasizes muscle strength and anaerobic power, with aerobic factors providing only part of general conditioning. The physiological demands are reflected in fitness measures and are accentuated by environmental stressors such as heat and altitude.


A considerableamount of data now describes the physiological characteristics of field hockey players of both genders. Such profiles need to be interpreted with caution, as competitive level, stage of season, player position and other factors should be considered. In contrast there have been relatively few attempts to measure directly the physiological demands of match-play in field hockey, hurling, shinty or lacrosse. Nevertheless, inferences have been made from model games and motion analyses. Information about conditioning has been gathered from fundamental research on training and its physiological effects, and from training studies on football players. Information on environmental stressors must as yet be borrowed from exercise physiology literature (or studies of soccer players) and applied to the specific context of these stickand-ball games, especially when play takes place in hot conditions.

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Introduction Mountaineering encompasses a broad range of physical activities, from the intense muscular conditioning and gymnastic agility of the rock climber to the durability and endurance of the high-altitude mountaineer.Common to all forms of mountaineering, from fast and difficult short ascents of artificial or real rock walls to remote ascents in unexplored regions, is the element of verticality, i.e. high-angle terrain where error or unforeseen events can result in death. Therefore, common to all forms of mountain climbing are such elements as difficulty, a variable quantum of risk and the need for skill, knowledge and judgement. Aside from the elements of risk and uncertainty, the physical demands upon the human body are analogous to those of other sports, such as gymnastics, skiing and endurance running. The unique element of mountain venture derives from the decrease in barometricpressure and the partial pressure of inspired oxygen. For example,at the summit of Mount Everest, the barometric pressure is but one-third of that at sea-level. The resulting hypoxia impedes performance and places special demands on the human body with regard to strength, endurance and nutrition. Certain illnesses caused by hypoxia may at times be fatal. In this chapter we will limit our discussion to the effects of high altitude upon human performance. We shall review the physiological adaptations to hypoxia, discuss the limits to maximum exercise at extreme altitude, define endurance in this environment, and consider attributes that are conducive to

better performance at high altitude. Additionally, we shall briefly discuss nutritional requirements and make suggestions for training.

The environment Although the high-altitude environment includes other environmental stresses such as cold and exposure to intense ultraviolet radiation which may have an impact on elements of performance such as muscle fatigue, dehydration, malnutrition and mental fatigue, the decreasing barometric pressure with increasing altitude is the unique problem for the high-altitude mountaineer (Table 62.1).Because of a variety of physiological adaptations, oxygen delivery to the tissues is remarkably well maintained in spite of the decreased partial pressure of oxygen (Po,) in the inspired air (Fig. 62.1).Adaptation minimizes the magnitude of steps in the oxygen cascade, helping to maintain an adequate delivery of oxygen to the mitochondria. Without any adaptation, a sudden exposure to severe hypoxia can result in a loss of consciousness and even death. Adaptation The body adjusts to hypoxia with changes in ventilation, gas exchange from the alveoli to the blood, haemoglobin affinity for oxygen, red blood cell mass and transfer of oxygen from the capillaries to the mitochondria (Schoene & Hornbein 1988). The most important recipients of oxygen are the exercising muscle and the central nervous system.



Table 62.1 Mean i s.d. of values for resting ventilation and arterial blood gases in seven subjects, measured during a simulated 40-day ascent of Mount Everest, in a chamber (Operation Everest 11). Modified from Goldberg and Schoene (1992)

Altitude Feet


Barometric pressure (Torr)

Partial pressure of inspired oxygen (Torr)

Pulmonary ventilation (Lmin-9

Partial pressure of carbon dioxide (Torr)


Partial pressure of oxygen (Torr)

Oxygen saturation (%)



15000 20000

26500 29029

760 429 347 282 240

o 4570 6100 8080


11.0 f 1.0

150 80 63 49 43

14.6 i 2.7 20.9 c 6.3 36.6 i 7.9 42.3 7.7





7.43 0.04 7.46 i 0.02 7.50 + 0.04 7.53 i 0.03 7.56 i 0.03

33.9 f 3.5 25.0 i 2.2 20.0 f 2.8

12.5 i 1.1 11.2 i 2.1



99.3 9.3 52.4 f 4.0 41.1 f 3.3 36.6 i 2.2 30.3 C 2.1

97.6 f 0.1 84.8 f 4.0 75.2 C 6.0 67.8 c 5.0 58.0 i 4.5


- - - - - - - desensitization



c 1oc 0,



4570 rn


p 75

e -n .!?

r, a





Years Time at high altitude

Many years

Fig.62.2 Course of ventilatory response to acclimatization to high altitude at different durations of exposure, from hours to a lifetime. From Weil(1986),with permission.








Inspired gas

Alveolar gas

Arterial blood

Mixed venous blood

Fig. 62.1 The cascade of oxygen partial pressures at four different altitudes.

Ventilation With the initial exposure to high altitude, breathing increases (Weil1986).The hyperventilation (relative to sea-level) is initiated by the peripheral chemoreceptors, notably the carotid body (Lahiri et al. 1981), although there is much inter-individual variability

in the magnitude of this response. Much of the increased ventilation occurs within the first few days after ascent, but a steady level of ventilation at a particular altitude may not develop for several weeks. Many years of residence at high altitude can result in a decrease of ventilation (Fig. 62.2) (Wed 1986).Hyperventilationresults in a decrease in alveolar Pco, and an increase in alveolar Po, which is reflected by an increased arterial Po, and oxygen content of arterial blood (West et al. 1983b). Ventilatory acclimatization is associated with renal bicarbonate excretion in compensation for the respiratory alkalosis. However, compensation is never complete, and there is a persistent respiratory alkalaemia.


Pulmonary function Upon initial ascent, lung compliance, vital capacity and air flow decrease and gas trapping increases (Coates et al. 1979; Jaeger et al. 1979; Gautier et al. 1982).These changes are attributed to an increase in interstitial lung water, which normally resolves within the first day or two at altitude. Lifelong residence at high altitude results in an increase of lung volume and diffusion capacity, documented in high-altitude natives of the Andes and Himalayas (Remmers & Mithoefer 1969; Frisancho et al. 1973; Vincent et al. 1978).

Gas exchange Alveolar hypoxia results in an increase in pulmonary arterial pressure, which at rest improves perfusion of non-dependent regions of the lung. Prolonged stay at high altitude can result in severe pulmonary hypertension, leading to chronic mountain sickness (Monge’s disease), characterized by


pulmonary hypertension, polycythaemia, mental slowing and cor pulmonale (Monge 1928; Winslow & Monge 1987).

Diffusion Transfer of oxygen from the air to the blood is decreased because of the lower driving pressure of oxygen in alveolar gas (Fig. 62.3) (West & Wagner 1980).This limitation to oxygen transfer from the air to the blood is accentuated during exercise, when a higher cardiac output results in a shorter transit time for red blood cells across the pulmonary capillaries and a briefer opportunity for end-capillary Po, to approach that in the alveoli (Fig. 62.3). The arterial oxygen desaturation that occurs with exercise at high altitude can be quite profound (Fig.62.4) (Westet al. 1983a).

Blood Two adaptations of oxygen transport occur at high

Fig. 62.3 Comparison of the calculated time course of Po, in the pulmonary capillary of a climber at rest on the summit of Mount Everest (Pe 250 torr, PIO,43 torr) (a) to sea-level values ( P , 760 torr, PIO, 150 torr) (b). From West and Wagner (1980),with permission. DMO,,membrane diffusion capacity for oxygen, P, barometric pressure; PIO,, inspired partial pressure of oxygen.



Sea level 90

6300 rn, 14% 0,






I altitude: (i) an increase in red blood cell production; and (ii) changes in the affinity of haemoglobin for oxygen (Fig. 62.5) (Winslow et al. 1984). The first adaptation is mediated by the hormone erythropoietin, which increases rapidly upon ascent to high altitude (Abbrecht & Littell 1972). An initial increase in haematocrit is probably secondary to haemoconcentration. Increases in red blood cell volume and total blood volume require several weeks to complete (Sanchez et al. 1970). There is marked variability in this response in both sojourners and high-altitude natives. An increase in haemoglobin concentration increases oxygen-carrying capacity but, if the increase is too great (haemoglobin > 190g.l-'1, blood viscosity also increases and a decrease in blood flow and oxygen delivery may result. Both sojourners and native highlanders who seem best adapted to high altitude maintain haemoglobin concentrations in the range of 160-180g.l-~ (normal sea-level value 130-150 g.1-I) (Beall & Reischman 1984).Chronic mountain sickness is one example of the adverse consequence of a surfeit of red blood cell production (Winslow & Monge 1987). The affinity of haemoglobin for oxygen influences











6 Altitude (krn)




Fig. 62.5 Effectors of oxygen-haemoglobin (Hb) affinity. The net result at extreme altitude is a protected arterial oxygen saturation. DPG, diphosphoglycerate.From Winslow et al. (1984),with permission.


both loading of oxygen at the lung and unloading at the tissues. At moderate altitudes a rightward shift of the oxyhaemoglobin dissociation curve enhances unloading of oxygen to the tissue (Aste-Salazar & Hurtado 1944; Moore & Brewer 1981).Although the arterial Po, is high enough to minimize the effect of the shift on arterial oxygen saturation, at very high altitudes (where alveolar Po, is much less), a leftshifted curve might better optimize intake of oxygen at the lungs (Fig. 62.5) (Winslow et al. 1984). Some animals who live at or birds that fly at very high altitude have left-shifted oxyhaemoglobin dissociation curves (Swan 1970; Faraci et al. 1984). and the marked respiratory alkalosis noted in humans at extreme altitude also results in a leftward shift of the curve (Winslow et al. 1984). Tissue adaptation Adaptation at the cellular level is less well understood. Some studies suggest that several weeks' exposure to high altitude results in increases in capillary and mitochondria1 density, as well as a decrease in cell size, all of which would decrease the


radial diffusion distance for oxygen from the capillaries to the mitochondria (Ou & Tenney 1970; Tenney & Ou 1970; Banchero 1975).There is controversy about what occurs to oxidative enzymes upon ascent to high altitudes (Hochachka et al. 1982; Green et al. 1989),but the sum total of all these mentioned changes is presumably beneficial to oxidative metabolism. Limitation to exercise Although little is known about endurance performance at high altitude, a great deal is known about maximal aerobic power. Maximal oxygen intake (f'oZmax) decreases with increasing altitude (West et al. 1983a; Reeves et al. 1987; Cymerman et al. 1989). Studies both in the field and in a high-altitude chamber have shown that at the summit of Mount Everest (barometric pressure of approximately 250 torr), f'02max is about 20% of the sea-level value (Fig. 62.6) (West et al. 1983a; Cymerman et al. 1989).Interestingly, even though individuals may start with different values of at sea-level, those who have been studied have similar values when exercis-

Summit of Mt Everest

F@. 62.6 Maximal oxygen intake (Vohau) against inspired Po,. There is a predictable decrease in

10 -

Basal 0,intake __________________-.___________________



ing at a barometric pressure equivalent to that at the summit of Mount Everest. The cause of the decrease in exercise performance is probably multifactorial, including impaired diffusion of oxygen from air to blood in the lungs and consequently a lesser availability of oxygen to the exercising muscles and brain (Gale et al. 1985; TorreBueno et al. 1985; Wagner et al. 1986, 1987).At very high altitude, diffusion of oxygen to the tissues may also be compromised by the low Po,. The ventilatory response to exercise at high altitude is a marked increase in ventilation. This helps maintain arterial oxygen saturation (Fig. 62.7) (Schoene 1984). but is not sufficient to reverse the diffusion limitation and the subsequent desaturation of arterial blood. In the high-altitude sojourner, a greater ventilatory response results in less arterial oxygen desaturation (Schoene et al. 1984), whereas in high-altitude natives who have a more blunted ventilatory response, desaturation is minimized in part by an increased surface area for oxygen transfer (diffusioncapacity) (Dempseyef al. 1971). For a given work rate, cardiac output is, for the most part, similar at high altitude to that at sea-level (Reeveset al. 1987).After exposure of several weeks or longer at moderate to extreme altitude, maximal heart rate is decreased (West et al. 1983a).Inhalation of oxygen results in an increase in maximum heart rate and in maximal aerobic power, although values remain well below those at sea-level. The

mechanism for the lower maximal heart rate is not understood. Limits to short bouts of intense exercise may reflect a failure of oxygen delivery to the brain rather than muscle. Hypoxia may impair central nervous system function. Numerous accounts exist of climbers at these heights who, upon further exertion, hallucinate, have narrowed or blurred vision, or come close to losing consciousness. Several studies have shown neurobehavioural dysfunction after return from extreme altitude (Cavaletti et al. 1987; Hombein et al. 1989; Regard et al. 1989).This is particularly notable in individuals with a more vigorous ventilatory response to hypoxia, an attribute that correlates with a better physical performance while at high altitude (Hornbein ef al. 1989). The authors speculate that the greater ventilatory response results in more profound hypocapnia and cerebral vasoconstriction,and consequently a larger decrease in oxygen delivery to the brain.

Endurance performance at high altitude For high-altitude mountaineering, endurance is defined not in hours, but in days, weeks or months. Therefore, data taken from brief, maximal exercise may not predict performance at high altitude. Much information on the effect of high altitude on athletic performance was obtained in the 1960s, at the time of the Mexico City Olympics (altitude 2300m). For


6300 m


.-E 80

. ‘E-


Sea level


.c .5




Fig. 62.7 The ventilatory response expressedas the ventilatory equivalent (V,/Vo,) in subjects at sealevel ( P , 755 torr) and at 6300m (P, 350 torr), demonstrating that the ventilatory response for a given metabolic rate is almost four times












events lasting for more than 2 min, some period of acclimatization is necessary for optimal performance. Most studies looked at Qo2max or performance time over measured distances (Dillet al. 1966; Buskirk et al. 1967; Grover et al. 1967). but improvement in submaximal exercise performance rather than intense exercise to exhaustion is more pertinent to high-altitude climbing (Maher et al. 1974). Here little objective information exists. As any highaltitude mountaineer can relate, at altitudes up to 5000m, performance improves with time. One study suggested that endurance time at 75% of Qo2max was greater at day 12 than at day 2 of exposure at 4300 m (Maher et al. 1974).This improvement was associated with decreased blood lactate concentrations, suggesting that improved exercise capacity resulted from better tissue oxygenation. No similar longitudinal studies have been performed above 6000 m. Based on anecdotes, an altitude of 55oom, where the barometric pressure is half that at sea-level, appears to represent the limit of permanent human habitation. Above that altitude, performance deteriorates after the initial period of acclimatization. It has become fashionable during expeditions to extreme altitude to acclimatize at moderate altitude with occasional short forays to extreme altitude, before making a final rapid ascent. This approach may optimize the adaptive processes while minimizing the deleterious effects of extreme altitude.

Training Although aerobic fitness is generally associated with greater speed of travel and thus safety in the mountains, it is not clear whether maximal aerobic power correlates with performance at extreme altitude. Aerobic training at low altitude or intermediate altitude is still the most beneficial way of enhancing performance at high altitude. Gains may be achieved by optimization of ventilation, haematological response, cardiovascular fitness and peripheral tissue adaptation, the benefits of which are common to both low- and high-altitude performance. Of these adaptations, those of the blood and tissues may be particularly important. At low alti-


tude, a modest increase in haemoglobin concentration is associated with improved endurance performance (Buick et al. 1980). One might presume that the high-altitude sojourner would gain similar benefits. All of these adaptations occur spontaneously over days to weeks at high altitude. In order to optimize performance, the mountaineer should ascend at a comfortable pace that will allow adaptation to take place, while minimizing the possibility of incurring altitude illness. Controversy has existed regarding the benefit of high-altitude training for low-altitude events. Anecdotal evidence suggested that living and training at moderate altitude, for the aforementioned reasons, conveyed benefit for the competitor in aerobic events at low altitude, but no good data were available to substantiate that claim until recently. Levine and Stray-Gundersen (1997) tested accomplished runners in four well-controlled situations. One group lived and trained at low (1250m)altitude, one lived and trained high (2500m), another lived high and trained low, while a fourth lived low and trained high. The group that lived high and trained low had the greatest improvement in maximal oxygen intake, sustainable time of maximal power output (Figs 62.8 & 62.9) and 5000-m run time. The improvement was attributed in part to the increase in haemoglobin and ability to maintain high-intensity workouts at the lower altitude which was not possible if training occurred at the higher altitude. The investigators found, however, that there was individual variation in the erythropoietic response such that not everyone responded to high-altitude training, and only enough data were available to substantiate the claim in men.

The Clite climber Unlike most sports in which elite performers have many common characteristics, the elite mountaineer cannot be so simply described. Several researchers have studied some physiological markers of mountaineers who have climbed on one or more occasions to 8000m or higher (Schoene 1982; Masuyama et al. 1986; Oelz et al. 1986). Factors such as hypoxic ventilatory responses, aerobic power, strength, muscle fibre type and bio-




* *





1 lead in


sea level I


altitude 1





8 High-Low

Mf 0 0

lead in

Fig. 62.8 Maximal oxygen uptake at baseline after sea-level training in Dallas (sea-level)and after altitude training camp or sea-level control (altitude). *P < 0.05 compared with previous time point for a given group.



sea level





altitude 6 Weeks







mechanics were investigated, to see whether any of these characteristics predicted climbing performance at extreme altitude (Oelz et al. 1986). Most, but not all, of the climbers had high Pohx values (>60ml.kg-~.min-~). On the other hand, one of the world's best climbers had a Pohm that was only moderately greater than the normal expected value (48mLkg-'.min-'). Previously, a very high Pornx was thought to be a requisite for the Himalayan climber. Perhaps the efficient climber may be able to climb for prolonged periods at a high percentage of

Fig. 62.9 Oxygen uptake (Pob,)at maximal steady state, determined from ventilatory threshold, at baseline, after sea-level training in Dallas (sea-level),and after altitude training camp or sea-level control (altitude).Group characteristics and figure symbols are defined as in Fig. 62.8.*P < 0.05 compared with previous time point.

their Pornx, in a manner similar to long-distance runners. The absolute value of ~ 0 2 m aatxsea-level may not be a relevant predictor of performance at extreme altitude, because the factors limiting at sea-level (primarily cardiovascular) are not those that limit performance at extreme altitudediffusion limitation at either the lung and/or the peripheral tissues becomes the critical factor. A number of studies have found that many successful climbers to extreme altitude have moderate to high ventilatory responses (HVR) to hypoxia


(Schoene 1982; Masuyama et al. 1986; Oelz et al. 1986) and exercise (Oelz et al. 1986).A greater alveolar ventilation ensures a higher alveolar Po, and subsequently minimizes the arterial oxygen desaturation during exercise (Schoene et al. 1984). This characteristic is probably only important for those who go to extreme altitudes, where a slight increase in ventilation can make a substantial difference in oxygen saturation. On the other hand, some individuals with blunted HVR and ventilation upon ascent appear to be more prone to mild and severe altitude illness (Hackett et al. 1982, 1988).A higher breathing response may, therefore, be a helpful but not essential attribute of the high-altitude climber. These studies have not found any characteristic common to all elite climbers. What may be more important are some of the less tangible traits without which no mountain can be climbed. A strong psychological drive, tenacity, patience, team work, knowledge, skill, judgement and joy in the activity are all prerequisites that are difficult to define by objective data. Nutrition Although many of the physiological responses to high altitude are well described, another key element to success or failure with prolonged stay at high altitude is nutrition. The well-described shift in food preference from fats and carbohydrates to primarily carbohydrates as one ascends may reflect the body’s needs. A unique factor found in highaltitude climbers is malabsorption in both the small and large intestines (Boyer & Blume 1984). This has been documented at altitudes above 6000 m. Carbo-


hydrates are probably better absorbed than other fuels; thus, to optimize performance, carbohydrates should be ingested to the point of tolerance to ensure adequate blood glucose, muscle glycogen and free fatty acid and triglyceride stores. Although weight loss is generally the rule in individuals climbing at high altitude for weeks or more, there is an individual variability in this response which may reflect the difference in preferences and tolerance for food (Boyer& Blume 1984). Both field and high-altitude chamber studies have documented a decrease in muscle mass, while fat stores (although decreased from sea-level) are still present (Boyer & Blume 1984; Green ef al. 1989). These findings reflect muscle catabolism, which suggests utilization of gluconeogenesis to maintain blood glucose and muscle glycogen. Interestingly, studies even at extreme altitude show adequate muscle glycogen stores (Green ef al. 1989).

Summary Physiological adaptations to high altitude optimize aerobic power in an environment characterizedby a diminished oxygen supply. Although these adaptations improve aerobic capacity during a stay at moderate altitude, sea-level capacities are never fully restored. Even less information is known about endurance performance for the high-altitude mountaineer during prolonged exposure to altitude. Much anecdotal evidencesuggests that, at moderate altitude, continual activity and adequate nutrition are the key elements in sustaining endurance and performance. At extreme altitude much more individual variability may exist based on psychological rather than physiological characteristics.

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Pugh, L.G. (1964) Cardiac output in muscular exercise at 58oom (19000feet). Journal of Applied Physiology 19,441-450. Reeves, J.T.,Groves, B.M., Sutton, J.R. et al. (1987)Operation Everest 11: preservation of cardiac function at extreme altitude. Journal of Applied Physiology 63,531-539. Regard, M., Oelz, O., Brugger, P. &I Landis, T. (1989)Persistent cognitive impairment in climbers after repeated exposure to extreme altitude. Neurology 39, 210-213. Renimers, J.E. & Mithoefer, J.C. (1969) The carbon monoxide diffusing capacity in permanent residents at high altitude. Respiration Physiology 6,233-244. Sanchez,C., Merino, C. & Figallo, M. (1970) Simultaneous measurement of plasma volume and cell mass in polycythemia of high altitude.Journal ofApplied Physiol08Y 28,775-778. Schoene, R.B. (1982)The control of ventilation in climbers to extreme altitude. Journal of Applied Physiology 53,886-890. Schoene, R.B. (1984)Hypoxic ventilatory response in exercise ventilation at sea level and high altitude. In: West, J.B. & Lahiri, S. (eds) Man at High Altitude, pp. 1930. American Physiologic Society Clinical Physiology Series.Waverly Press, Baltimore. Schoene, R.B. & Hornbein, T.F. (1988)Respiratory adaptation to high altitude. In: Murray, J.F. & Nadel, J.A. (eds) Textbook of Respiratory Medicine, pp. 196-220. W.B. Saunders, Baltimore. Schoene, R.B., Lahiri, S., Hackett, P.H. et al. (1984) Relationship of hypoxic ventilatory response to exercise performance on Mt. Everest.Journal of AppliedPhysiology 56,1478-1483. Swan, L.W. (1970) Goose of the Himalaya. Natural History 79,6875. Tenney, S.M. & Ou, L.C. (1970)Physiological evidence for increased tissue capillarity in rats acclimatized to high altitude. Respiration Physiology 8,137-150. Torre-Bueno, J.R., Wagner, P.D., Saltzman, H.A.,Gale,G.E. & Moon, R.E. (1985)Diffusion limitation in normal subjects during exerciseat sea level in simulated altitude. Journal of Applied Physiology 58, 989-995. Vincent, J., Hellot, M.F., Vargas, E., Gautier, H., Pasquis, P.& Lefrancois, R. (1978) Pulmonary gas exchange, diffusing capacity in natives and newcomers at high altitude. Respiration Physiology 34, 219-231. Wagner, P.D., Gale, G.E., Moon, R.E.,TorreBueno, J.R., Stolp, B.W. & Saltzman, H.A. (1986)Pulmonary gas exchange in humans exercising at sea level in simu-


lated altitude.Journal ofApp/ied Physiology 61,280-287. Wagner, P.D., Sutton, J.R., Reeves, J.T., Cymerman, A., Groves, B.M. & Malconiun,N.K. (1987)Operation Everest 11: pulmonary gas exchange during a simulated ascent of Mt. Everest. Journal of Applied Physiology 63,2348-2359. Weil, J.V.(1986) Ventilatory conhol at high altitude. In: Fishman, A.P., Chemiack, N.S.,Widdicome, J.G. & Gieger, S.R. (eds) HandbookojPhysiology. The Respira-

tory System, Section 3, Vol. 11, Control of Breathing, Part I, pp.730-737. American PhysiologicSociety, Bethesda, MD. West, J.B. & Wagner, P.D. (1980)Predicted gas exchange on the summit of Mt. Everest.Respiration Physiology 42.1-

16. West, J.B., Boyer, S.J.,Graber, D.J. et al. (1983a) Maximal exercise at extreme altitudes on Mt. Everest.Journal ofApplied Physiology 55,68%702.


West, J.B.,Hackett, P.H.,Maret, K.H. etal. (1983b)Pulmonary gas exchange on the summit of Mt. Everest. Journal ofApplied Physiology 55,6784337. Winslow, R.M. & Monge, C.C. (1987) Hypoxia, Polycythemia, and Chronic Mountain Sickness. Johns Hopkins University Press, Baltimore. Winslow, R.M., Samaja, M. &West,J.B. (1984)Red cell function at extreme altitude on Mt. Everest. Journal of Applied Physiology56,109-116.

Chapter 63 The Physiology of Human-Powered Flight ETHAN R. NADEL AND STEVEN R. BUSSOLARI

Introduction Humans have always been fascinated with the concept of flight, yet throughout history the actuality of flight has been relegated to winged animals or assigned to the realm of myth. Only in very recent times has an understanding of the requirements of flight and the development of strong and light structures enabled flight to be accomplished under human power alone. The first record of human-powered flight was from the ancient Greek civilizations. As first reported by Homer around the 8th7th century BC,a Mycenean craftsman and inventor named Daedalus fashioned wings from feathers and wax and flew under his own power from a hillside cleft in King Minos’ Labyrinth, in which he was imprisoned, across the Aegean Sea to his freedom. According to later versions of the myth, Daedalus flew with his son, Icarus, who, ignoring his father’s advice, flew too close to the sun and fell to his death when the heat of the sun melted his wings. Drela and Langford (1985) have charted the progress of human-powered flight since the time of Daedalus. They noted that only within the past 30 years or so has human-powered flight progressed beyond the realm of extended glides from a catapult take-off. This was undoubtedly because the early human-powered aircraft required more power to maintain steady flight than the pilot could produce. Progress in the realm of human-powered flight was stimulated by the challenge of competition for monetary prizes established by the British industrialist Henry Kremer in 1959. The first Kremer prize,


awarded for flying a human-powered aircraft around a 1-mile (1609-m), figure-of-eight course under human power alone, was claimed in 1977 by Bryan Allen, flying the Paul MacCready-designed Gossamer Condor. The second Kremer prize of €iooooo went to the same team, when Bryan Allen pedalled the Gossamer Albatross across a 37-km strait of the English Channel in 1979. This was indeed an endurance event; the flight time was nearly 3h. In 1988, Daedalus, designed by a team of engineers from the Massachusetts Institute of Technology, flew under human power from the north coast of Crete to the island of Santorini, a distance of 119km, in just under 4 h.

Aeroplane aerodynamics To understand the reasons why human-powered flight has become possible only in recent times, it is important to appreciatethe basics of aeroplane aerodynamics (for an expanded discussion see Shevell 1983).Four forces-lift, weight, thrust and dragare the determinants for flight. As an aircraft moves through the air, the shape of its wing imparts differential velocities to the air passing over its upper and lower surfaces, creating a higher pressure beneath the wing and a lower pressure above the wing. This results in a net upward force called lift. In level flight, lift is balanced by the downward force of gravity, the aircraft weight. A horizontal thrust force is furnished by the propeller which is driven by the aircraft engine. In level, unaccelerated flight, thrust balances the total horizontal resistive force, drag, which is produced by a combination of the move-


ment of air past the exposed surfaces of the aircraft (form and parasite drag) and the disturbance of the air caused by the wing as it produces lift (induced drag). The power required for flight is the product of thrust and velocity, or, in level flight, drag and velocity. Since form and parasite drag increase roughly as the square of the velocity, the power (force x velocity) required to overcome these components of drag will increase as the cube of velocity. Thus, doubling the airspeed of a given aircraft would require roughly an eight-fold increase in the power applied by the engine (the human engine in the case of a human-powered aircraft).A more exact relationship between power required and aircraft design parameters may be obtained by consideration of the equations that describe the production of lift and induced drag:

where p is the air density, S is the wing area, Wis the total weight of the aircraft including payload (in a human-powered aircraft, the pilot is a significant fraction of W), and C, and C, are coefficientsof drag and lift that depend on the aircraft shape. The above equation confirms that it is important for the aircraft designer to minimize weight and drag, while main-

Fig. 63.1 The Daedalus undergoing flight-testing at Edwards Air Force Base in California. In April 1988, K. Kanallopoulos flew the Daedalus between the Greek islands of Crete and Santorini, a distance of iigkm, in just under 4 h. The distance and duration are the current world records for humanpowered flight. Photo courtesy of the Daedalus Project, Massachusetts Institute of Technology.



taining a high lift and a large wing area to keep the required power low.

Design strategies Over the years, human-powered aircraft designers have attempted to solve the problem of reducing the power requirement to that which a human could be expected to maintain by adopting several strategies. One strategy was to design a very light structure with a large wing area by using external wire bracing. Compensation for the high parasite drag of the wire bracing was achieved by keeping the design airspeed (velocity) low to minimize its contribution to the power required. The success of the Gossamer human-powered aircraft was the result of this design strategy. The disadvantage of this type of aircraft is its low speed, which requires its pilot to remain aloft for a long time in order to cover a given distance. The development of strong, lightweight graphite-epoxy and other composite materials allowed designers to eliminate the external wire bracing, while maintaining a large wing area with little weight penalty. The Daedalus aircraft (Fig. 63.1), with its 34.1-m semicantilever wingspan, is an example of this design strategy.




Table 63.1 Characteristics of the 25 final pilot candidates. Parameter

Mean + s.d. value

Maximal oxygen intake (semirecumbent position) (ml oxygen,min-',kg-')

69.2 5.2

Maximal mechanical power output (W.kg-')

5.25 + 0.53

70% maximal power output (W.kg-')

3.54 f 0.36

Mechanical efficiency ('30)

24.1 f 3.7

Power requirements for flight The outcome of aerodynamic and materials innovations led to the design of a low-power, moderatespeed aircraft that could be flown for extended periods. Preliminary calculations and measurements, derived largely from tow tests of the aircraft, showed that the mechanical power requirement to fly the Daedalus was about 3.0-3.5 W,kg-' pilot weight at the design speed of 24km.h-'. Assuming the pilot's ability to convert 24% of the potential energy of stored fuels to mechanical work in the muscle machinery (Astrand & Rodahl 1986), the pilot must maintain a fuel conversion rate of nearly 15W.kg-', requiring an oxygen intake of about 45 ml oxygen.min-'.kg-', to generate mechanical power at 3.5W.kg-'. This metabolic cost is approximately the same as that required to pedal a bicycle over level ground at a speed of 37km.h-1 (Whitt & Wilson 1982).Based upon knowledge of performance characteristics, the metabolic cost of flying the Gossamer Albatross at its design speed of 18km.h-' has been estimated to be 20% higher, a remarkable output to maintain throughout the English Channel crossing. (Note: a human-powered aircraft is flown like any aircraft; the pilot adds power to gain altitude and decreases power to descend. Because the human-


powered aircraft flies within 6m of the surface, the loss of altitude due to a reduction in power for more than a few seconds will cause the aircraft to land, or worse.) As human-powered aircraft designers have refined their designs and used lighter and stronger materials, the power requirements for flight have come into the realm of the possible for more than just the elite endurance athlete. It is notable that the Daedalus pilot team of five athletes was selected from more than 300 initial applicants (Nadel & Bussolari 1988). The maximal mechanical power production of the 25 athletes who were invited for objective testing was 5.25 W.kg-' (Table 63.1). The 70%maximum power, which most fit people should be able to sustain aerobically for extended periods, was therefore 3.54W.kg-', higher than the most conservative estimate of power required to maintain steady flight in the Daedalus. The ability to generate power at this rate is the critical factor for extended flight. Factors that can limit prolonged flight include hyperthermia, dehydration and/or hypoglycaemia, the same factors that can limit other endurance exercise bouts (for a discussion of the strategies to limit the development of these factors during the Daedulus flight, see Nadel & Bussolari 1988).

References Astrand, P.-0. & Rodahl, K. (1986)Textbook of WorkPhysiology. McGraw-Hill, New York. Drela, M. & Langford, J.S. (1985)Humanpowered flight. Scientific American 253, 144-151.

Nadel, E.R. & Bussolari, S.R. (1988)The Daedalus project physiological problems and solutions. Scientific American 76,351-360. Shevell, R.S. (1983)Fundamentals ofFlight. Prentice Hall, New Jersey

Whitt, F.R. &Wilson, D.G. (1982)Bicycling Science. MIT Press, Cambridge, Massachusetts.

Chapter 64 Endurance in Other Sports PER-OLOF ASTRAND

Individual sport events with demands for endurance during training and competition have been discussed in preceding chapters. Orienteering was mentioned only in passing, but it is certainly an endurance sport because it involves long distances of cross-country running (the 'ideal' time is about 1 h 3omin for men and about 1 h for women). Armed with a compass and a map, the competitor must find his or her way to checkpoints in the terrain (see Creagh & Reilly 1997).Many countries have annual meetings with up to 5 days of competitions. In Sweden, more than zoooo people participate, with classes from beginners up to elite, and age groups from children up to master athletes. The endurance training for orienteering follows the same principles as those discussed in Chapters 28 and 57. Orienteering is also a popular sport when performed on skis. Many other events are time consuming with regard to both training sessions and competition time. However, physical activity during competition is often not continuous but intermittent, i.e. short bursts of vigorous exercise are followed by rest or low-intensity activity. The physiology of this type of exercise was briefly discussed in Chapter 2. A few examples of such events are given below. Several studies on soccer have been carried out (see Ekblom 1986; Chapter 61). On average the players cover about 10km during the go-min game, and it has been estimated that top-class performers in British premier-division teams walk and run 13.5 km in total (see Ekblom 1986). Soccer involves high-intensity, intermittent exercise although the total number of tackles in a game per player is only some 15-20, with 10-15 headings of the ball. Even

so, the heart rate is often high and close to the player's maximum. Ekblom estimated that the average oxygen intake during the game could be about 80% of the maximum. The maximal aerobic power of players in good national teams seems to be around 65-67ml.kg1.min-', with individual values exceeding 70 ml.kg-'.min-'. Peak blood lactate concentrations above izmmol.l-' have frequently been measured. It is evident that soccer players must devote time to endurance training. In the recent world championships many games were extended by z x 15-min periods. (See also Ekblom 1994.) Other games involving high-intensity, noncontinuous, intermittent exercise are European handball, basketball, volleyball, netball, field hockey, ice hockey and water polo. A high maximal aerobic power can lower the demand on anaerobic energy yield. The importance of myoglobin oxygen stores was discussed in Chapter 2 (see Fig.2.1). However, training does not seem to increase the myoglobin concentration in human skeletal muscle. One aspect of the importance of separate endurance training for players is the fact that training sessions often last for 2-2.5 h. A similar situation arises in racquet sports. A tennis match can last for 4 h or more, sometimes in a hot environment. In fable tennis, the three sets may take from 20 to 3omin. In the Swedish national team, which included world champions, the maximal oxygen intake averaged 65 rnl.kg-'.min-'. The mean oxygen intake during games was about 70% of the maximum. During major tournaments a player must often play several matches per day.






Fencing is another event with many matches per day; this complicates food and water intake. A competition often lasts for 2 days, and the fencers are usually active for 10-12h on each day of competition. Six members of the Swedish national CpCe team have been studied. Altogether, the fencers won 13 gold, one silver and four bronze medals in world championships and Olympic games. The mean maximal oxygen intake was 5.2l.min-', 67.3ml.kg-'min-' (Nystrom et al. 1990). Endurance training is considered an important part of their training. The muscle mass was significantly larger


in their 'forward leg' than in the contralateral leg, although the fibre composition was similar. This list could be much longer. The conclusion is that the training of aerobic power has importance for all athletes, not least because habitual physical activity is essential for optimal function. In addition, there is the health aspect. Many studies have shown convincingly that training of the oxygen transport system can significantly reduce the morbidity and mortality from cardiovascular disease (for references see US Department of Health and Human Services 1996; Astrand 1997; Chapter 51).

References h a n d , E-0. (1997) Why exercise? Advances in Exercise and Sports Physiology 3 (2), 45-54. Creagh, U. &I Reilly, T.(1997) Physiological and biomechanicalaspects of orienteering. Sports Medicine- (6), 404-418. Ekblom, B. (1986)Applied physiology of soccer. Sports Medicine 3,5040.

Ekblom, 8. (1994)Football (Soccer).Blackwell ScientificPublications, Oxford. Nystrom, J., Lindwall, O., Ceci, R., Harmenberg, J., Svedenhag, J. & Ekblom, B. (1990) Physiological and morphological characteristicsof world class fencers. International Journal of Sports Medicine 11, 136-139.

US Department of Health and Human Services (1996)Physicnl Activity and Health: AReport ofthe Surgeon General.Superintendent of Documents, P.O. Box 371954, PA 15~50-7954,S/N 017-02300196-5, USA.


Page numbers in bold refer to tables; page numbers in italics refer to figures. This index is in letter-to-letter order whereby spaces and hyphens between words in main entries are ignored in alphabetization. 'Training' refers to endurance training unless otherwise noted. Likewise, all athletes and performance levels relate to endurance athletes and endurance performance. abortion, spontaneous 536-537 accessory respiratory muscles 54 accidents 33 see also injury, sports acclimatization 614 cold stress 294 heat 265,288,288-289 high altitude 12,296,614,617-619, 932.937 muscle blood flow 111 soccer in hot environment 904905 accumulated oxygen deficit (AOD) canoeists 893 rugby players 913 acetazolamide 321,622 acetyl coenzyme A (CoA) 757 Achilles tendinosis 462,469 Achilles tendon 777 blood supply 777 chronic tears 783 pain 780 rupture 779 complete 780-781,783 partial 780,783 tightness 786 Achilles tendon overuse injuries 777-783 aetiology 778-779 anatomy 777 classification 777778 diagnosis 780 differential diagnosis 781 investigations 781 pathogenesis 779-780 prevention 783

treatment 781-783 acid-base balance 320-322 high altitude 61&617 measurements 3 2 ~ ~ 3 2 1 modifications 321-322 pregnancy 532 acid-base imbalance acute mountain sickness 621 respiratory acidosis 321 respiratory alkalosis 321,532 see also metabolic acidosis acrophase 640 actin eccentric exercise effect 166-167 F-actin/G-actin 164 monomers 164 myosin interactions 1 5 ~ 1 6 0 action potentials changes in fatigue 29,30 failure in repetitive activity 174 sarcolemma and T tubules 171 activities of daily living (ADL) 566, 753 actomyosin failure 158 interactions 159-160 see also actin; myosin acute mountain sickness 296,618, 62c-621 acute phase proteins 802 adaptatiods) 501 adverse 528 see also overtraining ATP regeneration 178 autonomic nervous system 596, 708 biochemical, to high-intensity exercise 180 Ca2+-ATFase177 canoeists 894 cardiac 7071,71,520 chronic, excitation-contraction coupling 176 circulatory 12 cycling 866 cytoskeletal system 179-180 ECG changes 677 enzymes see enzymes

'first in, last out pattern' 122 high resistance training 168 membrane excitability 177 mitochondria see mitochondria mountaineering 931,935 muscle see muscle, adaptation neurones 136 overuse injury prevention 766 pulmonary system 59,6164 regression after discontinuation of training 130 respiratory muscle training (RMT) 62-64 respiratory system 59,61-64 sensorimotor systems 144 signalling systems 177 skiing 852,854 tissue, mountaineering 935 to training 97,501 ATP regeneration 178 in women see women ventricular function 75 see also plasticity adductor injuries 791,792-793 adductor longus, injuries 792 adenosine 96 adenosine diphosphate (ADP) 21, 331 adenosine monophosphate (AMP) 21

adenosine triphosphatase (ATPase) see ATPase adenosine triphosphate (ATP) 21, 330-331 intermittent exercise 10-11 muscle blood flow control 96 regeneration 178,334 energy requirement 31 structure 331,332 synthesis 179,271,33~+331 fatty acid degradation 336-337 g~yco~ysis 333,334-336 phosphocreatine 334 sites 177 triathlon 872 utilization 84,279 adipose tissue 329 bloodflow 107




adipose tissue (continued) fat mobilization 28 in pregnancy 534 triglycerides 201 seealso fat, body adolescents anthropometric characteristics 41-42, 42 athletic success prediction 41 cardiovascular screening see cardiovascular screening growth spurts 397,398 height increase 397,398 injuries 462,466-468 marathon running 399 maximal oxygen intake ( V O ~ ~ ~ , ) 512 age-related changes 45,47 body s u e relationship 45,45,46 endurance training effect 509 menstrual cycle 514,720 overuse injuries 462 scaling factors, submaximal Vo2 48t49 talent identification and development 400 training 509 see also children adrenaline (epinephrine) 184,185 muscle sensitivity,training effect 130 overtraining marker 494 response to endurance exercise 184,185 secretion increased by caffeine 441 use prohibition 653 adrenergic blocking agents 549 alpha-blockers 567 beta-blockers 567,569 adrenergic receptors 184,634 adrenocorticotrophic hormone (ACTH) 185-187 actions 493 decreased, overtraining marker 493 E-endorphin correlation 188-189 response to exercise 185-186 training effect 186-187 adult respiratory distress syndrome (ARDS) 802 aerobic activities 866,867 injuries in elderly 558,559 see also aerobic exercise training aerobic-anaerobic threshold 318 cycling 866,867 economy of movement and 247 swimmers 828 see also anaerobic threshold aerobic capacity 311,318 alcohol effects 447 cycling 857,868 definition 301

smoking effect 445 see also anaerobic threshold aerobic conditioning 533-534 aerobic exercise training benefits 458 children see children diffusive oxygen flux 9-1 muscle blood flow 90-91 pregnancy 533-534,537 women 518-519 aerobic fitness 767 guidelines for elderly 554,555 hot environment 289-290 maximal oxygen intake as marker 507 soccer 907 see alsq maximal oxygen intake (VOZmax)

aerobic metabolism canoeing 894-896 continuous exercise 13 glycolysissee glycolysis hockey 922924,924 isokinetic ergometer 278 rowing 839-840 skeletal muscle 84 skiing 846 swimming 824,825 training in women 521 transition to anaerobic 311,315 see also anaerobic metabolism; anaerobic threshold aerobic power age-related decline 714 body fat relationship 350 elderly 552-555 as input to perception of effort 377 maximal see maximal oxygen intake (Vo,,) measurement 271,272 peak, disabled persons 566 post-myocardial infarction 566 pregnancy 533 rate of loss with age 753 swimmers 824 tiathletes 88~882,881 seealso oxygen intake aerodynamic drag 253,279 aerodynamics 252-253,279 aeroplane aerodynamics 942343 A-frame stands 609 afterload 34 age, chronologicalus biological 397-398r513 age-related changes 38-40,548-551 Achilles tendon overuse injuries 778 aldosterone 550 baroreceptor reflex function 549 blood pressure 549 body composition 555,556 boneloss 551

cardiac function 548,550 cardiovascular disease risk 701 catecholamine response to exercise 185 circadian rhythm control 640 endurance athletes 38-40 endurance preparation 397-401 flexibility loss 558,756 hepatic function 550 hyperthermic exercise effect on vasoconstriction 112 injuries associated 466-468 jet lag response 641-642 . maximal oxygen intake (VoZmax) 45,47.713-714,753,756 musculoskeletal changes 550551 peak height velocity (PHV) 397, 398 performance at and prediction of success 399 physical limitations 547 physiological/ pathological changes 547-551 rating of perceived effort 390 renal function 549-550 renin-angiotensin-aldosterone 550 stress fracture 768 temperature intolerance 548 tissue injury and inflammation 805-806 vasoconstrictor responses 107 see also elderly air-liquid partition coefficient 23 air pollutants 628-638 carbon monoxide 297,635-636 ozone see ozone performance reduced 629-630 primary 297 respiratory discomfort 628 secondary 297-298,298 sulphur dioxide 297,634435 air pollution 53 episodes 298 high altitude 298,615 air quality 297-298 assessment 298 air resistance cycling 857,859,860 energy costs 252 high altitude 252--253,614-615 shielding from 254 skiing 846 triathlon 878-879 air travel 639 sedative use with 646447 see also jet lag airway hyperresponsiveness to ozone 632 inflammation 632


ozone pollution effect 632 resistance 53,632 alcohol 445-448 adverse effects 447 catabolism 446 consumption 760 rugby football 9x5 social 447 content of drinks 445-446 effects on CNS 446 as energy source 446 misuse 447-448 oxidation 328 physiological effects 446 warning before mass participation events 661 aldosterone 190 elderly 550 high altitudes 616 alertness, maintenance after jet lag 646’ 647 alkalosis input to perception of effort 376 respiratory 321,532 allelic variations 234 allergies, medical screening before competition 653 allometric equations 44,45 allometry 44 alpha-adrenergic receptor blockers 567 A-motoneurones 137,139 altitude acclimatization see acclimatization high see high altitude moderate acute effects 6 6 6 1 7 diet 618 training see high altitude, training altitude chamber, rowing training 842 alveolar-capillary surface area 53 alveolar hyperventilation 55 alveolar macrophage 737 alveolar oxygen pressure high altitude 616 rowers 841 alveolar to arterial partial pressure gradient (A-aqo,) 55 alveolar ventilation (V,) 52 alveoli, oxygen transport from 23 amantadine hydrochloride 581 amenorrhoea adolescents 514 bone (density) loss 361,718,719 causative hypotheses 723-725 characterization 72cP723 consequences 718-719 eumenorrhoeic athletes comparison 720 factors associated 721723 ovarian function and hormone

changes 72c~721 secondary 410,514 sports injuries and 805 stress fractures 466 American Academy of Orthopedic Surgeons 479-480 American College of Sports Medicine (ACSM) exercise for cardiorespiratory / muscular fitness 554 exercise prescription for elderly 557 heat stress 287 American football/footballers 915917 background and principles 915 characteristics of players 916 dehydration 917 heart rate 916 jet lag effect 643-644 maximal oxygen intake 916 protective equipment 478,479 rule and injuries 464 training 916-917 American Heart Association 667-668,668,672,715 Americans with Disability Act (ADA) 565 amino acids branched-chain see branched-chain amino acids (BCAAs) changes in fatigue 33 essential 329 ingestion 201,203-204 supplements 201,204-205 synthesis 329 5-aminolevulinic acid 133 amphetamine 43~440,657 derivatives 439 effects and dosages 440 amputations, lower extremity 576-577 amyotrophic lateral sclerosis 582-583 anabolic-androgenic steroids ( U S ) 443,443-444 abuse 657 adverse effects 444 effect on bone mass 358 mechanisms of action 444 anaemia 424-425 erythropoietin treatment 428 haemoglobin levels 424 iron deficiency 415 ’sports’ 190,424-425 anaerobic capacity 318 anaerobic conditions, aerobic training session with 12 anaerobic events, swimming 824 anaerobic metabolism 311-328, 41-411


American footballers 916 canoeing 891-893 concepts 311-312 congestive heart failure 91 cycling 866 glycolysis 328,331,335 maximal power 334,336 hockey 922 inefficiency 312 intermittent exercise 10 interval exercise I 1 isokinetic ergometer 278 lactate accumulation limitation 312 markers of competitive performance 312 middle-distance running and 819-820

pace training effect 519 rowing 840 skiing 847 swimming 824,825 training influence 312 transition to 311,315 anaerobic threshold (lactate threshold) 13-14,3r5,318-320 altitude acclimatization 618 canoeing 893-894 carboxyhaemoglobin effect 635 concept 318 cycling 863,866,867 definition 315 economy of movement and 247 endurance performance and 403-404 exercise below 27 first/second breakpoints 318-320 as marker for training intensity 381,382,389-390 measurement methods 320 overtraining marker 489,490,491, 492

pace training in women 519,521 perception of effort 381,382 performance and 524-525 pregnancy 533 rating of perceived effort 389-390 rowers 840 rugby football 914 running, training effect 407-408, 408 running velocity (VLa4)and 403-404 soccer 902-903 swimmers 828 training at speed corresponding 404 triathlon 883 ventilation curves and 318 ventilatory threshold relationship 54 women 521-522, 524



anaerobic threshold (cont i m e d ) see also aerobic capacity anaesthetics, local injection 657-658 analysis of covariance (ANCOVA) 44 anaphylactic reactions, dextran infusions 432 androgenic steroids 443-444 aneurysms 56&569,577 aortic 568 circle of Willis 712 exercise/ training guidelines 569 angina pectoris 548,695 angiotensin I1 190 angiotensin-converting enzyme (ACE)gene 234-235 I / D polymorphisr-. 235 angiotensin-converting enzyme (ACE)inhibitors 567 ankle braces for stabilization 480,480 dorsiflexion 779 injury 476 taping 481 venous pressure 97 ankle drop protocol 788 anorexia nervosa 723 anovulation 720 anterior cruciate ligament injuries 465,471' 472,473 injury prevention 476,477 anterior tibia1 muscle, chronic stimulation effect 118,120 anthropometry 37-38 biological age 397 body composition assessment 349 canoeing 891 characteristics of athletes 38-40, 38-41 child and adolescent athletes 41-42,42 Heath-Carter protocol 38 heat loss and cold stress 292-293 physiological/ biomechanical considerations 43 rugby football 912 somatotype 37-38,232,233 see also body size; height; physique anticholinergic drugs 584 anticoagulants 568 anticonvulsants 578,583 antidepressants 570,582 antidiarrhoeals 660 antidiuretic hormone (ADH) 190, 432,447 antihypertensive agents 572,578 anti-inflammatory agents 808-809 see also non-steroidal antiinflammatory drugs (NSAIDs) anti-inflammatory cytokines 738,802 anti-inflammatory effects 802,803 antioxidants 417 anxiety 214

benefits of exercise 759 fatigue association 33 input to perception of effort 382 performance relationship 215,456 precompetition 214--215,456 aorta aneurysms 568 enlargement 568 rigidity, elderly 549 rupture 670 aortic valve stenosis 670 appetite, diminished in overtraining 496 arachidonic acid (AA) 802 arctic trips 663-664 area equipment 463-464 arousal 216,760 arrhythmias see cardiac arrhythmias arterial oxygen saturation see oxygen; oxygen transport arterial pressure see blood pressure arteries occlusion, muscle blood flow reduction 91 rigidity, elderly 549 arteriovenous oxygen difference 103, 104,224 age-related changes 548 elderly 552 arthritis 575 rheumatoid 575,752 see also osteoarthritis arthropathies, Achilles tendon injuries 779 articular cartilage see cartilage aspirin 808 association-dissociation factors 216-217,454 input to perception of effort 383, 388 pain and discomfort management 456 association football see soccer asthma 53,298 benefits of exercise 750 exacerbation by exercise 634 exercise training effects 569 ozone effect 629,632 sulphur dioxide effect 634 training recommendations 570 atherosclerosis 77,566,568 benefits of exercise 695 stroke due to 696 sudden death due to 712 atherosclerotic plaque 691 'athlete's heart' (concept) see heart athleticism, personality impact 211-212

Athletic Motivation Inventory (AMI) 368 atmosphere, high altitude 296,615, 931

ATP see adenosine triphosphate (ATP) ATPase muscle cells 170 myofibrillar see myofibrillar ATPase myosin 160,164 atrial natriuretic factor/peptide (ANF; ANP) 190,683 during and after exercise 685,685 atrioventricular accessory pathway 79 atropine sulphate 632 attentional focus, input to perception of effort 381 'augmenters,' input to perception of effort 382-383 Australian Rules football 917-919 maximal oxygen intake 9x9 autonomic nervous system adaptation induced by training 596,708 circulation control 103 failure, blood pressure changes 105

awareness of effort 374,388 axotomy 149 back pain gestational 536 stress fractures 771 triathletes 877 badminton, rules and injury prevention 464 banned substances 439,439,657 blood doping 427,657 drugs used for bronchospasm 653 ephedrine 443 erythropoietin 430,657 reasons for use 439 barometric pressure 294-295 baroreceptors 113 baroreflex 112-113 blood pressure control 112-113, 113 elderly 549 sensitivity in exercise 112,113 base, excess 321 baseball, rules and injury prevention 464 basketball, left ventricle dimensions 76 Bassler hypothesis 77 baths, heatstroke management 610 Bayes theorem 715 B cells 495,732 Becker muscular dystrophy 580 benzodiazepines 646 Bergstrhm needle biopsy 342,343 beta-agonists 634 beta-blockers 567,569 beta-endorphin see E-endorphin


betamethasone, cerebral oedema 621-622 bicarbonate 26 buffering action 321 cerebral fluid, high altitude 617, 619 doping 26,322 measurement and normal level 321

metabolic acidosis 321 biceps femoris 789 bicycle, types 857 biochemical markers, of overtraining 491-492 biochemical tests, muscle metabolism 338-341 bioelectric impedance analysis 349, 685 biological age 397-398 chronological DS 397-398,513 training effect in children 513 biological factors, endurance performance 21 bioluminescence assays 340 biomechanical constraints 245-258 drag forces 252,253 economy of movement relationship 2 5 ~ 2 5 1 fluid resistance and 252-253 mechanical power and economy 246,246-248 performance 'us controlled conditions 245 stride length and speed 250-251 see also mechanical power biomechanics Achilles tendon overuse injuries 778 anthropometry 43 canoeing 888-891 orthotics (shoe) 482 rowing 838 stress fracture prevention 773-774 biophosphates 576 biopsy, muscle 118,338,342-343 biopsy needles 342,343 b1adder catheterization 606 spinal cord injuries and 579 blindness 586 blood PH 321 redistribution during exercise 684 removal and re-infusion 427 solubility factors for gases 23,23, 24-25 storage, glycerol cell-freezing technique 426 blood doping 425,657,682 blood viscosity changes 425-426, 427 detection 427-428

erythropoietin 428-431,657 maximal oxygen intake 425 time course of RBC changes 427 blood flow 103-117 adipose tissue 107 blood pressure and vascular resistance 104-i05,105 cerebral 107 cutaneous see cutaneous blood flow to legs in runners 34 maternal 535 oxygen consumption relationship 103,104 pooling below heart level 263, 264

redistribution 103,104 blood pressure maintenance 104-105 reduced cardiac output 106 restriction in excess muscle contraction 31,32 skeletal muscle see muscle blood flow uterine 107 blood glucose see glucose blood-muscle oxygen exchange capacity 89 blood packing see blood doping blood pressure autonomic failure 105 baroreflex control 112-113,113 blood flow and vascular resistance relations 104-105,ios canoeists 896 control 689 elderly 549 endurance exercisebenefits 689-691 dose-response 691 exercise types 691 intensity threshold 689 maintenance 104-105 measurement 305-306 myocardial work rate 711 preliminary screening before competition 654 raised 689691 incidence 690 in isometric/isotonic exercise 751 response to endurance exercise 751.751 see also hypertension rowing 840,841 systolic see systolic blood pressure unconscious patient 603 women and effect of training 520 blood samples, doping detection 427-428, blood transfusions autologous 426,428,657


erythrocythaemia induction 426 risks associated 657 blood viscosity agents reducing 568 increased 425-426 adverse effects 429 altitude acclimatization 618,934 erythropoietin use 429 blood volume 682 central 683 after exercise 685,685-686 fall in 'heat exhaustion' 594 increase during exercise 683 prolonged standing effect 684 changes 427 decreased, hot environment 263, 264 estimation 431

see also volume loading pregnancy 531-532,534 regulation 683 role in oxygen transport 431-435 see also plasma volume body awareness 759 bodybuild 4 body clock see circadian rhythm body composition 346-365 assessment 346-349 criterion methods 346-349 errors 348 field methods 349 definition 346 elderly 555,556 endurance athletes 351-362 bone mass/density 350,355-361 extreme leanness, problems 361-362 fat-free mass 350,354-355 female 351 male 352 percentage fat 351-354 genetic influences 232-234 menstrual disorder mechanism 724 models 346 multiple-component 346, 348-349 three-component 348,349 two-component 43,346,347-348 performance 349-350 role of specific genes 238 triathlon 879-880 young athletes 353-354 body mass amenorrhoea 'us eumenorrhoea 721, Australian Rules football 918 calculations 347 canoeists 891 children and adolescents 41,42



body mass (continued) cycling 859 distribution (male and female) 41 economy relationship 250 excess 43 fat see fat, body fat-free (FFM)see fat-freemass (FFM) genetic influences 233-234 maximal oxygen intake relation 45,405,817, monitoring during intensive training 654-655 rugby players 912 scaling 44,48,49 skiers 850,850 smokers 757 for specific sports 38-40 triathlon 878,879,879 see also fat, body body mass index (BMI) genetic influences 233-234 maximum oxygen intake measurement 307 obesity 574 body shape, athletes 757 body size 38-40,346 assessment 37-38 consequences for performance 43, 48-5or49 economy of movement and 250 'ideal' values 37 individual variability 42-43 performance in cold conditions 292-293 physiological/ biomechanical considerations 43 runners 39,40,42,43 running performance and 817-819 scaling see scaling submaximal energy cost of locomotion 47-48,48 VoZmaxrelationship 45,45-47, 48-49,817 children and adolescents 45,45, . 46 Volsubmaxrelationship 47-48,48, 49 see also anthropometry body surface area left ventricular volume ratio 897 thermoregulation and 43 volume relationship 44 body temperature see temperature, body bone age 397 density see bone mineral density exercise effect 356,358,361 force applied 768 loss amenorrhoea 718,719

elderly 551 women 4x5 mass anabolic steroids effect 358 endurance athletes 355-361 injuries in women and 466 performance and 350 see also bone mineral density microtrauma 399 mineral content (BMC),gender and 355,356' 357,359-761 remodelling 768 spinal cord injuries 579 stress fractures due to 768 training in children 513 bone mineral density benefit of exercise 752-753 benefits of training children 512 endurance athletes 350,355-361 heritability 358 influences/factors affecting 752, 754-755 oligomenorrhoea/amenorrhoea 361 performance and 350 women 361,415 see also bone, mass bone scans 772,787 stress fractures 771,772 boredom 33 Borg's scale 374,376,384,384,389 boundary layer (air) 27 bowel maintenance programme 579 braces ankle stabilization 480,480 elbow 480 injury prevention 479-481 knee 480 patellar stabilizing 776,785 bradycardia, fetal 535 brain blood sugar decrease effect 28 see also entries beginning cerebral branched-chain amino acids (BCAAs) 204 mountaineers 618 oxidation 499 performance improvement 419, 655 transport to brain 205 tryptophan relationship 499 breakfast, pre-competition 198-199 breast cancer, risk reduction 758 breast milk, lactic acid 539 breath-by-breath equipment 283,284 breathing excessive work during prolonged exercise 56 increase at high altitude 932 input to perception of effort 376, 381

mechanics during exercise 53-54 ozone-induced alterations 629,632 pregnancy-induced changes 532 rate 53,54,64 respiratory muscle training effect 64 work 58,60 see also ventilation (VE) breathlessness see dyspnoea 'bright light,' jet lag management 647-648,648 bronchial C fibres 633 bronchitis, chronic 750 bronchoconstriction, pollutants causing 629,634 bronchodilators 571,632 bronchospasm, exercise-induced 653 Brozek formula 347,349 buffering capacity 321 altitude acclimatization 617-618 intramuscular 320 bundle branch block 617 burnout see overtraining bursae 777 Ca2+-ATPase170,170 chronic adaptation effect 177 content in muscle fibres 85,85, 172-1 73 function 172 sarcoplasmic reticulum 172-173 cadence, stride length and speed 250-251 Caesarean section 539 caffeine 201,441~442 content of drinks/products 441 dosages 441-442 effects and mechanisms 441 ergogenic benefit 201-202,657 health risks 442 calcaneal spur 787 calcitonin 576 calcium/calcium ions cycling and free calcium levels 175,176 in fatigue 29-30,r70-i7i intake, children 514 muscle contraction 28,29-30 post-tetanic potentiation 163 release, prolonged exercise effect 176 sarcoplasmic reticulum 169-170 supplements 415,753 troponin complex action 164 calcium channel blockers 567 calcium ion (pCa)-force relationship 164,165,166 chronic adaptation effect 168 calcium release channel 170,173 repetitive activity and 175 T tubule interface 173-174 calf muscle pump 596


calisthenics 560 calories 5 caman 926 camogie 926 Canadian technique, canoeing 889, 889-891,890 cancer, benefits of exercise 758-759 canoeing 888-899 accumulation oxygen deficit (AOD) 893 adaptations 894 aerobic metabolism 894-896 kayakers us canoeists 894-895 anaerobic metabolism 891-893 anaerobic threshold 893-894 anthropometry 891 biomechanics 888-891 blood lactate levels 891-892,894 blood pressure 896 Canadian technique 889,889491, 890 cardiovascular system 896 equipment 888 ergometers 274,274,275,276 force exerted during paddling 889, 890 heart rate 894 historical aspects 888 isokinetic data 891,891 kayak technique 888-889,889,890 isokinetic data 891,892 metabolic/cardiac parameters 281 monitoring 897 left ventricular mass 896,897 muscle fibre type 891 muscle force 891 paddling efficiency 895 speed canoeing 888 watercraft types 888 whitewater canoeing 888,889,893 capillarization, muscle, training effect 122,127-i29,128,130,169 capillary bed, gas exchange 23 capillary density 13,520 capillary electrophoresis (CE) 340 carbohydrate(s) 197-207 availability,and perception of effort 379,387 classification 199 cyclists 869,870 energy per gram 329 energy source 27,198,847 food containing 199,413 high-CHO diet 197,411-412,757 before/during exercise 420 effect on glycogen stores 418 jet lag management 646 ingestion 197-201,4ic-4ii amino acids with 201 children 514 cyclists 869,870,870

effecton glycogen stores 417 during exercise 200 glycogen resynthesis rate 412, 412

immediately pre-exercise 200 post-exercise 200-201,870 precompetition meals 198-199 prior to exercise 198-200,870 timing during exercise 200 women athletes 205-206,525 loading regimens 198 rugby football 91 1 women 525 low-CHO diet 418 metabolism 27,198 alcohol effects 447 pregnancy-induced changes 531 training in women 521 oxidation (aerobic glycolysis) 329-330,334,336 requirements 410,411-412 restriction, hypoglycaemia with 606 sources 412 sports drinks see carbohydrate beverages stores 197-198,411 elevated and detrimental aspects 198 ’supercompensation’ 198 supplementation 741 immune benefits 740 synthesis 329,329 threshold, cycling 863 utilization rate 411-412 carbohydrate beverages 200,201, 742 benefits on immune system 731, 740-74L741 seenlsu sports drinks carbon cycle 329,329 carbon dioxide adverse effects 24 arterial partial pressure 52 blood solubility factor 24-25 conductance 24,24-25,25 output as input to perception of effort 377 pregnancy 534 partial pressure (ambient air) 24 retention/accumulation 31,321 total flux 24 transport 24 underwater athletes 24,31 carbonic anhydrase inhibitors 621 carbon monoxide air pollution 297,635-636 binding to haemoglobin 635,684 diffusing capacity see pulmonary diffusing capacity (DLco) exposure, causes 635


high altitude interaction 615 carboxyhaemoglobin 635,636 cardiac arrest/events 306,601 mass participation events 663 reduced risk by exercise 696 risk at high altitude 622 see also myocardial infarction; sudden cardiac death cardiac arrhythmias 653,654 fetal bradycardia 535 sudden death 670,712 tachycardia 320,594 ventricular fibrillation 306,696 cardiac disease see cardiovascular disease cardiac failure 58,604 congestive see congestive heart failure detection methods 709 cardiac fatigue 69,80 cardiac hypertrophy 708 benefits 713-714 biochemical and cellular changes 75 endurance sports effect 7677, 708-709 haemodynamic basis 70-71,708 health impact 714 historical aspects 68,708 investigation methods 709 molecular triggers 71 myocardial ischaemia and 710-711 pathological 71-75,78,709 indicators 710 physiological 71-75,709,711,713 pathological us 68,71-75,73, 709,710 types of sport and 76,7677 septa1 710,712 stimulus causing 70 wall stress 71,72 wall thickness 709 cardiac output 34 central limitation of effort 34 distribution 58 elderly 548,552 genetic influence 228-229 high altitude 617,936 hot environment 112 increased 70,682 pregnancy 531-532 reduced, blood flow redistribution 106

rowers 840 triathlon 873 cardiac reserve, children 513 cardiac transplantation 106 cardiomegaly, physiological 70, 70-71 see also cardiac hypertrophy cardiomyopathy 73 dilated 75,670



cardiomyopathy (continued) hypertrophic see hypertrophic cardiomyopathy (HCM) overdiagnosis, danger 708,709, 713 cardiorespiratory fitness 701 ACSM recommendations 554 cardiorespiratory function age-related decline 714 hockey 924 screening before competition 653 cardiothoracic ratio 708 cardiovascular abnormalities, sudden death and 668-671 cardiovascular benefits, of exercise 688-707 blood lipids and lipoproteins 698-699 blood pressure 689-691 confounding factors in studies 688-689 coronary heart disease prevention 691496 exercise recommendations see exercise glucose intolerance 699 insulin sensitivity 699 obesity 698 research methodological issues 688-689 stroke risk reduction 696-698 cardiovascular consequences of exercise in children 508 of respiratory muscle work 57-58 women and effect of training 520 cardiovascular disease 566-571, 688 age-related risk 701 epidemiology, exercise link 691-696~693~694 exercise testing 306 reduction by exercise 458 skeletal muscle blood flow and 91-92 see also cardiovascular system; coronary heart disease cardiovascular drift 54,109, iog-iio cardiovascular fitness 776,781 cardiovascular resistance, oxygen transport 24 cardiovascular risks, of exercise 671, 708117 see also cardiac hypertrophy; sudden cardiac death cardiovascular screening 667-681 abnormalities/disorders 668-671 American Heart Association guidelines 667468,668,672, 715 cost-efficiency 671,676,715 definitions and background 667-668

efficacy/limitations of noninvasive tests 675-677 ethical considerations 671 examiners 673,674 expectations of strategies 674-675 impact and limitations 675,715 importance 714-715 legal considerations 672 limitations in use 673,715 methods/diagnostic testing 676 obstacles 671 practice in US 672-673 purpose 667 questionnaires 673,673,674 race and gender aspects 677-678 cardiovascular system alcohol effects 446 canoeing 896 cycling 864,865 genetic aspects 228-229 pregnancy 531-532 see also cardiovascular disease carnitine 336,416 carotid body 932 cartilage benefit of exercise 751752 degeneration with age 551 catecholamines 184 cardiac hypertrophy 70 effect of strenuous exercise 184, 185,440,682 glycogenolysis stimulation 185 input to perception of effort 379 myocardial response, in elderly 548 overtraining marker 494 release in exercise 184,185,864 sudden cardiac death due to 79-80 see also adrenaline; noradrenaline catheterization bladder 606 muscle metabolism analysis 341-342 Cattell sixteen personality factor questionnaire (16PF) 368,370 cavusfeet 469 CD25 (IL-2R),overtraining marker 495 cell trafficking, cortisol effect 735 central fatigue see fatigue central limitations, of effort 34-35, 301,304 see also fatigue, central central nervous system (CNS) alcohol effect 446 thermoregulatory centre 262 central venous pressure exercise in hot environment 263 rowers 840-841,841 cerebral blood flow 22,107,759 velocity, rowers 8413841,841 cerebral fatigue 28-29,29

cerebral hypoxia 623 cerebral oedema 598-599,606 acute mountain sickness 621-622 treatment 621-622 cerebral oxygenation, rowers 841, 842 cerebral palsy 583-584 Cerebral Palsy-Intemational Sport and RecreationAssociation (CP-ISM) 3 583 cerebral perfusion 759 cerebral vascular accident (CVA) 577 see also stroke cervical spine injuries 464 cervix, incompetent 539 C fibres, bronchial 633 channel swimmers, body temperature 266,600 chemiluminescence,enhanced 338 chemokines, inflammation 800 chemoreceptors 54,932 chest disease, carbon dioxide conductance 25 childbirth, training after 539 childhood, 'disappearance' 515 children 507 aerobic trainability 507-512 implications 511-512 mechanisms 509-511 reduced response to training 509-5'0 anthropometric characteristics 41-42, 42 athletes 507 athletic success prediction 41 biological age 397-398,398 bumout 515 carbohydrate intake 514 early maturers 398-399 early specialization in sports 398-399 energy expenditure 510 growth 397 growth spurts 397,398,399 heart rate 510 heart size and cardiac reserve 513 height development 397-398,398 injuries 466-468 late maturers 398 maximal oxygen intake (VohaX) 45j47r227,507-509J508, 511 body size relationship 45,45,46 musculoskeletal system 513 nutrient deficiencies 513 nutrition 513-514 oxygen intake variations 509 participation in sport 507 performance trainability 512 physical activity levels 510 psychosocial variables 514-515


scaling factors, submaximal Vo2 48r49 selection of wrong sport 398-399 sexual maturation 5x4 soccer, early selection 399 stroke volume 510,511,513 talent identification and development 400 tennis, early selection 399 thermoregulation 514 training 399,507-516,512 benefits and risks 512-515 effect on growth 41-42,513 weight 514 cholesterol, reduction by exercise 69M99r757 chondromalacia 473 chondromalacia patellae see patellofemoral pain syndrome (PITS) chronic fatigue syndrome 499,660, 742 plasma glutamine 500,500 chronic pulmonary disease (CPD) 569-570 chronic stimulation, electrical see electrical stimulation chronological age 397-398,513 cigarette smoke, composition 445 cigarette smoking see smoking ciprofloxacin 660 circadian rhythm 639-641 adjustment 644-645 bright light and exercise 647449,648 improving 645-649 maintaining alertness 646,647 meal timing/composition 646 melatonin 647 process 645446 schedule to facilitate 645446 sedatives 646-647 control 639 desynchronization see jet lag exercise 640 factors affecting 640 intensity of exercise 641 phase delay and advance 645 rectal temperature 640,645 signals controlling 644-645 ventilation WE) 640,641 circle of Willis, aneurysms 712 circulation control 103 coronary see coronary circulation gastrointestinal 105 maximal aerobic power and 13 pregnancy 531-532T537.538 problems, fatigue development 31-32 rowers 836,841A41 splanchnic see splanchnic

circulation circulatory discomfort, in heat stress 265 circulatory failure 32,594 cisternae, terminal 172 citrate synthase 119 citric acid (Krebs)cycle 25,332,333, 337 branched-chain amino acids 205 enzymes 119,120 increased in altitude acclimatization 618 claudication, intermittent 91,568 clothing cold stress 291,294 economy of movement and 253 hot environments 29c-291 mass participation events 663 soccer 905 wind chill reduction 291 clumsiness 29,32 cognitive disorders 584-586 cognitive factors 216-217 cognitive strategies 453,456 input to perception of effort 383 cold environment 259-267,291-292 exercise in 265-266 shivering 260 soccer 905 cold injuries 465 prevention 481 risks during competition 291-292 skiers 855 cold stress 265-266,291-294 acclimatization 294 assessment 291-292 clothing 291,294 determinants 291--292 hydration 294 performance factors ~92-294 poor air quality and 298 cold tolerance 293,294 cold water 292 collagen disorders 779 collapse 607 conditions causing 601,601 diagnosis 598 exercise-associatedsee exerciseassociated collapse (EAC) management 601607 in conscious patient 606-607 diagnostic information required 603 diagnostic steps 602-604 flowchart 611 initial 601-602 protocols 604406,606-607 in unconsciousness 604406 postexercise see exercise-associated collapse (EAC) rates 601,602 rectal temperature 663


risk reduction by prerace planning 608-609 severity assessment 602,602 vasomotor 594 see also hypoglycaemia; unconsciousness colonic cancer, reduction 758 coma 603 common colds 742 communication system, prerace planning 609 compartment syndrome, hamstring 791 competition anxiety before 214-215,456 carbohydrate meal 198-199 cold injury risks 291-292 diet 417-419 high altitude, strategies 296-297 hot environment, strategies 288-291 international see international competition medical supervision during 659-660 mental preparation 453-454,456 return to after childbirth 539 Competitive Reflections 456 complement, in inflammation 800 computed tomography (CT), stress fractures 771,772 concanavalin-A, overtraining marker 495 concentric actions 475 Concept I1 rowing ergometer 275, 275 conchotome technique 342-343 Conconi principle 320 Conconi test 13,320,827 conditioning, endurance 4,402-408 hamstring injury prevention 791 oxygen intake 405 physiological factors 402-405 safe limits in pregnancy 536538 training considerations 405-408 see also training conductance, definition 22 conductance analysis 22 conductance theory 22-28 carbon dioxide 24,24-25 heat 26,2&27 lactate 25,25-26 metabolites 27-28 oxygen 22-24 confectionery 412 confounding factors, benefits of exercise 688-689 congestive heart failure 580 anaerobic metabolism 91 muscle blood flow reduction 91 vasodilatation impairment 91,92 continuous exercise 12-14,15



contractile proteins 159-164 failure i5%159 types 161 convection,heat 260 cooling-down 474-475 elderly athletes 557 coordination failure, fatigue 29 training for injury prevention 476 core temperature see temperature, body coronary anomalies, congenital 669-670~676~712 coronary arteries, intramural (tunnelled) 670 coronary circulation 696 impairment 653 coronary heart disease 691 anabolic-androgenic steroid increasing 444 benefits of exercise 691-696 epidemiological features 692-693 mechanisms 695 risk assessments 692,692-694, 693,694 benefits of training children 512 ECG and diagnosis 549 elderly 548-549 ephedrine effect 443 lower extremity amputees 577 marathon runners 77 risk factors 548,551 reduction by exercise 695 sudden cardiac death 670 see also cardiovascular disease; myocardial infarction cor pulmonale 569 corpus luteum 719 corticosteroids anti-inflammatory actions 808 injections 658,809 adverse effects 477 contraindication 782,783 corticotrophin-releasinghormone (CRH) 185 cortisol 185-187 consequences of elevation 186 elevated levels in amenorrhoea 7231 725 input to perception of effort 380 local infiltration 808-809 neutrophil / lymphocyte count changes 735 overtraining marker 492,493,656 response to exercise 186 testosterone ratio 493,656 training effect 186-187 COSMED telemeter 304 C-urotein 160 creatine 416

loading 201,911 muscle stores 416 supplements 416-417 creatine kinase (CK) 236 adaptation to chronic stimulation 121

overtraining marker 491 creatine kinase, skeletal musclespecific (CKh4h4) fatigue resistance and 236 gene 236-237 maximal oxygen intake linkage 236 creatinephosphate 21,416 critical power 317,318 see also anaerobic threshold cromolyn sodium 634 cross-country running, rating of perceived effort 390 cross-reinnervation 144-145 cruciate ligament injury see anterior cruciate ligament injuries crutches 790 cryotherapy 807 cutaneous blood flow 26,103-117, 107-109,263 alcohol effect 447 body temperature relationship 107-108,108 exercise in hot environment 263 muscle blood flow competition 108-109,iio, 263 role in cardiovascular drift 109, 109-110

thermoregulation 596 threshold temperature for vasodilatation 108 vasoconstriction 108-109 cyanmethaemoglobin assay 424, 73e39 cybex strength testing 790 cycle ergometer/ergometry 274, 865-866 cerebral palsy 583-584 diabetics 573 disabled persons 565 incremental test 866 maximal oxygen intake measurement 11-12,304, 865-866 overtraining 489 wetsuit effect 873 cycling and cyclists 857471 adaptations 866 aerobic-anaerobic transition 866, 867 aerobic capacity 857,868 aerodynamic clothing /equipment 253 age, body size and physique 38 air resistance 254,857,859,860 anaerobic metabolism 866

bicycle variables affecting economy 252 blood glucose 869,870 blood lactate 861,864,866,869 bodyfat 352 body mass effect 859 body surface area 859,860 cadence and economy 251 caffeine intake effect 442,657 cardiovascular system 864,865 catecholamine release 864 circadian rhythm control 640 cross-country races 858 dehydration 865 diet 869-870,870 drafting 857458,859 economy of movement 245,524, 885 energetics 861-864,864-865 energy consumption 857-858 energy costs 517,859 per unit of body mass 250 energy sources 864,865 environmental conditions 869 events 857,858 external/internal locus of control 383 fatigue mechanism 34,869 fluid ingestion 597 fluid requirements 869 functional capacity assessment 865470 glycogen loading 655 gravity effect 614 heart rate 865,867,869 heatloss 873 immune system changes 732 ketone bodies 865 laboratory see cycle ergometer/ergometry left ventricle dimensions 76 long-term, physiology 864465 lower extremity amputees 577 maltodextrin/low fructose beverage 869 maximal oxygen intake 863,867 medium-term, physiology 861-864 metabolic data 282 metabolic rate 409 metabolic thresholds 863 motor system 861,864 muscle enzymes 863 muscle fibres 861,864 area 863 recruitment patterns 127 ozone effect 630,631 pedalling rates 251 perceived effort application 385 performance structure 862 power output 866 pregnancy 537


protein catabolism 865,868 recovery, diet and 86S869 respiratory muscle training effect 61 road 858 rolling resistance 252 short-term events, physiology 861-864 sitting positions 858-859,859,860 speeds 857,858 factors influencing 857-860 wind resistance 279,280 sudden cardiac death 711 tactics 857,860 track 857,858 training follow-up 866,867 intensity 866-868 physiology 861 rating of perceived effort 390 for world record 860,86@861 years required 861 training load 860,861~861,861 triacylglycerolcontent of muscles 864 triathlons 873,874,885 wind speed/direction effect 253 in wind tunnel 279,279 work components 246,246 cyclooxygenase 802 cyclooxygenaseinhibitors 633,803 COX2 inhibitors 803,808 cystic fibrosis 61,570-571 cytochrome c oxidase 119 cytochromes 337 cytokines anti-inflammatory 738,802 ex vivo production reduced 739 increased by prolonged exercise 738-739r739 inflammation process 802,808 pro-inflammatory 73%739,802 C toskeletal system, muscle cells 177-178 adaptations 179-180 disruption by eccentric exercise 167

Daedalus 942, 943,944 dancers, amenorrhoea 724 dead space ventilation 53 deafness 585-586 deceleration, work 6 decompression chamber 620 deep vein thrombosis, in air travel 639 degenerative changes, elderly 468 dehydration air travel 639 American football 917 cold environments 294 cyclists 865

due to fluid restriction 591-592 elderly, susceptibility 550 during exercise zoo wartime studies 595 exercise-associatedcollapse 607 fatigue due to 419 heart rate increase 14 heat cramps association 592-593 heat exhaustion 593,607 heatstroke and 596 hot environment 290 impaired performance in 597,598 physiological changes 597 pre-exercise 595 role in heat illnesses 591-592, 597-599 triathlon 873-874 unconsciousness 605 delayed hypersensitivity 738,738 delayed-onset muscle soreness (DOMS) 808 densitometry 347 depression 214 benefits of exercise 759 detraining 147 dexamethasone, plantar fasciitis 787 dextran 432 dextran infusion 432,434 blood volume increase 432 dextroamphetamine 439 diabetes mellitus 572-574 benefits of exercise 757-758 complications 758 effects of exercise training 573,699 endurance training recommendations 573-574 gestational 534,572-573 injury predisposition 473 reduced risk with exercise 699, 757-758 type I (insulin-dependent; juvenileonset) 572,758 type 11 (non-insulin dependent; adult-onset) 572,758 lower extremity amputees 577 obesity reduction 574 prevention 573 dialysis 571,572 diaphragm, shortening 63 diaphragmatic fatigue 54,5&57,57, 61 diarrhoea, traveller’s 659 diastasis recti 536,539 diastolic blood pressure, elderly 549 diastolic function 75 training-induced changes 70 diclofenac 808 diet acute mountain sickness prevention 621 benefits of exercise 760


carbohydrate ingestion see carbohydratefs) for competition 417-419 cyclists 869-870,870 recovery 868-869 at high altitude 618 high-carbohydrate see carbohydrate($ high-fat 202,412,413,757 high-fat, low carbohydrate 412-413 high-fibre 203,204 infection prevention 742 injury prevention 477 luteinizing hormone pulsatility 726 meal timing/composition, jet lag 646 pre-competition 418 pre-exercise 418 prerace advice to athletes 609 rugby football 9x5 soccer players 908 training 409-417 energy substrates 409-413 micronutrients 414-415 protein intake 413-414 supplements 415-417 vegetarian 203,415 see also nutrition; individual nutrients dietary fibre, high 203,204 dietary supplements see nutritional supplements dihydropyridine receptors (DHPR) 170,176 dimensionality theory 44 diphenoxylate 660 2,3-diphosphoglycerate 618 disabilities classification 567 definition 565 see also individual disabilities disability, persons with 565-587 endurance training principle 565 importance of training 566 discomfort, cognitive control strategies 456 disease, classification 567 dissociation 216,454 see also association-dissociation factors diuresis, caffeine effect +p diuretics 606 effect on exercise training 567,570 diurnal rhythm see circadian rhythm dopamine reduced 584 role in central fatigue 419 dopaminergics 584 doping 657-658 bicarbonate 26,322



doping (continued) blood see blood doping erythropoietin see erythropoietin hormones 191,194,657 international competition 657-658 see also banned substances dorsal root ganglion 151-152 neurones 142-144.151 succinate dehydrogenase activity 151-152 dorsospinocerebellar neurones 138 Douglas bags 305,905 Down’s syndrome 585 drafting, cycling 857-858,859 drag forces 252,253 drinking stations 658,661 drinks 200 caffeine content 441 composition during exercise 420 glycerol-containing 419-420 sodium addition 420,421 see also carbohydrate beverages; sports drinks drugs 438 ergogenic see ergogenic drugs injury prevention 477 for medical facilities at races 610, 611 prohibited 657 bronchospasm treatment 653 see also banned substances social (recreational) 438,439, 444-448 dual-energy X-ray absorptiometry (DXA) 349 Duchenne muscular dystrophy 580 duration of exercise/training ACSM recommendations 554 elderly 552 input to perception of effort 380, 386,388,389 application 385-386 metabolic changes 125-127 muscle metabolism 125-127 periodization and 527 pregnancy 538 dye dilution technique 341 dynamic stretching 476 dyspn0e.a 546549 development 750 reduction in performance enhancement 64 respiratory muscle loading/unloading 58,63 ear guards 479 East Germany, swimming medals 400,400 eating, grazing pattern 412 eating disorders 362,514,723 eccentric exercise 475 effect on cytoskeletal system 178

effect on myofibrillar proteins 166-167 muscle strain injuries 788 triceps surae 781-782 echocardiography 69 abnormalities detectable 676 hypertrophic cardiomyopathy 6751 709 M-mode 74,74 prescreening of competitors 675, 676,715 two-dimensional 677,709 use and misuse 709710 ecologicalphysiology 44 economy index, triathlons 884 economy of movement 245-258,402 biomechanical measures and 250-251 body size relationship 250 cycling 245,524,885 equipment relationship 251-252, 253 external resistance forces 252-254 footwear 248,251-252 kinematic/kinetic measures 251 lower limb flexibility 249 mechanical power relationship 246-248 optimization 254 performance relationship 245,524 exceptions 7.45 running see running skiing 251 small improvement with large benefits 245-246 stretch-shortening cycle 248-250 technique affecting 251 triathletes 875,884-885 utilization of maximal aerobic capacity 402-403 variations 246 women 521,524 ecstasy 439 ectomorphy 37-38,41,42 education Achilles tendon injury prevention 782 health 477 prerace planning 608 stress fracture prevention 773 effectivetemperature (ET*)288 efficiencysee economy of movement efficiency ratio 247 effortawareness 374,388 Ehlers-Danlos syndrome 779 eicosanoids 802 role in inflammation 802-803 eicosapentaenoic acid 803 ejection fraction 709 elbow braces 480 Pads 479,479

tennis 463,480 elderly 547-564 ACSM recommendations for exercise 554 activity level 547 baroreceptor reflex function 549 blood pressure 549 body composition 555,556 cardiac function 548 cardiac hypertrophy benefits 713714 cerebral performance improvement 759 chronic disease 547 cool-down exercises 557 coronary artery disease 548-549 dyspnoea 750 eccentric exercise not recommended 475 electrocardiography (ECG) 549 endurance training effects 552-555 exerciseprescription 555-560 guidelines 555-559 to prevent disease 551 falls 576 frail, exercise programme 756 graded exercise testing 548-549 hepatic function 550 hyperkalaemia 550 injuries associated 468,558,558, 805 intensity of training 558 , maximal oxygen intake (V0-J 552-5558553 medical examination, clearance for exercise 477,551,551-552 muscular strength training 555 musculoskeletal changes 550-551 physical activity levels 753 physiological/ pathological changes 547-551 prolongation of independence 753756 renal function 549-550 renin-angiotensin-aldos terone system 550 strength training 559-560 sudden deaths 670 tennis 468 warm-up exercises 557 electricalimpedance 349,685 electricalstimulation, chronic effectson muscle 118,120-122, IZI enzyme changes 118,119 electrocardiography (ECG) 69 cardiovascular screening for training 672,677 changes due to training adaptations 677 elderly 549 electrode placement 305 exercise test 305


high altitude 617 hypertrophic cardiomyopathy 677 long QT syndrome 677 ST depression 549 electroencephalography (EEG) 646 electrolyte analysers 610 electrolytes administration, exercise-associated collapse 607 balance, women during training 525-526 heat cramps and 593 loss during sweating 419 replacement 42c-421,421 see also potassium; sodium electromyography (EMG) 141,174 electrophoresis, erythropoietin determination 43cq3i elite athletes 239 anxiety 214,215 body composition 351,352 cognitive factors 216,217 genetic markers 234 infections 732 maximal oxygen intake (Vo02max) 402 mental skills 452 mountaineering 937-939 overtraining 487 performance determinants 271, 2 72

pulmonary blood-gas barrier impairment 53 skiing 850-852 veteran, injuries 468 emergency departments, mass participation events 661 emergency evacuation see evacuation of athletes emergency transport, prerace planning 609 emotional risks, training of children 512,514-515 endergonic reactions 330 endocrine response highaltitude 616 see also hormones endometrium, oestrogen and progesterone effect 719 endomorphy 37,41,42 P-endorphin 188-189,749 ACTH release correlation 186, 188-189 euphoric sensations 189,749 input to perception of effort 379 response to exercise 188-189 secretion (‘runner’s high’) 749,759 endotenon 777 endothelium-dependent vasodilatation 96-97 congestive heart failure 92 endotoxin 801

endurance definition 7-8,37 perceived effort relationship 385 endurance activities 9-16 categories 653 endurance conditioning see conditioning, endurance endurance factors 184-207 endurance time 12-13 energetics cycling 861-864,864465 running see running energy ATPresynthesis 31,331 ba1ance negative see below women 525 chemical 5,21 consumption (internal) 6 costs(C,) 813 air resistance 252 competitive walking 282 cycling 857458 fluid resistance 252-253 reducing see economy of movement rowing 839 running see running elastic 248,249 expenditure activities of daily living (ADL) 753 chldren 510 cycling 517,859 hockey 92921,925 international competitions 655 leisure, optimal 747 resting 6 rugby football 911 running 517,815 ‘running and walking’ 814 skiing 846-847 soccer see soccer in training 410 weight maintenance 700 women 517-518 ‘free‘ 21 intake 410,414 amenorrhoeic vs eumenorrhoeic athletes 721 cyclists 869,870,870 runners 410,410 women athletes 202,205,410 kinetic 6,97 low availability consequences 725 menstrual disorder mechanism 724,725 metabolism elderly 550-551 pathways 331-334,332,333 for muscle cells 158,329,330-331


negative balance decreased bone density due to 752 swimmers 830-831 origins 329 potential 5 protein oxidation 414 relationship to work 6 release 330,331,411 anaerobic glycolysis 335 replenishment, cyclists 868-869 requirement for women 5x7 luteinizing hormone pulsatility 725,726 requirements during exercise 410, 411 reserves 22 resting expenditure 6 sources p9,4m-413 alcohol 446 carbohydrate 27,198,847 for cycling 864,865 fat see fat for skiing 846-847 see also glycogen stores 5,330 submaximal costs of locomotion 47-48r48 supply and demand, skeletal muscle 84,85-86,98 utilization by muscle 330-331 ’energy drain’, amenorrhoea in dancers 724 English Channel swimmers, hypothermia 266,600 enhanced chemiluminescence (ECL) 338 environmental conditions conditions for event cancellation 662 contribution to competitive success 4 cycling 869 injuries associated 465 mass participation events 662,663 potential hazards 658 rugby football 911 soccer 904-905 environmental extremes assessment 287-300 stressor interactions 298 see also cold environment; high altitude; hot environment enzyme immunosorbent assay (ELISA) 340 enzymes 330 adaptation 12c-121,122-124 citric acid cycle enzymes 120 adaptations, training-induced mechanisms 131-133 chronic electrical muscle stimulation effect 118,119



enzymes (continued) endurance training effects 122-124,124 aerobic enzymes 27,314 lifespan 131 in mitochondria 332 muscle metabolism 118 genetic determinants 231,232 overtraining effect 656 reactions catalysed by 330 synthesis rate 131 vastus lateralis muscle, cyclists 863 ephedrine 442-443 side-effects 443 epic expeditions 653 epinephrine see adrenaline (epinephrine) epiphyseal plate (growth plate) injuries 399 children 513 epitenon 777 equipment arena 463-464 canoeing 888 economy of movement and 251-252,253 medical facility at race finish 609-611,610 poor, injuries due to 463 preventive 478-482 braces 479-481 shoes 481-482 tape 481 protective 478,478-479 ergogenic aids 438 alcohol 446 caffeine 442 creatine 41&417 MacrodexTM434 ergogenic drugs 438,439-444 reasons for use 439 see also banned substances ergometer pools 276-277 ergometers canoeing 274,274,275 Concept I1 rowing 275,275 cycle see cycle ergometer/ergometry Gjessing-Nilsen 275,275,276,831 isokinetic 277-278,278,891 lower extremity amputees 577 for maximum oxygen intake (Vqmax) 304,865-866 rowing 275,275-276,276 skiing 276,277 stroke and head injury patients 578 types 274-279 wheelchair athletes 278,278 ergometry 273-274 definition 273-274

muscular dystrophy 580 erythrocytes see red blood cells erythrocythaemia 425-428 induction methods 425,426 input to perception of effort 376 erythrocytosis, autosomal dominant 235 erythropoiesis altitude training in women 526-527 increased by anabolic-androgenic steroids 444 signs 682 erythropoietin (EPO) 190,236 abuse 190 actions 190 anaemia treatment 428 blood doping method 428-431, 657 dangers of use 429 effect on training on serum levels 429-430 gene 235-236,428 improved aerobic power 428 recombinant 428,429 anabolic-androgenic steroids effect 444 detection 430-431 renal failure therapy 572 sudden cardiac death 711 role 428 serum level determination 430 synthesis 428 urine levels 430 erythropoietin receptor (EPOR) gene 236 Escherichia coli diarrhoea due to 659 phagocytosis 735,736 ethics, cardiovascular screening 671 ethnic aspects blood pressure and exercise effect 689-690 cardiovascular screening 677-678 sudden death 678 ethyl alcohol see alcohol eumenorrhoeic athletes, characterization 720-723 evacuation of athletes 609,664 wilderness trips 664 evaporation 260-261 examination, medical cardiovascular 672,673 impact and limitations 675 seealso cardiovascular screening pregnancy 536537 before sports for injury prevention 477 excess post-exerciseoxygen consumption (EPOC) 574 excitation-contraction coupling see muscle

exercise benefits 547,551,688-707 see also cardiovascular benefits bronchospasm 653 circadian rhythm 640 deaths related to 712 see also sudden cardiac death; sudden deaths definition 3 duration see duration of exercise/ training effect on heart 68,688 elderly see elderly health benefits see health benefits infection reduction 732 intensity see intensity of exercise/ training intermittent see intermittent exercise jet lag management 647-649 lack 688 leisure-time coronary heart disease risk 692, 6924594,693,694 high blood pressure incidence 690 reduced risk/mortality of stroke 697 lipids and lipoproteins 69EL-699 medical clearance for in elderly 551,551-552 in peripheral vascular disease 91 programme for frail elderly 756 recommendations cardiovascular health 699-700, 7ovo1 by health organizations 70-701 stress, menstrual disorder mechanism 723,7q-725 types and injury relationship 805 whilst unwell, recommendations 742-743 year 2000 goals in US 701 exercise-associatedcollapse (EAC) 594,595 diagnosis 607 management 606-607 exercise-induced arterial hypoxaemia (EIAH) 55-56,62 exercise machines, lower extremity amputees 577 exerciserehabilitation, chronic pulmonary disease 570,750 exercise testing contraindications 306,306,551 ECG 305 elderly 546549,551 graded see graded exercise testing (GXT) precautions 306,306 exergonicreactions 330 expiratory flow limitation (Em) 56


expiratory flow rates 53,59 external oblique aponeurosis 795 external resistance forces 252-254 extrasarcomeric proteins 178 extroversion 382,640 circadian rhythm 640 exercise intensity relationship 382 eye, injury prevention 478-479 eye-protecting devices 478-479 Eysenck Personality Inventory (EPI) 382 face masks 464 protective 478,478,479 facioscapulohumeral dystrophy (FSHD) 580 falls, elderly 576 fasting, short-term 413 fast-twitch muscle fibres see muscle fibre types fat 197-207,201 avoidance by athletes 202 energy per gram 329 as energy source 329,519,847 high-fat diet 202,412,413,757 increased utilization after training 60 inflammation and 807 ingestion/intake 201-202 metabolism 27,521 pregnancy-induced changes 531 mobilization 28,201-202 oxidation 410-411 requirements 412 stores 197 see also lipids fat, body adverse effects of accumulation 757 aerobic power relationship 350 American footballers 916 critical level and amenorrhoea aetiology 724 density relationship 347 endurance athletes 351-354 excessive 349-350 gender influences 293 genetic influences 233-234 increasing prior to prolonged exercise 655 intra-abdominal in elderly 555 mass 43,346 assessment 347 performance and 349-350 two-component model and 346, 347 men, by sport type 354 percentage determination 347,349 endurance athletes 351-354 reduction in diabetics after exercise 573

tissue insulation in cold water immersion z92-293,293 women 353,410,525 young athletes 353-354 fat-free mass (FFM)43,346 assessment 347 calculation 347,348 constituents 346,348 elderly 560 endurance athletes 354-355 gender differences 354-355,355 genetic influences 233 interindividual variations 347-348 performance and 350 resistance training effect 555 two-component model and 346, 347 fatigue 22,28-33,418-419 accident risk 33 acute after training session 501 anxiety association 33 branched-chain amino acids role 205 causes 28,259,336 central causes 28,205 dopamine role 419 nutrition and 418-419 overtraining 499 susceptibility 33 central vs peripheral limitations 34-35 cerebral 28-29,29 clumsiness 29,32 cumulative chronic 32 cyclists 34,869 definition 259,903 dehydration causing 419 diaphragmatic 54,56-57,57,61 excitation-contraction coupling 174 failure of drive mechanisms 28-30 failure of power supply 31 glycogen reserves and 31,411 heart rate 259 high-frequency 174 homeostasis failure 31-32,95 hormonal 32 hot environment 419 hyperthermia relationship 111 hypoglycaemia as cause 336 hypothermia susceptibility 294 immune system deterioration 32, 33 inappropriate calcium level 29-30, 170-171 injuries 461 interindividual differences 33-34 intermittent exercise protocol 11 internal temperature and 111,419 marathon runners 31 masked by amphetamine 440 medical aspects 33


mental, goals in soccer 904 metabolic i20,158,166,178-180 avoidance 166 cause (theory) 205 protective role 166 metabolic acidosis 95 mitochondria1damage 33 muscle see muscle myocardium 110 myofibrillar function 165-167 neural component 29,29 neuromuscular 146,153 neurotransmitters involved 419 non-metabolic 178-180 perceptions 33 peripheral cause, onset speed 33-34 perseverance aspect 453 physiological 28-32 projected 32-33 psychological 3 ~ 3 3 , 4 5 3 resistance 180 adaptations in myofibrillar system 167-168 enzyme activities 146 low CKMM activity 236 Na+/K+pump role 177 soccer 904 training effect 168-169 respiratory muscles see respiratory muscles soccer see soccer time to, acclimatization effect 111 travel 639 triathlons 874,875 warm environment 419 fatigue fractures 33 fat pad atrophy 788 fatty acid-binding protein (FABPPM) 334 fatty acids degradation, ATP production 336-337 energy metabolism 333,334,337 essential 803,807 free see free fatty acids (FFA) long-chain 202 metabolism 337 oxidation 332,336-337 chronic stimulation effect 119, 119,120 polyunsaturated (PUFAs) 807 short-chain 202 transport across mitochondria 334, 336 transport to muscle 31 Federation Internationale des Societes dAviron (FISA) 836, 837,839 feedback, body 216,217 perceived effort 375,386-387,388 feed-forward mechanisms 54



femur, stress fracture 768,769,770 fencing 946 fenoterol, prohibition 653 fetus bradycardia 535 growth, endurance exercise effect 535 heart rate 534-535,535,538 obstetric outcomes 536 response to maternal exercise 534, 534-535 stress 538 fibrinolysis 696 fibula, stress fracture 768,770 Fick principle/equation 103,510 Ficks first law 89 field games physiological demands 900 pitch dimensions 900 types 900 see also rugby football; soccer field hockey see hockey field independent input, to perception of effort 383 field sports 90-30 first-aid helpers 609,660 first-aid stations mass participation events 662,663 positions 609 fishoil 803 fitness 3-4 ACSM recommendations for exercise 554 aerobidanaerobic 767 see also aerobic fitness athletic 767 basic level for injury prevention 473-474 blood pressure control 689 cardiorespiratory 554 cardiovascular 776,781 hurling and lacrosse 92-27 rugby football 912-915 soccer 907 sport-specific 767 Five-Nations Championship 910 flexibility age-related loss 756 elderly 558 injuries due to 47c-471 stretch-shortening cycle and 49-50 training 471 ACSM recommendations 554 elderly 558 to prevent injury 475-476 flight see air travel; human-powered flight; spaceflight flow-volume loop 53,56 fluid absorption 599 accumulation 598-599

advice before international competitions 659 balance, women during training 525 ingestion during exercise 597 marathon running 592 mass participation events 661 loss diarrhoea 659 see also dehydration overload in prolonged exercise 598-599 diagnosis 604 management 606 see also hyponatraemia replacement 420-421, 421 see also hydration requirements 4iy-421 cyclists 869 before exercise 419420 postexercise 420-421 resistance 246,246 work to overcome 252-253 restriction during exercise 591 retention 598 pathogenic mechanisms 599 see also drinks; genetic determinants; water fluid-regulating hormones 190 fluorescein isothiocyanate (FITC) 175 fluorometric pyridine nucleotide method 338,339 follicle-stimulatinghormone (FSH) 719 foods advice before international competitions 659 glycaemic index 199,199-200 see also diet; nutrition food supplements see nutritional supplements foot care 477-478 dorsiflexion 779 football American see American football/ footballers association see soccer Australian Rules 917-919 Gaelic 917-919 rugby see rugby football footwear Achilles tendon injury prevention 778179 cushioning effect on energy costs 252 economy of movement and 248, 251-252 energy storage and economy of movement 248

heel (shoe) 778-779 heellifts 782 ideal 481-482 injury prevention 481-482, 778-779 mass participation events 663 motion control 779 plantar fasciitis 786 running 248,481 stress fracture prevention 774 force 5,768 aeroplane aerodynamics 942943 drag, rowing 838,838 forced expiratory volume in 1 s (FEV,) 629 forced vital capacity (FVC) 629 forcevelocity curves, canoeists 891, 892 fractures fatigue 33 Jones' 771 risk after menstrual disorders 718 stress see stress fractures tibial, anterior cortical 770 vertebral 576 Frank-Starling mechanism 520,548, 683 free fatty acids (FFA) availability,input to perception of effort 379,387 degradation 33G337 intravenous administration 655 metabolism, caffeine effect 441 mobilization 201 free radicals damage to muscle 417 Na+/K+pump susceptibility 175 reactive oxygen species 801,802, 806 frostbite 291,654 fructose, uptake by liver 199 fruit, carbohydrate content 199,200 fuel reserves, catecholamine effect 185 functional field test, rugby 913 Gaelic football 917-919 gait analysis 780,787 kinetic chain 471-472 gamma (y)-motoneurones 137-138 gas exchange 52-53 capillary bed 23 maternal-fetal 532 mountaineering 933 prolonged exercise 52 training effect 59 gastric emptymg 420 gastrocnemius muscle 777,788 gastrointestinal circulation 105 gel electrophoresis 341


GENATHLETE Study 235,236,237, 239 gender differences aerobic trainability of children 509 blood pressure and effect of exercise 690 body fat 293,353,354 bone mineral density/content 355, 356, 357,359-361 cardiovascular screening 677678 fat-free mass 354-355,355 heart size 75-76 jetlag 642 maximal aerobic power, adolescents 397,398 nutritional needs 205-206 performance 523 rating of perceived effort 390 sluing distance-velocity relationships 846 stress fracture 767,768 tissue injury and inflammation 805-806 seealsowomen genes amplification in motor units 142 candidate for endurance performance 237,239 contribution to competitive success 4 genetic determinants 21,223-242 bone density 358 cardiovascular 228-229 maximal oxygen intake 224-228 familial resemblance assessment 224-225,225 heritability 225-227 maternal effects 227 response to training 227-228 molecular markers 234-238 muscle 229-232 muscle blood flow control 97 physique and body composition 232-234 quantitative studies 224-234 research directions 23&239 sluing performance 846 genetic markers, performance phenotypes 234-238 genuvarum 468 Gestalt rating 384,748 gestational diabetes 534,572-573 Gjessing-Nilsen ergometers 275,275, 276,831 glandular fever 660 glaucoma 586 glomerular filtration rate (GFR) 549-550 glucagon 189-190 glucocorticoids 570 see also corticosteroids

gluconeogenesis 31,198,313,329, 336 glucose advice before international competitions 659 blood amenorrhoea us eumenorrhoea 721 cerebral decrease in fatigue 28-29 cyclists 869,870 improved control by exercise 573 pregnancy-induced changes 531 insulin secretion stimulation 189 intake 27-28 intolerance, benefits of exercise 699 preliminary screening before competition 654 reduction by endurance exercise 758 regulation 336,654 replacement 606 solutions, ingestion/absorption rate 27-28 sources during exercise 198 supplements 27-28,29,387 synthesis 31 glucose analysers 610 glucose-electrolyte solutions, mass participation events 662 glucose/polymer solutions 27-28 glutamine 33,204 chronic fatigue syndrome 500,500 depletion 417,740 overtraining marker 491-492,492, 492.496,500 role in immune system 496 supplements 204,740 gluteus medius, weakness 776 glycaemic index 1 9 ~ 2 0 0 foods 199,413,418 glycerol, hyperhydration 419420 glycerol cell-freezingtechnique 426 glycerol-containing drinks 419-420 glycogen 328 breakdown 411 depletion 411,418 Gaelic football 918 hypoglycaemia 606 overtraining marker 491 oxidative enzyme relationship 131 rate 27 specific muscles 847 swimming training 830 ultra-long distance events 313 glYcolYsis 333.334-335 loading 655,925 muscle stores 198,336,411,417 amphetamines effect 440


Australian Rules football 918 diet to increase 417-418 rugby football 911 soccer 904,906 type of carbohydrate diets 417, 418 replenishment after exercise 655 cyclists 870 joggingeffect 519 reserves fatigue development 31,411 utilization rate 27 women 521 resynthesis rates 412,412 sources, skiing 847 storage 200,314,864 structure 335 glycogenolysis 185,328 see also glycolysis glycogen phosphorylase, regulation 185 glycolysis 328,333,334-336 aerobic 334,335,336 anaerobic 328,331,334,335 energy release 335,411 maximal power from 334,336 muscle 334-336 pathway 331 reactions 333,334-335 terminology 328 glycolytic enzymes 126 chronic stimulation effect 118,119, 119,121 inhibition by hydrogen ions and lactate 312 muscle cell content 127 training effect 127-129 goals outcome / performance / process 455 setting 216,455-456 training 518 gonadotrophin-releasing hormone (GnRH) 719,72~-721,723 gonadotrophins 188 Gossamer human-powered craft 942, 943 graded exercise testing (GXT) disabled persons 565 elderly 548-549 granulocytes 735,737 gravitational unloading syndrome (GUS) 144 gravity at high altitudes 614 neuromotor responses 144,151 potential energy stores 5 reduced (spaceflight),effects 144, 146,149,151 groin mass 792 pain 79'792



growth submaximal energy costs of running 48,48 training in childhood effect 41-42, 513 growth factors, inflammation 800 growth hormone 187-188 actions/effects 187 response to training 187-188,511 growth retardation, intrauterine 539 growth spurts 397,398,399 flexibility exercises after 475 injury predisposition 466 muscle strength imbalance 466 gunshot wounds 577 gymnasts growth and training effect 513 injuries 467,467,513 stress fractures 771 haematocrit 424 determination 427 improvement in women 526 increase with erythropoietin use 429 optimal 425 haematoma, hamstring injury 789, 790 haemoconcentration 191,618 haemodilution, from volume expanders 433 haemodynamic overloading 70 haemoglobin 423-437 altitude acclimatization 617,934 blood volume changes and 427, 43' carbon monoxide binding 635,684 control of levels 429 erythrocythaemia and 425-428 see also erythrocythaemia maximizing before competitions 655-656 oxygen affinity, high altitude 934, 934 oxygen-carrying capacity 423 oxygen transport 423-431 structure 423 see also anaemia haemoglobin A 423 haemopoiesis increase, altitude acclimatization 618 suppression after return to sealevel 620 see also erythropoiesis Haglund's deformity 470,781 hamstring 789 hamstring compartment syndrome 791 hamstring injuries 7 8 ~ 7 9 1 avulsion 790 strains 470

treatment 790-791 hand grip, strength after spinal cord injuries 579 'handicapping,' allometric scaling for 50 Hanin's individual zone of optimal functioning (IZOF) 456 'hardiness,' coping with training 498 Hawthorne effect 216 head injury 577-57%578 protective equipment 478,478 healing, after tissue injury 802 health, perceived 748-749,749 consequences of changes 749-750 health benefits, of exercise 699, 747765 cardiovascular see cardiovascular benefits humoral disorders 756-758 immune function 732,759 independence prolongation 753-756 lifestyle 7 6 7 6 1 metabolic 756-758 musculoskeletal 750-753 neoplasms 758-759 psychological function 759-760 respiratory function 750 in specific diseases 747,748 health promotion 458 hearing aids 585 hearing difficulties 585-586 heart conduction abnormalities 79,710 failure see cardiac failure function, elderly 548 malformations 668 murmurs 674 rhythm abnormalities 653 see also cardiac arrhythmias size effect of training of children 513 enlargement 70-71 genetic influence 229,710 hockey players 924 see also cardiac hypertrophy training effect see heart, athlete's transplantation 106 heart, athlete's 68-83,75-76 characteristics 71-75 concept relating to 70-09 diagnostic advances 69 gender issues 75-76 historical aspects 68-69 hypertrophy see cardiac hypertrophy natural selection and 710 shape 73 sudden death see sudden cardiac death systolic and diastolic functions 70

ventricular performance 69-70 see also ventricular remodelling heart rate age-associated decline 548 American footballers 916 anaerobic threshold measure (Conconi test) 13,320,827 body temperature relationship ro9,iio canoeists 894 children 510 cycling 865,867,869 deflection point 827 elderly 555,557,560 environmental factors effect 14 factors affecting 280-281 in fatigue definition 259 fetal 534,535,538 hockey 924 increase 107 input to perception of effort 376, 385 intensity of endurance training 14 interval exercise II,II marathon runners 385 measurement 14 myocardial work rate 711 overtraining marker 490 pace training in women 519 peak 14,490 power output relationship 13,320 pregnancy 533,537,538 reserve 14,555,557,560 rugby football 914 skiing 849 soccer 905,908 swimming 826-827,827 training recommendation 14 in unconscious patient 603 women during sustained distance training 518 heat acclimatization 265,285,288, 288-289 conductance 26,26-27,260 water immersion 27,292 convection 260 dissipation 26,27 environmental see hot environment flux 27 generation 7,26,108,260 injury children 514 prevention 481,481 intolerance by elderly 548 10SS 260,419 cold conditions 291 importance 108 mechanisms 107-108,260-261, 419 predictions 292


reduction in mass participation events 663 skiing 855 triathlon 873 response to exerciseby children 514 storage 260 tolerance 289 transfer 260,261,262,290 during exercise 263 water immersion 261 wetsuit effect 872,873 heat cramps 592-593 heat exhaustion (syncope) 593-596, 607 Heath-Carter anthropometric protocol 38 heat illnesses 591~599,663 heat prostration (exhaustion) 593-596 607 heat retainers 481 heat-shock proteins 802 heat strain 593,595,597 heat stress 263-265,287-288 see also hot environment heat stress index (HSI) 288 heatstroke 288,592,59&597 amphetamine interactions 657 body temperature 595 diagnosis 603 emergency treatment 601 management 604405,610 mortality 605 physiologica1changes 604 predisposing factors 596 heelpain 786 height canoeists 891 increase in boys 397,398 peak height velocity (PHV) 397, 398 triathletes 877-878,878 see also body size; stature helmets, aerodynamic 253 Henry’s law 423 hepatic blood flow, exercise in hot environments 264-265 hepatic function, elderly 550 hepatitis B, protection against 659 hepatitis C, protection against 659 heritability 224 maximal oxygen intake 225-227, 226,865 see also genetic determinants HERITAGE family study 227,228, 228,233,234,237 hernia, sports 794796 herniography 795 herniorrhaphy 796 hexokinase (HK) 120 high altitude 294-297.614-627, 931

acclimatization 12,296,614, 617419,932 acid-base balance 616617 acute effects(moderate altitude) 61-17 air density reduction 296,615 air quality deterioration 298,615 air resistance decrease 252-253 assessment 294-295 cardiac output 617,936 competing above 3000m 619 competitive strategies 29&297 disorders associated 620-623 endocrine response 616 endurance performance 936-937 heat conductance 27 hyperventilation 321,932 hypoxia ~5~58,616,933,936 lung volume 933 maximum oxygen intake (VohaX) 558 2958295496 medical conditions at 614,622-623 muscle oxidative capacity 133 oxygen partial pressure reduced 2 9 ~ ~ 2615416,931 9s~ performance relationship 295-296, 296 physical environment 614-616 polycythaemia 619 pulmonary arterial pressure 617, 933 pulmonary oedema 296,622 risks of competitions at 614 training i2,296-297,32i-322 for low-altitude events 937 rowing 841-842 rugby football 911 women 526-527 see also mountaineering high-altitude training camps 619620 high-density lipoprotein (HDL) 566, 698 increased by exercise 698,700,701, 757 high intensity training see training high-performance liquid chromatography (HPLC) 339-340 high ventilatory response 938-939 examination 784 injuries 770 loss of rotatory function 473 rotation abnormality 792,793 ’hitting the wall’ 27,216,313 dissociation methods linked 216-217 HIV infection 657,659 hockey 919-926 cardiorespiratory system 924 demands of specific positions 920


dribbling, and demands of 92921 energy expenditure 92921,925 exercise intensity 920 fitness profiles 922-924 men 924-926 women 921,922-924 heart rate 924 historical background 919-920 maximal oxygen intake 922, 922-923,923,924-925 muscle performance 922 physical strain 925-926 playing surfaces 921 positional role 921 rules/principles 920 training 923,925,926 ventilatory threshold 924 homeostasis failure 31-32 signs 28 homocystinuria 779 hormonal fatigue 32 hormone replacement therapy (HRT) 576 hormones 184-207 abuse 194 adolescents, training 511 doping 191,194,657 exercise-induced changes 192-193 fluid-regulating 190 markers of overtraining 492-494 measurements 191 Na+/K+pump regulation by ‘76-177 peptide, doping 657 pregnancy-induced changes 531 prolonged events 313 response to training 191,511 sympathoadrenal 184-185 variables affecting 191 horseradish peroxidase 139 hospitals admission in heatstroke 605 liaison for mass participation events 661 warning in prerace planning 609 hot environment 259-267,287-291 aerobic fitness 289-290 caffeine effect 442 cardiac output 1x2 casualty number prediction 608 circulatory homeostasis failure 32 clothing 29-291 competitive strategies 288-291 exerciseheat acclimatization 285, 288,288-289 exercise in 262-265,287-291 fatigue 419 fluid and electrolyte loss 419 fluid intake 597 heart rate increase 14 ‘heat exhaustion’ pathogenesis 594



hot environment (continued heat stress assessment 287-288 hydration levels 290 intolerance by elderly 548 mineral depletion 656 muscle blood flow i i i , i i z soccer 904905 temperature regulation influence 110,290 training in women 526 see also heat stress human-powered flight 942-944 aeroplane aerodynamics 942-943 characteristics of pilots 944 design strategies 943 factors limiting prolonged flight 944 historical aspects 942 power requirements 943,944 humidity, soccer 904 hunger, exerciseand 726 hurling 926-927 demands 926 fitness 926-927 maximal oxygen intake 926-927 hydration 290,294 rugby footballers 911 hydride ions 334,335,337 hydrogen ions accumulation decreased by respiratory muscle training 64 infatigue 29-30 muscle 312 repetitive activity 166 effect on lactate transport 26 high-intensity exercise 95 muscle blood flow control 95 pregnancy 533 3-hydroxyacyl CoA dehydrogenase (HAD) 119,119 yhydroxytryptamine see serotonin hygiene 477-478 hyperbaric chamber 621 hypercapnia, as input to perception of effort 377 hypercarbia 620 hypercortisolism 186-187 hyperextension, injury risk factor 4671 467 hyperglycaemia 572 hyperhydration 290,419-420 hyperinsulinaemia 699 hyperkalaemia 550 hyperlipidaemia 698 hypermobility 471 hyperoxia, in perception of effort 376 hyperpnoea, exercise 53,54,56 hyperpronation, compensatory 468, 469 hyperreactivity, in perception of effort 382

hyperreflexia, amyotrophic lateral sclerosis 582 hypersensitivity, delayed 738,738 hypertension benefits of endurance exercise 688 elderly 550 risk factor for disease 689 risk factor for stroke 578 screening 671 systolic 549 see also blood pressure hyperthermia 26,591613,659 American footballers 917 cooling procedure 604 fatigue relationship 111 malignant 597,605 in triathlon 872 visceral vasoconstriction 111-112 hypertrophic cardiomyopathy (HCW 71-72,79,654 athlete's heart vs 72,74 detection 674,675 diagnostic criteria 713 ECG screening 677 false-negative screening 677 gene mutations 669,713 overdiagnosis 708,709,713 pathology 669 as post-mortem finding 711,712 race and gender aspects 677 screening by genetic testing 675-676 sudden cardiac death 78,712713 hypertrophy, cardiac see cardiac hypertrophy hyperventilation 54,312 altitude acclimatization 617,932 compensatory 55 exercise-induced 54 high altitude 321,932 hypervolaemia 7~~71,431-432 see also blood volume; volume loading hypnosis, fatigue and 28,29 hypocapnia, high altitude 616 hypoestrogenaemia 514 hypoglycaemia cause of fatigue 336 coma 603 detection 602 effects 313-314 management 606 precautions against 573-574 preliminary screening before competition 654 reactive 418 hypoglycaemic agents, oral 573 hypoglycaemic crisis 654,758 hypogonadism 188 hypohydration see dehydration hyponatraemia diagnosis 603

emergency treatment 601,602 of exercise 598-599,599 management 605-606 mass participation events 662 triathletes 874 hypotension 579 postural see postural hypotension hypothalamic dysfunction, overtraining 493 hypothalamic-pituitary-adrenal axis 186,740 hypothalamic-pitui tary-ovarian (HPO) axis 719,720 amenorrhoeic vs eumenorrhoeic athletes 72c-721, 721 causative hypothesis for amenorrhoea 724 hypothalamus 262,639 hypothermia 261,266,591613,659 cold exposure 291 consequences 600 high altitude 615 management 605,610 predisposing factors 600 during running 599-600 susceptibility in fatigue 294 water immersion 266 hypovolaemia 263,264 hypoxaemia, arterial, exerciseinduced (AIAH) 55-56,62 hypoxia adjustment in mountaineers 931 aerobic training session combined 12

cerebral 623 diaphragmatic fatigue 56 high altitude 55,58,616,933,936 input to perception of effort 376 oxygen dissociation curve 616 ice, inflammation management 807 'iceberg profile' (mood states) 212, 212,213 personality 370 ice-cold water, hyperthermia therapy 604,610 ice hockey 464 protective equipment 478,478 ilioinguinal neuralgia 792 iliopsoas bursitis 792 iliotibial band friction syndrome 462, 469 imagery, mental 215 immobilization, adverse effects 474 immune system 731746 benefits of regular exercise 732, 759 detenoration in fatigue 32,33 endurance exercise adverse effects 73%735-740 countermeasures 740-742 implications 734745


‘open window‘ theory 731, 735740 policy recommendations 742-743 see also immunosuppression impairment by overtraining 656, 731732 marker of overtraining 494-496 monitoring before competition 654 non-athletes vs endurance athletes 731-733 soccer players 908909 immunity adaptive 732 innate 732734 immunoblotting 338 immunoglobulin, overtraining marker 495-496,656 immunoglobulin A 735-736 decreased after prolonged exercise 735-736 nasal 735-736 overtraining marker 495-496 salivary, reduced in athletes 734, 735-737 immunomodulators 740 immunoradiometric assay 430 immunosuppression, exerciseinduced 735-740,759 countermeasures 740-742,741 immunosuppressive agents 575 impact force protective equipment role 479,479 shoes to prevent 481 sports surface 462 impact injuries, chronic 468 ‘impaired competitor’ policy 609 impedance, electrical 349,685 inactivity, physical and injuries 474, 779 independence, prolongation 753-756 ’indifferencepoint’ 684 ‘individual zones of optimal functioning’ (IZOF) 214-215, 456 infections benefits of regular exercise 732, 759 fatality rates 712,732 IgAlevels as risk marker 734-735 overtraining association 494,712, 732,742,74?-750 prolonged exerhon linked 731732t 734, 759 prevenhon recommendations 742 tropical, prevention 658 infectious mononucleosis 660 infertility,female athletes 718 inflammation 8 0 d 1 0 age and gender effect 805406 chronic 807

damage due to 802 initiation 800,801,805 nutritional influences 806-807 overuse injuries 800,804 polyunsaturated fatty acids affecting 807 prevention and treatment 807-809 non-pharmaceutical 807 pharmaceutical 808-809 process/reaction 8oo,801,804-807 prolonged exercise causing 735 regulation 802,805,806 role 80c-802 training form and status affecting 804-805 inflammatory mediators 738739, 800

influenza, vaccination 742 inguinal hernia 794 injury, sports 458,749,803 acute 460,461 aetiological factors/mechanisms 460-461 arena equipment 463-464 environmental conditions 465 extrinsic factors 461-465,462 ineffectiverules 464 intrinsic factors see below poor equipment 463 sports surface adjustment 462-463 training errors 462,462,766767 age relationship 805 chronic impact injuries 468 elderly 468,558,558-559 epidemiology 460 exercise type relationship 805 fatigue 461 impact 461 intrinsic factors causing 465-473 mass participation events 660 mechanisms, education on 477 overuse see overuse injuries/syndromes previous and reinjury 472-473 reinjury risk 470 repeated overload 461 running mileage link 805 sites, triathlons 876-877 skiing 463 societal costs 458 surveillance system 460-461 tennis 463 tissue inflammation see inflammation; tissue injury triathlon 876-877 women 465-466 injury prevention 458-465 cold environment 481 cooling-down 474-475 general methods 473-475


at individual and group level 458-459 inflammation and tissue injury 807 load and speed decrease 461 inobesity 574 preparation for sports 478 preventive equipment see equipment preventive training 475-478 coordination and proprioceptive 476 diet and drugs 477 education 477 flexibility 475-476 hygiene 477-478 medical examination 477 muscle training 475 sport-specific 476-477 primary 459 risk factor identification 459 secondary and tertiary 459 sequence 459,459-460,460 slow progression 475 at societal level 459 tactics 458-460,459 warm-up 458,474 inspiratory capacity, decreased 629 inspiratory flow rates, training effect 59 insulin 189-190,572 amenorrhoeic us eumenorrhoeic athletes 721,723 basal levels in athletes 189 decreased secretion 189,572 hypoglycaemic crisis 654 pregnancy 531 receptor density 699 resistance 572 secretion 189,531 sensitivity improved by exercise 573,699 of muscle 132-133 therapy 573 insulin-like growth factor (IGF) 71, 187,723 insulin-like growth factor-binding protein I (IGFBP-I) 721,723 insulin receptor substrate-i 337 intellectual performance 759 intensity of exercise/ training ACSM recommendations 554 anaerobic threshold as marker 389-390 -=-3 children 508 circadian rhythm 64; disabled persons 565 effect on blood pressure 689 elderly 552,557,558 high-density lipoprotein increase 701 hockey 920 importance in training 125-127






intensity of exercise (continued) input to perception of effort 381, 382,386 maximal oxygen intake 406 metabolic effects 125-127 periodization and 527 personality relationship 382 pregnancy 537-538 rating of perceived effort 390 soccer 907 interactional theory, personality assessment 370 interferon-y,inflammation 801 interleukin-1 (IL-1) 741 interleukin-2 (IL-z),receptor (CD25) 495 interleukin-6 (IL-6) 739,800,805 intermittent claudication 91,568 intermittent exercise 9-11,14-15 international competition 653-660 cardiovascular screening 714-715 doping 657-658 immediate preparation 658-659 medical supervision during 659-660 nutrition 654-656 overtraining 656-657 preliminary medical screening 653454 preliminary site visit 658 preparation 654-658 International Conference on Overtraining in Sport 486 International Olympic Committee banned substances see banned substances standards for medical/athletic facilities 658 interval training ii-iz,15 aerobic 518 continuous us 391 elderly 559 lactate data role 314 swimming 830 women 518-519 interventricular septum, thickness 710 intervertebral disc, loading in hockey players 925-926 intestinal ischaemia 1x2 intracellular signalling, muscle 337-338 intracerebral haemorrhage 696 intramuscular pressure, arterial supply reduction 31,32 intrasarcomeric system 178 intravascular fluids, decrease in hot environment 263,264 intravenous fluids, hyponatraemia misdiagnosis 606 introversion 382,640 inverted U-hypothesis 214

iontophoresis 787 ion transport, in muscle cells 169 iron altitude acclimatization 618 deficiency 424-425 intake recommendation 425 losses 425 supplements/therapy 415,656 ischaemia-reperfusion injury, Achilles tendon 779 isokinetic ergometer 277-278,278, 891 isokinetic training 475 isoleucine, supplements 204 isometric exercise 475 isoprenaline, prohibition 653 Italy, preparticipation screening 672, 6757 676 jet lag 639,641-642 age and gender differences 641-642 effects on performance 642-644, 649.644 management see circadian rhythm symptoms 641,647 jogging injuries in elderly 558-559 lactate removal 519 joint instability 471,472 laxity, injury predisposition 471 malalignments 468-469 mobility and flexibilitytraining 475 Jones’ fracture 771 joules 5 jumper’s knee see patellar tendinitis jumping fat mass and performance 349 patellar tendinitis 784 repeated overload 461 stress fractures 768,771 stretch-shortening cycle contribution 249

KzCOSMED 281 Q b z metabolimeter 282,283,284 Q R Q metabolimeter 281,282,282, 283 kayak canoeing see canoeing kayak ergometer 274,274,892,895 ketoacidosis 572 ketoacids 328 ketone bodies, cycling 865 kinematic measures 251 kinetic chain 471-472 kinetic measures 251 knee braces 480 examination 775,784 imaging 776

injuries 766 pain 775,783 referred pain 775 sprains 463 unstable 480 knee-bend, stretch-shortening cycle 248 knee ligament, instability 471,472 Krebs cycle see citric acid (Krebs) cycle kyphosis 576 lacrosse 92-27 demands 926 fitness 92-27 maximal oxygen intake 926-927 lactate 314-318 accumulation 311,318,319 adverse effects 312 benefits of limitation 312 decrease by respiratory muscle training 63-64 effect on standard bicarbonate 321 factors influencing 312 as input to perception of effort 3771387 mechanisms 316-317 in muscle 25,312 muscle endurance and 312-313 patterns during exercise 315-316 practical applications 317-318 see also anaerobic threshold blood levels accumulation 318,319 Australian Rules football 918 canoeists 891-892,894 cycling 861,864,866,869 factors affecting 316,317 during hyperthermic exercise 111

implications of data 314 increase during exercise 111,316 maximal oxygen intake correlation 313 maximum levels 25,311 measurement 315 overtraining marker 490,491 patterns during exercise 315-316 power output relationship 3 16, 316 rowers 840 rugby football 91crgii skiing 847 soccer 905,905-906,90~07 swimming 827,827-828 training 318 buffering, high altitude 616 conductance from muscles 25, 25-26


curve, shift 404 implications of data on 314 input to perception of effort 377, 378.387 intermittent exercise 9,1o, 11 intramuscular levels 316,335 marathon running 11 maximal steady state 828 measurement methods 314-315 metabolism 25,317,335 post-exercise 316 production 335,377,387,521 rating of perceived effort and 498, 498 removal 12,317,335 continuous jogging 519 gentle exerciseafter intense exercise 335 increasing 656 running 312 salivary 315 threshold see anaerobic threshold tolerance, rugby football 911 transport from muscle to blood 25-26 turning point see anaerobic threshold ventilation relationship 60 lactate dehydrogenase (LDH) 119 lactation, exercise and 539 lactic acidosis, hyperventilation 54 Laplace, law 71,711 lateral retinacular release 776777 lateral retinaculum 774,775 leanness, extreme, problems 361-362 lean soft tissue (LST),calculation 348 left anterior descending coronary artery 670,895 left main coronary artery, anomalous 669470,676 left ventricle dimensions 71,72,72 endurance sports 7 6 7 7 hypertrophic cardiomyopathy 78 for specific sports 76 strength training 76'77 training effect 76 ejection time 520 end-diastolic diameter 710 end-diastolic volume 683 canoeists 896 increased 70-71 gender-related differences 75-76 hypertrophy 71,708 detection 69 patterns and haemodynamics 73 physiological ZE pathological 73, 74 women 76 mass ACE gene alleles and 235

canoeists 896 women 520 mass index (LVMI) 72 structure, genetic influence 229 volume 72-75,520 ratio to body surface area 897 training-induced changes 69 wall stress/tension 71,72 wall thickness 72-75,709,710 1% length discrepancy 46~470,769, 775 raises 776 stiffness, measures 248 see also limb blood flow legal aspects, cardiovascular screening 672 leptin, diurnal rhythm 721,723 leucine, supplements 204 leucocyte count, overtraining 494-495 leukotrienes 802,806 inhibitors 808 life expectancy 68 cross-country skiers 760,760,761 effect of exercise 747 endurance athletes 714 quality-adjusted 714,748 lifestyle 438 benefits of regular exercise 76-761 benefits of training children 512 effect on biological age 398 healthy, importance 478 rugby football 915 ligaments, benefit of exercise 75'752 light exposure, jet lag management 647449,648 limb blood flow effect of respiratory muscle work 58-59 'steal effect' of respiratory muscles 57-58t63 lipids blood, benefits of exercise 698-699, 757 peroxidation, reduction 806-807 see also fat lipogenesis 329 lipolytic enzymes 699,757 lipoprotein(a) 698 lipoproteins, benefits of exercise 698-699 little leaguer's elbow 467 liver carbohydrate stores 198 function, elderly 550 ischaemia 112 locomotion, energy costs 47-48,48 locus of control, input to perception of effort 383


longevity, exercise benefit 747 long QT syndrome 670,677 loperamide 660 low back pain see back pain low-density lipoprotein (LDL) 698 lower extremity amputees 576-577 lower limb, flexibility 249 lower motor neurones, degeneration 582 Lown-Ganong-Levine syndrome 79 lumbar spine, hyperextension 771 lung anatomical dead space 53 minute volume 22 size 684 vital capacity 750 volume canoeists 896 high altitude 933 static, effect of training 59-60 seealso entries beginning pulmonaty lung disease 566-571 chronic 569-570,750 exercise rehabilitation 570,750 obstructive 750 lung fluid movements 682-687 exercise-induced changes 683-684, 684 see also blood volume lung function 684 mountaineering 933 ozone effect 629,629 training effect 59-60 luteinizing hormone (LH) amenorrhoeic us eumenorrhoeic athletes 722 pulsatile secretion 719,722,725 low energy availability disrupting 725,726 lymphatic drainage 53 lymphocyte(s) 740 mitogen-induced proliferation 732,738 overtraining marker 495 reduced counts due to cortisol 735, 736 see a h B cells: T cells McArdle's disease 54,319 macrocycles 527 MacrodexTM432,434 macronutrients 197-207 macrophage 737,800 alveolar 737 Mader's two-point test 828 magnesium deficiency, sudden death 79 intravenous therapy 607 magnetic resonance imaging (MRI) cardiac 69,676 use and misuse 709-710 plantar fasciitis 787



magnetic resonance imaging

(continued) stress fractures 770,772 major histocompatibility complex (MHC), class 11antigens 739 malabsorption, high altitude 939 maladaptations, of overtraining 528 malalignments 468-469,769 malaria 658 malpractice liability 672 maltodextrinl low fructose beverage 869 marathon runners carbohydrate fluid ingestion 74-741 children and teenagers 399 coronary heart disease and 77 dissociation methods 216 fatigue 31 fluid ingestion rules 592 fluid restriction 591-592 hypothermia 600 immune system and infection reduction 732 injuries associated with environment 465 lactate levels 11 maximal oxygen intake 13 mood state profiles 212,212 perceived effort application 385-386 psychological response 213 serum erythropoietin 429-430 see also running marathons first-aiders 660 speeds 815,816,816 seealso mass participation events; ultra-long distance events Marfan’s syndrome 568-569,670, 673,675 Achilles tendon injuries 779 massage, deep friction 782 mass participation events 653 application forms and waiver clauses 661 casualty types 660 clothing and equipment 663 conditions for cancellation 662 detailed planning 661-662 immediate preparation 662 initial preparation 660-661 medical supervision 660-663 participants’ information sheets 661 plan of treatment 663 route planning 661 withdrawal from 662 see also marathons Masters athletes high altitude 623 infection reduction 732

conditions for 303 injury prevention 468 contraindications 306 medical condition screening 654 cycle ergometer 304,865-866 smoking cessation 760 ergometer choice 304 maximal accumulated oxygen deficit factors adversely affecting 303 (MAOD),rugby 913 field tests 307,309 maximal aerobic power 13,259,301 halting, indications 306 see also maximal oxygen intake preparations 303 maximal isometric force 161 principle 301,302 ~ ~ J maximal oxygen intake ( V O ~22, reproducibility 309 224,301-310 result interpretations 309 age-related changes 45,47,107, safety precautions 306307 713-714.753,756 standard errors 307 alcohol effect 447 submaximal tests 307 American footballers 916 uses 309 Australian Rules football 9x9 mountaineers 935,935936,938 benefits of exercise 714,750 muscle 87 blood doping to increase 425 muscle specific creatine kinase link blood lactate correlation 3x3 blood volume effect 431-432 236 overtraining effect 309,489 body mass relationship 405 ozone effect 631432 body s u e and see body size plasma volume expansion effect carboxyhaemoglobin effect 635, 433 63 6 cardiovascular responses 12, IZ pregnancy 533 pre-/post-pubertal differences 510 children 227,303,507,508 prolonged exercise 52 endurance training effect 509, respiratory muscle training and 61 511 rowers 840 criteria 301-303 cross-country skiers 400 rugby 914,914 running 403,405,815,852 cycling 863,867 speed correlations 308 definition 301 significance 301 determinants 224 skiing see skiing disabled persons 566 elderly athletes 552-555,553 soccer 902+03,905,907 swimming see swimming elite athletes 402 endurance performance training effects 14,406 relationship 402 running 406,406 factors affecting 309 women 522,524 fatigue development 31 triathletes 880-882,881 Gaelic football 919 fractional utilization 882-884 gender differences in adolescents utilization and economy of movement 402-403 397,398 genetic aspects see genetic values by specific sports 302,945, determinants 946 wheelchair athletes 34 heritability 225-227,226,865 women 5q-520,522-524 high altitude effects 55,295,295, meal, timing and composition 646 295-296,617 measurement of endurance hockey 922,922--923,923,9q-925 hot/cold environment effect 259 factors 271-272,272 laboratory and field 273-286 hurling and lacrosse 92-27 input to perception of effort 377 sport-specific 273-286 intensity of endurance training 14 mechanical constraints see interindividual differences 309 biomechanical constraints intermittent exercise 9 mechanical efficiency 6-7 interval exercise 11-12 mechanical power 246-248 economy and 247-248 marathon runners 13,402,404-405 measurement 271 measures 247 ancillary equipment 305 reduction, benefits 247 medial collateral ligament, training blood pressure during 305 cardiac arrest and 306 effect 752 medial tibia1 stress syndrome 462 central limitation of effort 301, medical examination see examination 304


medical facility organization 607411 collapse prevention by prerace planning 608-609 first-aid stations positions 609 flowchart for management 611 layout 609,610 for mass participation events 662 medications needed 610,611 planning/equiping at race finish 609-611,610 prerace 607-608 rate of admission to 601 triage 603,604 medical history, in cardiovascular screening 674,675 medical records 658-659 medical screening hypertension 671 international competition 653454 see also cardiovascular screening medical surveillance 653-666 international competition 653460 mass participation events 66&63 wilderness expeditions 663-664 see also international competition; mass participation events medications, for medical facilitiesat races 610,611 melatonin 639,647 levels and temperature effect 640, 647 secretion 642,647 supplements 647 membrane permeability, increased in fatigue 33 memory loss, cerebral hypoxia 623 men (athletes) age, body size and physique 38-39 body composition 352 body fat, by sport type 354 body mass distribution 41 bone mineral density 355,356,359 exercise, benefit on cardiovascular disease 693,693 fat-free mass 354-355,355 hockey 924926 reproductive disorders 723 menarche, average age 399,514,720 menstrual cycle changes in eumenorrhoeic athletes 72-721 follicular phase 719 jet lag severity 642 length and regularity variations 719-720 luteal phase shortening 718,719 regulation 7iy720 sports injuries relationship 466, 805 menstrual disorders/ irregularities 718

adolescents 514,720 clinical consequences 718-719 effect on bone mineral density 361 hypotheses relating to 723-725 induction experiments 725 injuries and 466,805 jetlag 642 prospective experiments 725-727 mental coping strategies 454 mental health model 211-212 mental imagery 215 mental preparation for competition 453-454 to optimize preparation 456 warm-up exercises 474 mental retardation 584-585 definition 584 mental skills development 455-456 goal setting 216,455-456 used by elite athletes 452 mental strategy training program 388,454 mental tension, adverse reactions 478 mental training 454-455 meromyosin 160 mesocycles 527 mesomorphy 37,41,42,232 metabolic acidosis 321 fatigue mechanism 95 high-intensity exercise 95 input to perception of effort 378 metabolic control hypothesis 94-95 metabolic disease 571-575,756-758 metabolic efficiency, perceived effort relationship 378 metabolic power (EJ, long-distance running 815 metabolic rate 409 input to perception of effort 377 metabolism 118-136 alcohol effects 446 heat generation 26 input to perception of effort 376-378,39’ muscle see muscle metabolism total body 328 metabolites conductance 27-28 muscle blood flow control 94-95 muscle fatigue 95 metatarsal, stress fractures 771 metatarsal heads 779 metatarsal shafts 770 methacholine 632 methamphetamine (speed) 439 methylene-dioxymethamphetamine (ecstasy) 439 methylxanthines 570 micro-Astmp apparatus 320 microdialysis technique 343-344


microgravity environment 144 micronutrients 414-415 microstatellites, erythropoietin receptor gene 236 Minnesota Multiphasic Personality Inventory (MMPI) 368 minute ventilation CV,) 53-54,54 decreased after training 60,64 ozone effect 630,631 rowers 841 minute voIume 22 ‘miserable malalignment syndrome’ 469 misoprostol 808 mitochondria adaptation 123,167,935 damage in fatigue 33 density in motoneurones 138, 138

density in muscles after training 13 high altitudes 935 intermyofibrillar pool 124 pools in skeletal muscle 124 subsarcolemmal pool 124 transport chain 22 mitochondrial DNA (mtDNA) 237-238 mitochondrial enzymes 87,332 increase by training 90 mitogen-activated protein kinases (MAPK) 338 mitogen-induced lymphocyte proliferation 732,738 mitral regurgitation 710 mitral stenosis 106 mitral valve prolapse 670 mixing-chamber metabolimeter 281 modified discomfort index (MDI) 287 Monge’s disease (chronic mountain sickness) 621,933 monoamine oxidase type 8 (MAO-B) inhibitors 584 monocytes 735 mood disturbances, training association 213 positive effect of exercise 749,759 ‘profile of mood states’ see Profile of Mood States (POMS) motivation 374 body temperature effect 419 decreased, overtraining marker 496 goal setting 455-456 maintenance, psychological aspects 453 poor, in fatigue 33 motoneurones 136-157 adaptive response 152-153



motoneurones (continued) changes with training/detraining 147 firing frequency 140 functions and conduction velocities 137 heteronymous 138 mitochondria density 138,138 modulation of myosin isoforms 144-145 muscle fatiguability and 140-142 muscle fibre type relationship 139-14Ot152 nucleus and myonuclei relationship 142 overloading effect 147-149 oxidative enzymes 140 properties 137--140,152 reduced loading effect 149 spaceflight effect 149,150-15i spinal cord 149-151 succinate dehydrogenase 148, 148-149 motor development 759 motor pools 137-140,139,147 motor system, cycling 861,864 motor units fatigue and 140-142, 146 mechanism 29,30 firing frequencies 140 gene amplification in 142 plasticity 146,147 properties and metabolism 137-340 recruitment 136-137,140,i53 training and detraining effects 147 mountain-biking 857 mountaineering 614,931-941 acclimatization 932,937 adaptation 931 blood changes 933-935 diet 618 elite climbers 937-939 environment 931-936 gas exchange 933 limitation to exercise 935-936 maximal oxygen intake 935, 935936,938 nutritional aspects 939 oxygen partial pressure and 615 oxygen transport 933 pulmonary function 933 respiratory alkalosis treatment 321 risks 931 tissue adaptation 935 training 937-939 ventilation 932,932 ventilatory response 936,936, 938-939 mountain expeditions 663-664 mountain sickness acute 296,618,620-621

chronic 621,933 prevention 621 mouthpieces, protective 479 movement economy of see economy of movement mechanics 245 velocity, aerobic energy relationship 517 mucociliary clearance, reduced 737 multiple sclerosis 581 muscle 158-183,159-169 action potential see action potentials active transport of ions 169 adaptation 122-124,167-169, 1787179,179J475 chromcally shmulated 167-168 genetic aspects 231-232 metabolism 120-121,i3c~i31 skiing 852,854 tostress 475 agonist / antagonist imbalance 470 area, adaptation to training 179 atrophy, fatigue 146 biopsy 118,338,342-343 blood flow see muscle blood flow capillarization 122,127-1~9,128, 130,169 catabolism, high altitude 939 chronically stimulated 167-168 conditioning programme, elderly 559 contractile characteristics 130 contraction 158 forces 93 frequency and muscle pump effect 97 increased after warm-up 474 initiation 28 maximal velocity 161 maximum voluntary 93 myosin heavy /light chain isoforms 162-163 pH effect and perceived effort 378 post-tetanic potentiation 163 sliding filament theory 159 training effect 168 contraction-relaxation cycle 93 cramps 593,607 creatine stores 416 cross-bridges 160-161 cycling 161,164 inhibition in fatigue 29-30 maximal isometric force 161 denervation 581,582 design and structure 84-91 discomfort, exercise during heat stress 265 disruptive injury 789

elasticity and need for warm-up 474 endurance 312-314 definition 312-313 training effects 314,526 women 526 energy supply and demand 84, 85-86,98 excitation-contraction coupling 169-177,vo adaptation to endurance training 178-179 caffeine effect 41 chronic adaptation effect '76-177 failure 176 repetitive activity 174-176 sarcolemma and T tubules 171-172 sarcoplasmic reticulum 172-173 T tubulesarcoplasmic reticulum Ca2+ 173-174 fatigue 33,57 fibre types and 86-87 input to perception of effort 379 metabolites involved 95 motor unit plasticity 146 motor units and 140-142 substrate availability aspect 379, 411 triathletes 874 force 121,891 force sharing 180 function in prolonged events 313 glycogen stores see glycogen growth hormone effect 511 heterogeneity 86 hypertrophy 314,413 injury 470,792 overuse 788-789 prevention by warm-up 474 insulin sensitivity 132-133 isometric contraction 248 lesions, in fatigue 33 mass elderly 550,560 perceived effort application 386 mechanical properties, training effect 169 membrane 169 metabolism see muscle metabolism mitochondria pools i q myofibrillar proteins and protein isoforms 161 nuclei, changes 123-124 overloaded 147-149 oxidative enzyme content 124,125 oxygen consumption 103,260 oxygen transport 682 peak blood flow 23 perfusion 97 potassium release 95


recruitment see muscle fibre types regulatory proteins 164-165 response to training, genetic aspects 231-232 sensitivity to epinephrine after training 130 strain 788,789 strength benefit of exercise 750-751 improvement 314,471 rowing 838-839 rugby football 912-913 strength imbalance 470 growth spurts and 466 injuries 470 renal failure 571 strength training elderly 555 women 526 stretch, failure 789 temperature, warm-up exercise


training, injury prevention 475 triacylglycerolcontent in cyclists


vascular resistance i04-i05,105 volume, oxygen consumption

303 weakness 178,179-180,470,75i muscular dystrophy 580 'wisdom' 140 muscle blood flow 26,84-102,93,263 capacity CQ,), 87,87,87-88,88 cardiovascular disease and 91-


chronic electrical stimulation effect 121-122

forearm 97 hot environments and 111,263,


hyperthermic exercise effect 111-112

impedance by maximum voluntary contraction 93 implications for endurance sport

97 increase to active muscle 93-94 injury prevention 474 input to perception of effort 379 limiting conditions 91-92 oxidative enzymatic capacity relationship 87-89 oxygen delivery 93 redistribution effect 104 regulation 93-98,94,99 endothelium-dependent 96-97 metabolic 94-95 muscle pump control 93,9798 myogenic control 96 nitric oxide role 97 resistance 93-94 response to exercise 92,9293

skin blood flow competition

108-109,110,263 steady-state 92-93 temperature regulation effect 111 training effect 90-91 muscle-building programmes, middle-aged 75c-751 muscle cells 159-169,331-332 cytoskeletal system 177-178 see also myofibrillar system muscle fibre types 85,85-86 adaptation 167-169 Ca2+-ATPasecontent 172-173 calcium ion (pcabforce relationship 164,165 calcium-releasechannels 173 canoeists 891 continuous exercise 13 cycling 861 detraining effects 147 distribution 8&87,229-231 men/women 162 elderly 550 energy supply and demand 85-86 fast-twitch 162 adaptations 167 cycling 861 endurance training effect 126 fatigue 29,379 forcevelocity characteristics

163,163 motoneurones 140 recruitment 318-319 types IIA and IIB 128,161 fast-twitch glycolytic (FG) 85,85 endurance training effect

12%129 functions 86 fast-twitch oxidative glycolytic (FOG) 85,85,86 forcevelocity characteristics 163, 1 63

functional properties 85,8546 functions of specific types 86 genetic aspects 229-232 hydrogen ion release 95 innervation 137-138 input to perception of effort 379 modification by endurance training 13 motoneurone relationship

139--140,152 Na+/K+AWase content and isoforms 171,171-172 neural modulation 144-145 plasticity 136 recruitment patterns 86,93,127 effects 126-127 fatigue and 86-87 training effect 126 women 521 rowers 838


rugby players 913 sarcoplasmic reticulum characteristics i72-173,173 size, endurance training effect 129 skiing 851 slow-twitch (type I) 85,85,86,162 endurance training effect 126,

128-129 enzymes 126 fatigue 379 genetic influence 230-231,231 long-distance cycling 864 marathon runners 13 motoneurones 140 rowers 838 skiing 13,851 in specific sports 7 succinate dehydrogenase 148,


training effect iz7-129,128--129,

147,168 type determination 127 muscle filaments, thick and thin 159,

159,160 muscle metabolism 328-345 A T production (from) 334-337 capacity determination 118-119,

337, citric acid cycle 337 endurance training effects

122-124,328 duration of exercise 125-127 enzyme changes 122-124 intensity of exercise 125-127 energy utilization 330-331 enzyme-catalysed reactions 330 enzymes 118 adaptation izo-izi profile, genetic influence 231,


rate-hmiting 337 genetic aspects 231 impairment in amenorrhoea 719 intracellular signalling 337-338 maximal adaptability iz0-12~ metabolic pathways ii8,328-330,

331-334 methods of study 338-344,339 oxidation-reduction 334 oxidative enzyme(s) 124,125 oxidative enzyme capacity 85,85, 123

high altitude 133 overloading and 147-149 oxygen exchange capacity linked


traimng effect 90,122-124,123 principles 329-330 rate variations 328 regulation 328 training-induced adaptation, significance r30-13i



muscle pump model 93,97-98 muscle spindles, innervation 137-138 muscular dystrophy 58-581 muscular fitness ACSM recommendations 554 rugby football 912 musculoskeletal system adaptation to stress 475 benefits of exercise 750-753 changes in elderly 550-551 children 513 injuries in elderly 558-559 medical screening before competition 653 problems, screening before competition 654 musculotendinous injuries 470 musculotendinous junction, overload 803 music, input to perception of effort 381 Mwave 177 mycolytic therapy 571 myocardial capillary development 71.' myocardial contractility 34 training-induced changes 70,520 myocardial function, increased 695 myocardial hypertrophy 708 see also cardiac hypertrophy myocardial infarction 566-568 endurance exercise after 688 exercise training effect 566 recommendations for training 567-568 risk at high altitude 622 risk factors 307 risk reduced by endurance exercise 694 myocardial ischaemia 566 cardiac hypertrophy and 710711 fatal 712 high altitudes and 615 transient 78 myocardial oxygen demand, reduced by exercise 695,696 myocardial perfusion 711 myocardial work rate 711 myocarditis 656,670,670,750 myocardium electrical stability increased by exercise 695 fatigue 110 response to catecholamines 548 myocyte, stretch 71,78 myofibrillar ATPase 127,170 assay 340 failure in repetitive activity 174 myofibrillar proteins isoform patterns 129,166 plasticity 168

types 161 see also myosin myofibrillar system 159-169, 331-332 chronic adaptations 167-169 composition 167-169 contractile proteins 159-164 see also myosin function 165-167 regulatory proteins 164-165 see also tropomyosin; troponin repetitive activity 165-167 myofibrils, structure 159,159 myoglobin 9,618,945 myonuclei 142,142 myosin 159,160 actin interactions 159-160 ATPase 160,164 eccentric exerciseeffect 16&167 filaments 159,159 force generation 160-161 heavy chains 145,160 adaptation effect 167 effects on contractile properties 162-163 fast-twitch/slow-twitch muscles 162 isoforms 161,161-162 submaximal exercise and 166 tropomyosin isoform association 165 isoforms, neural modulation '44:'45,147 light chains 160 adaptation effect 167 effect on force-velocity characteristics 163 effects on contractile properties 162-163 heterogeneity 162 phosphorylation 162,163 structure 160 Na+/K+pump 169,170 chronic low-frequency stimulation effect 176,177 content/isoforms in muscle fibres 171,171-172 free radical susceptibility 175 hormonal regulation 176-177 increase in skeletal muscle 95 muscle fibre membrane content 171-172 role in muscle contraction 177 sarcolemma and T tubules 169, 171-172 structure 171 training effect 176,179 naproxen 808 nasal patches 911 natural killer (NK) cells 33,732-733 activity measurement 732-733

decreased by prolonged exercise 656,737.737,759 enhancement by exercise 732-733, 734 as overtraining marker 495,656 navicular stress fractures 768, 77-71 nedocromil 571 neoplasms benefits of exercise 758-759 risk associated with athletes 758 neoprene, for triathletes 872,873 neoprene sleeves 481 nerve conduction 29 net efficiencyvalue, definition 6 neuralgia, ilioinguinal 792 neural modulation, myosin isoforms 144-145 neuroendocrine system 184 neuromuscular aspects, in perception of effort 378 neuromuscular disease/conditions 471,577-578 neuromuscular fatigue 146,153 neuromuscular junction, physiology of fatigue 29 neurones adaptations 136 dorsal root ganglion 142-144,151 dorsospinocerebellar 138 ionic balance 137 pseudounipolar 151 size, succinate dehydrogenase activity and 142,143 ventral horn 149-151 see also motoneurones; sensory neurones neurosis 382 neurotransmitters 144 neutrophils cortisol-induced changes 735,736 inflammation 800,801 overtraining marker 495-496 prolonged exercise-induced changes 735,736 role 733 suppressed activity in athletes 733734 newtons 5 nicotinamide adenine dinucleotide ("3 332,334,375 nicotinamide adenine dinucleotide phosphate (NADP) 338,339 nicotine 444-445 infusion 445 nifedipine 622 night pain 769 night splints 781 nitric oxide 803 muscle blood flow control 97 role in inflammation 802-803 synthesis 97,803


vasodilatation due to 97 nitric oxide synthase 803 nitrogen balance, protein intake and 413 disposal 414 negative balance, high altitude 618 nitrogen dioxide 297,634 Nobel-Robertson model 375,375 non-steroidal anti-inflammatory drugs (NSAIDs) 575,781,808 complications 808 mechanism of action 803,808 noradrenaline (norepinephrine) 184, 185 age-related response 107 levels reduced by exercise 696 overtraining marker 494 response to endurance exercise 184,185 Northern blot 341 nuclear magnetic resonance (NMR), muscle 343 nuclei, muscle cells 123-124 nutrient deficiencies, children 513 nutrition advice for competition preparation 654 central fatigue and 418-419 children 513-514 gender differences in requirements 205-206 injury prevention 477 mountaineers 939 pregnancy 537 preparation for international competition 654456 rugby football 9x5 strategy 409 tissue injury and inflammation affected 806-807 women 525-526 see also diet; foods nutritional supplements 414-415, 415-417 cyclists 869870,870 role on immune system 731,740 obesity 574-575,698 avoidance 756-757 benefits of exercise 698,756-757 injury prevention 574 training recommendations 574-575 obturator nerve 792 oedema 622 see also cerebral oedema; pulmonary oedema oestrogen menstrual cycle 7x9 replacement therapy 576,719 response to exercise 188 supplementation 514

Ohm’s law 22,88 oligomenorrhoea 361 see also amenorrhoea Olympic Games 1968 (Mexico) 12,42,616,619 blood doping ban 427 cross-country skiing 844 erythropoietin doping ban 430 Seoul Congress 400 women participation 517 omeprazole 808 one-leg model 341,342 ‘open window’ theory 731,735740 orienteering 945 orthopaedic conditions 575-577 orthotics, shoe 482 Achilles tendon injuries 782 biomechanical goals 482 injury prevention 482 leg length discrepancy 469 malalignment correction 469 patellofemoral pain syndrome 776 stress fracture prevention 774 Osgood-Schlatter disease 467,473 osteitis pubis 793-794 osteoarthritis 468,575 after anterior cruciate ligament injury 472,473 post-traumatic 471 risk in athletes 751752 vitamin E supplements 806 osteopenia 576 osteoporosis 514,551,575-576 effects of exercise training 576 menstrual disorders causing 718 postmenopausal 576 premature 361 risk after hypoestrogenaemia 514 spinal cord injuries 579 training recommendation 576 treatment 576 ovarian axis see hypothalamic-pituitary-vari an (HPO)axis ovarian follicles 719 overfatigue see overtraining overhydration 598 overload 147,710 musculotendinous junction 803 overpronation 778 overreaching 486,488,500 continuum with training/ overtraining 501,501 see also overtraining over-the-counter medicines 657 overtraining 4,656-657,766 avoidance 527-528,742 child athletes 515 cold tolerance compromised 294 continuum with training 501, 501 definition and terminology 486-487


diagnosis 656-657 effect on maximum oxygen intake 309 framework 499-502 immune system impairment 731732 incidence 487,487 infection association 494,712,732, 749T750 monitoring 486-504 mood disturbances 214 need for redefinition 500-501 potential markers 48%499,489, 656,743 biochemical 491-492 central fatigue mechanisms 499 hormonal 492-494,656 immunological 494-496,656 performance 488-491 psychological 496-499 preparation for international competition 656-657 prevention 501,657 research 486,487-488 signs and symptoms 487,528,656 swimmers 830 women 527-528 overuse injuries/syndromes 766199,803 Achilles tendon see Achilles tendon overuse injuries adductor injuries 792793 aetiological mechanism 461, 803-804 causes 462,462 children/adolescents 462,466-467 definition 803 elderly 468 epiphyseal 513 groin pain 791792 hamstring injuries 789791 incidence 458 inflammatory response 800,804 muscle injuries 78-89 osteitis pubis 793-794 patellar tendinitis see patellar tendinitis patellofemoral pain see patellofemoral pain syndrome (PFPS) plantar fasciitis 785-789 prevention 579,766,807 rest periods 766-767 slow progression to prevent 475 stress fractures see stress fractures tennis 463 triathlons 876,877 types 766 women 466 E-oxidation see fatty acids, oxidation oxidation-reduction, muscle 334 oxidative burst 733,737



oxidative enzymes adaptation to chronic stimulation 120

fat metabolism and 131,132 glycogen depletion relationship 131 motoneurones 140 muscle see muscle metabolism muscle blood flow and 87-89 regression of adaptations after training cessation 130 soccer players 907 thigh muscle 127 training effects 122-iq, 124,125, 224 oxidative phosphorylation 137,153 oxygen arteriovenous differencesee arteriovenous oxygen difference consumption blood flow relationship 103,104 energy costs determination 813 muscle 103,260,303 ‘plateau’ 301,302 splanchnic tissue 103 swimming 827 see also oxygen intake costs of skiing 851 costs of ventilation 53-54 deficit see accumulated oxygen deficit (AOD) ’deficit,’ rowers 840 delivery 93 oxygen extraction relationship 103-104,lO4 demand benefit of exercise 695,696 exceeding intake 11 increased myocardial 653 desaturation, high altitude 933 diffusion, high altitude effect 933 diffusive flux 89,9c-91 excess post-exerciseconsumption (EPOC) 574 exchange capacity 84-91 blood-muscle 89 muscle oxidative capacity and 89-90

training effect 90-91 haemoglobin affinity at high altitude 934,934 kinetics, measurement 282,283 maximum consumption see maximal oxygen intake (VOZrnax)

myocardial supply/demand 653, 695 partial pressure 22 byaltitude 932 arterial 52 capillary (high altitude) 933,933

at high altitudes 295,295, 615416,931 intracellular 96 radicals 801,802, 806 requirements, intermittent exercise 10

saturation, high altitude and 616, 933,934 solubility factor 23,23 sources 329 submaximal cost 47-48,48,283 supply in intermittent exercise 9-10

oxygen dissociation curve 423,616 left shift by carboxyhaemoglobin 635 at very high altitude 935 right shift in altitude acclimatization 618,935 oxygen intake children 509 heat generation 26 high altitude effect 12 intermittent exercise 9 interval exercise 11 maximal see maximal oxygen intake (Vo2,.,& measurement in swimmers 827 mountaineers 938 peak, effect on heat flux 27 ‘plateau’ 301,302 reduction by respiratory muscle unloading 58-59 rowers 285,839 running 11 skeletal muscle fibre types 85,85 skiing 849 stroke volume relationship 12 ’supramaximal’ 311 swimmers 84,825 see also aerobic power oxygen transport 22-24,423 altitude training in women 526-527 from alveoli to blood 23 athletic selection 4 barriers (air to muscle) 23,23, q benefits of endurance exercise 753 blood volume role 431-435 conductance determinants 23, 23-24 conductance theory 22-24 driving pressure and 22-23,24 effect of training 4 fatigue development 31 haemoglobin role 423-431 maximal 4,12, 24 mountaineering 933 tomuscle 682 performance limitation 55 rowers 841

rugby football and altitude effect 911 ozone 53,628-633 acute inhalation effects 630,632 concentrations and effects 629 effect on maximal oxygen intake 631-632 endurance performance 629-631, 630 exercise interactions 628 at high altitude 623 interventions 633 mechanisms of adverse effects 632-633 pollution 297 pace strategy, perceived effort 387 pace training, women 519,521 pain Achilles tendon 780 cognitive control strategies 456 defective recognition and tissue injury 800 inhibition, dangers 477 input to perception of effort 379, 380 knee 775 night 769 osteitis pubis 793 perception 802 perseverance and psychological aspects 453 referred, knee 775 spinal cord injuries 579 stress fractures 769 tolerance 217 pain relief Achilles tendon injuries 781 counterproductive effects 800 mechanisms 803 patellofemoral pain syndrome 776 pancreas, E cell changes 189 pancreatic enzyme supplements 571 pancreatic hormones 189-190 parallel processing hypothesis 375, 380 paraplegia 578 parasympathetic system 107 paratenon 777 paratenonitis 777-778,780 tendinosis with 778,780,781783 treatment 781783 Parkinson’s disease 584 PARmed-X for Pregnancy 536,537, 536543-545 pars interarticularis, stress fracture 768,771 patella bracing/taping 469,776 hypermobile 776 stabilizing brace 776,785 subluxation prevention 480


patella alta 469,473,775,776 patella baja 775,776 patellar tendinitis 775,783785 aetiology 784 anatomy and classification 783-784 diagnosis and differential diagnosis 784 treatment and prevention 785 patellar tendon 783 patellar tracking 774,775,776 patellofemoral ligaments 774 patellofemoral pain syndrome (PFPS) 469,766,774-777 anatomy and aetiology 774-775 diagnosis/differential diagnosis 775 investigations 776 treatment / prevention 480, 776-777 peak height velocity (PHV) age 397, 398 perceived effort 33,374-394 endurance relationship 385 intensity inputs 377 measurement 383-384,384 models 375,375,380 physiological inputs 376-380,387 non-specific mediators 379-380 peripheral mediators 378-379, 387,391-392 respiratory-metabolic mediators 376-378,391 thresholds 377-378 practical applications 385-391 performance 385-389 training 389-391 psychological inputs 380-384,388 dispositional factors 382-383 situtational factors 380-382,382, 392 psychophysiological model 374-376 rating see rating of perceived effort (RPE) perception 374 of health see health, perceived performance blood volume role 431-435 body composition and 349-350 body size consequences 48-50,452 cognitive factors 216-217 deterioration in fatigue 28 determinants 224,271,272,423, 451,501 at early age and prediction of success 399 environmental extremes see specific environmental extremes gender differences 523 genetic determinants see genetic determinants

glucose administration 29 improvement, pulmonary system 62-64 respiratory muscle training 61-62’62 jet lag effect 642444,643,644 limitations by pulmonary system 54-59 mental health model 211-212 overtraining effect 488-491,490, 528 ozone exposure affecting 629-631, 630 peak oxygen deficit and 312 perception of physical effort 374-394 applications 385-389 see also perceived effort personality and 369-370 pregnancy effects 532,532-533 psychological aspects 214-215, 452-453 psychological interventions 215-216 women and training relationship 522 see also individual sports performance-enhancing drugs 657-69 see also banned substances; doping perfusion pressure 32 periodization 501,527 peripheral arterial disease 91,568 peripheral blood flow, fatigue development 34 peripheral limitations of effort 34-35 see also fatigue, peripheral peripheral vascular disease 91 elderly 549 peripheral vascular resistance, in heat stroke 604 peritendon 777 personality 217,366-373 athletes from different sports 369-370 athletes of different skill levels 370 athlete DS non-athletes 369 controversies 366 definition 366 iceberg profile 370 impact on sport 211-212 implications for practitioners 370-371 input to perception of effort 382 interactional theory of assessment 370 measurement 366-369 sports performance and 369-370 theories 366,368-369,370 traits in endurance athletes 370 Perthes’ disease 473 pes cavus-type foot 786


PH blood 52,321,378 intracellular, high-intensity exercise 95 as marker for training intensity 389-390 phagocytosis 735,736,801 phenotypes 223-224 phenylpropanolamine 442-443 phlebotomy 427 phosphate 21,166 phosphate-binding agents 572 phosphate compounds, high-energy 21

phosphocreatine 332,334 ATP production in muscle 334 cycling 861,863 intermittent exercise 10-1 I threshold, cycling 863 phosphofructokinase 118 photosynthesis, products 329 phrenic nerve, supramaximal stimulation 56 physical activity 3 minimal and optimal levels 699, 70°1 747 see also exercise Physical Activity Readiness Medical Examination for Pregnancy 536’ 537,538,543-54.5 physical fitness see fitness physicians legal aspects of cardiovascular screening 672 malpractice liability 672 requirements for wilderness expeditions 664 physiological fatigue see fatigue physiotherapy, at race finish 611 physique 37-38,38-40,346 genetic influences 232-233 individual variability 42-43 see also body size; height phyto-haemagglutinin, response to 495,732,733 piroxicam 808 pituitary hormones 185-189 placental growth, endurance exercise effect 535 placental injury 539 plantar aponeurosis, tear/strain 785-789 plantar fasciitis 785-789 aetiology 786 anatomy 785-786 diagnosis / differential diagnosis 786-787 investigations 787 treatment and prevention 787788 plantaris muscle 147,777 plasma volume 682 altitude training in women 527



plasma volume (continued) decrease 432 at high altitude 619 spaceflight 683 effect on hormone measurements 191 increased 432,682 at sea-level 620 response to training, adolescents 511 see also blood volume plasticity muscle fibre types 136 myofibrillar proteins 168 sensorimotor systems 144 see also adaptatiods) Poiseuille‘s law 94 poliomyelitis, anterior 581-582 polycythaemia, high altitudeinduced 619 polymerase chain reaction (PCR) 341 polymorphonuclear neutrophils see neutrophils polysaccharides, for cyclists 869 polyunsaturated fatty acids (PLJFAs) 807 positron emission tomography (PET) 343-344 postmenopausal women 468,576 post-polio syndrome 581-582 post-tetanic potentiation 163 postural hypotension 603 after exercise 607 collapse after exercise 594-595 heat exhaustion and 594 posture blood pressure changes in elderly 549 hockey players 925 muscle pump control of blood flow 97 postviral fatigue syndrome see chronic fatigue syndrome potassium in fatigue 30,95 interstitial 95 raised levels 550 regulation 95 release from muscle 30,95 serum levels, elderly 550 potassium spectroscopy 347 power 6,13 ‘power strokes‘ 161,166 pre-eclampsia 536,539 pregnancy 531-546 acid-base balance 532 aerobic exercise 537 ‘anabolic phase’ 531 blood flow and redistribution 535 carbohydrate metabolism 531 disorders 536 duration of exercise 538

effects on performance 532, 532-533 effects on response to aerobic conditioning 533-534 fetal response to maternal exercise 534.534-535 gestational diabetes 534,572-573 heart and circulation 531-532,537, 538 response to conditioning 533-534 heart rate 533,537,538 medical screening 536-537 nutrition 537 outcomes 535-536 physiological effects 531-532 practical advice 546 reasons to contact physician 539, 546 respiration 532 response to strenuous exercise 533 safe limits for conditioning 536-538 safety considerations 546 thermoregulation 532 training after childbirth 539 twin 536-537 unintended due to menstrual disorders 718 preload 3 4 , m 70 premature labour 536-537,539 premenstrual syndrome 805 preparticipation screening, cardiovascular see cardiovascular screening prerace organization 607-608 collapse reduction 608-609 mass participation events 660-661 see also international competition prerace seminars 608-609 pressure sores, spinal cord injuries 579 Profile of Mood States (POMS) 212, 212,368-369,370, 371 identification of ‘distress’ 497 overtraining marker 496-497 rating of perceived effort and 498-499 progesterone 188 menstrual cycle 719 suppression in athletes 718 prolactin 188 pronation 780 control by shoe orthotics 482 increased 468,469,778 maximum point 468 plantar fasciitis 786 proprioceptive training, injury prevention 476,476 prostaglandin El analogue 808 prostaglandin E, 633,802 prostaglandins 802,803

prostate cancer 758 prostatitis 792 protective equipment 458,478, 47s479 protein 197-207,203 catabolism cycling 865,868 prolonged exercise 203 as energy source 329,414 in fat-free mass 346,348 high protein meals, jet lag prevention 646 intake 203-204,413,413-4i4,4q cyclists 869,870,870 monitoring in high-risk groups 203 recommended 413 oxidation to energy 414 requirements 203,413,413-414 women athletes 205 vegetarian diets 203 proton accumulation 11 see also hydrogen ions; pH pseudoephedrine 442-443 psychological aspects 211-221 benefits of regular exercise 75w60 challenges/demands in endurance sport 453-454 chronic pulmonary disease 569 group (nomothetic) factors 217 individual (ideographic) factors 217 input to perception of effort 380-384,388,392 mental health model 211-212 muscular dystrophy 580-581 pain tolerance 217 performance 454-455 characteristics related to 452-453 impact on 451-452 interventions 215-216 precompetition anxiety 214-215 ‘profileof mood states’ see Profile of Mood States (POMS) response to endurance training 212-214 psychological markers, overtraining 496-499 psychological preparation 451-457 factors included 452-453 psychological skills training 454455 psychological toughness 8,21 psychopathology, sport capacity and 211

psychophysiological model, perceived effort 374-376,375 psychosocial variables children 514-515 input to perception of effort 380


psychotherapy, overtraining prevention 657 puberty, maximal oxygen intake and 510 pubic rami, stress fracture 794 pulmonary arterial pressure 52-53 high altitude 617,933 pulmonary blood flow 53 pulmonary blood-gas barrier, impairment 53 pulmonary diffusing capacity (BLco) 53,59,682,683-685,684 postexercise reduction 682,684, 684 pulmonary disease see lung disease pulmonary function see lung function pulmonary oedema 53,604 chest X-ray 623 at high altitudes 296,622 high-permeability type 622 management 622 presentation and risk factors 622 pulmonary vasoconstriction 622 pulse pressure, rowers 840 pygmies, running and energy costs 818 pyruvate 25,335 quadriceps fatigue in cycling 34 fibre type distribution 86 strength and injuries 470 strengthening exercises 776 tendonitis 775 was,% 775 quadnceps tendon, pull during contraction 774 quadriplegia 464,578,579 quality-adjusted life expectancy 714, 748 quality of life 714,748-750,749 Qu6bec Family Study 237,234,238 questionnaires, personality assessment 367-369 race organizers 661 races (sports) casualty number prediction 607-608 cool/warm conditions 608 participant screening/qualification 608 planning course 608 plans 453-454 scheduling 608 seminars before 608-609 see also mass participation events racial aspects see ethnic aspects racquet sports 945 radiation see ultraviolet radiation radioactive techniques, muscle metabolism analysis 341-342

radiography cardiac hypertrophy 708 neoplasms associated 758 osteitis pubis 794 stress fractures 771772 rain suits 600 rating of perceived effort (WE) 374, 376,377’ 378,392 constant level 386-387 continuous us interval training 391 disabled persons 565 elderly 559 exercise duration and 389 overtraining marker 498 peripheral arterial disease 568 POMS scale relationship 498-499 pregnancy 538 scale 384,384 submaximal exercise intensity 390 for training 390,391,392,568 women during sustained distance training 518 rating scales, personality 367 reactive oxygen species (ROS) 801, 802,806 see also free radicals recovery area, for mass participation events 662 rectal temperature circadian rhythm 640,645 collapse 601,663 heat exhaustion and 593,594 heatstroke 604 hot environment 289,290 mass participation events 663 raised 604 emergency management 601, 604 malignant hyperthermia 605 rugby footballers 911 swimmers 266 unconscious patients 603 rectus femoris, injury 788 red blood cells altitude acclimatization 297,618, 934 in bronchoalveolar lavage fluid 53 counts 424,618,934 erythropoietin role 428 mass 682 testosterone effect 511 volume expansion, high altitude 297 redox reactions 334 ‘reducers,’ input to perception of effort 382-383 refrigerator facility 610 regattas 83-77 regulatory proteins 164-165 see also tropomyosin; troponin


rehabilitation, chronic pulmonary disease 570,750 rehydration, rugby footballers 911 reinjury 470 renal blood flow elderly 549-550 reduced during exercise 599 renal failure 32,571-572,606 NSAIDs causing 808 transient 599 renal function, elderly 549550 renal vasoconstriction 105,106 renin-angiotensin-aldos terone system 190,550 repetitive activity Ca2+-releasechannel 175 cytoskeletal proteins in muscle 178 excitation-contraction coupling 174r176 myofibrillar proteins 165-167 Na+/K+pump changes 174,175 reproductive changes 718-730 females see menstrual cycle; menstrual disorders males 723 resistance training 526 ACSM recommendations 554 adaptations 168 fast-velocity and slow-velocity 526 fat-free mass 555 post-polio syndrome 582 women 526 respiration see breathing; ventilation respiratory acidosis, compensated 321 respiratory alkalaemia 932 respiratory alkalosis 321,532 respiratory chain 332,335,337 ATP production 334 enzymes 119 function and structure 337 respiratory discomfort, air pollution 628 respiratory exchange ratio (RER) 533 respiratory infections, management 659 respiratory muscles 52 accessory 54 endurance increase 63 exercise stress and maximum bloodflow 60 expiratory 57,63 fatigue 56-57,57,61 reduction by training 63 fibre hypertrophy 62-63 increased activity in exercise 53 loading/unloading effects 58,63 performance limitation 57-59 prolonged exercise 53,56 recruitment 57 steal of locomotor muscle perfusion 57-59,63



respiratory muscles (continued) training see respiratory muscle training (RMT) work 56,63 cardiovascular consequences 57-58 respiratory muscle training (RMT) 60,61-62,62 adaptations due to 62-64 respiratory quotient (RQ)24,338, 813,830 respiratory rate (fJ, input to perception of effort 376 respiratory system 52-67 adaptations by training 59,6144 alcohol effects 446 benefits of exercise 750 endurance training effect 59-61 failure and performance limitations 52,54-59 function 52 improvement of performance 62-64 input to perception of effort 376-378t391 respiratory muscle training 61-62 response to exercise 52-54 respiratory therapists 570 rest periods, importance 766-767 restricted fragment length polymorphism (RFLP) 237 retinal haemorrhage 621,622 retinal oedema 622 rhabdomyolysis 597 rheumatic disorders 779 rheumatoid arthritis 575,752 right ventricular dysplasia 670,676 right ventricular hypertrophy 69 risk, sports and sudden death 671 roller-skiing training 854 Rorschach test 367 rowing and rowers 836-843 ACE gene alleles 235 aerobic metabolism 839-840 age, body s u e and physique 38,40 altitude training 841-842 anaerobic metabolism 840 biomechanics 838 blood lactate 840 blood pressure 840,841 boat weights and type 836,837 body fat 352-353 bodymass 43 central venous pressure 840-841, 841

cerebral oxygenation 841,842 circulation and cardiac output 836, 840-841 competitions 836 duration 837-838 coxswain 836 distance and speed improvement

837 drag force 838,838 energy costs 839 per unit of body mass 250 ergometers 275,275-276,276 health problems 836 immune system changes 732, 734 maximal oxygen intake 840 muscle strength 838-839 oxygen intake measurement 285 oxygen transport 841 regattas 836-837 sculling 836 sweep rowing 836 training 842 15x5 training method 831 ventilation 841 weight categories and gender 837-838 work components 246,246 ‘rowing strength’ 838 rugby football 99-915 aerobic measures 914 altitude training 911 anaerobic threshold 914 anthropometry 912 blood lactate 910-911 bodymass 912 dehydration and body temperature 9x1 demands of specific position 909, 912 diet and nutrition 915 distance covered in game 910 energy expenditure 911 environmental factors 911 field tests 913 fitness 912-915 heart rate 914 historical aspects 909-910 injuries 911 lifestyle 915 low-intensity / high-intensity activity 910 MAOD test 913 maximal oxygen intake 914,914 muscle fibre types 9x3 muscle glycogen 911 muscle strength and endurance 912-913 training 915 women 909-910 work rate 910-911,911-912 Rugby League 912 Rugby Union 909,912,913 workrate 910-911 rules ineffectiveand injuries due to 464 for sport in environmental conditions 465 ’runner’s high 749,759

‘runner’s trots’ 662,758 running and runners 9,813-823 association and dissociation methods 216,454 blood flow to legs 7,34 body fat 349,352 body size and 39,40,42,43, 817-819 cardiac parameters, track vs treadmill 281 cortisol levels, perception of effort 380 cross-country,rating of perceived effort 390 decreased atmospheric density 615 dehydration in triathlon 874 distance, age, body size and physique 39,40 economy 247,402-403,407 hill training 403,407,407 lower limb flexibility 249 maximum oxygen intake vs 403, 405 performance relationship 524 speedand 250 training effects 406-407 elderly 560 endurance conditioning 402-408 energetics 813-823 bottleneck affecting (equation) 815,817 long-distance running 815817 middle-distance 819-822 treadmill 813 energy costs (C,) 281,517,813-817, 814 accleration from start 821 body mass relationship 250, 817-818 ground contact time 285 increase with distance 817 interindividual variability 813 long-distance running 815-817 track vs treadmill 281 energy expenditure 814,815 energy intake 410,410 fat mass and performance 349 fluid ingestion 597 genetic determinants 227 gravity effect 614 heatstroke, management 604 hill training 403,407,407 hypothermia 5 9 e o o imagery use 215-216 injuries 462,468,469,482,766 lactate levels and 312 left ventricle dimensions 76 limitation by central vs peripheral factors 34-35 malalignment injuries 468,469


marathon see marathon runners maximal aerobic speed 818,819 maximal metabolic power (Emax) 815 maximal oxygen intake 11,815, 852 training effect 406,406 mechanical power and economy 247 metabolic power (E,) 815 metabolic rate 409 middle-distance 819-822 theoretical us best times 821,821 mileage link to injury 805 ’miserablemalalignment syndrome’ 469 muscle fibre recruitment patterns 127 oestradiol level prediction by energy balance 724 overuse injuries 766 pace strategy 387 performance and body size 817-819 physiological variable affecting performance 402-404,404 pregnancy 537 repeated overload 461 shielding from air resistance 254 shoes 481 speed 250,815,816,816 maximal oxygen intake correlation 308 protection against hypothermia 600 strength training in elderly 559-560 stress fractures 768,770 stretch-shortening cycle contribution 248,249 submaximal oxygen cost 47-48,48 sudden deaths 670 technique assessment (video) 770 training errors 462 triathlon 874,883 velocity (VLa4)403-404 visual impairment and 586 warm-up exercises 474 wind speed/direction effect 253 work and energy expenditure 248 work components 246,246 see also marathon runners ryanodine receptor 597 sacroiliacjoint, dysfunction 472,793 sarcolemma 169,171-172 sarcomeres, structure 159,159160 sarcoplasmic reticulum 169-170, 172-173 Ca2+-ATPase172-173 characteristics 172-173,173 function 172

repetitive activity effect 175-176 T tubuleCa2+channel interface 173-174 T tubule coupling failure 176 satisfaction, in athletes 749 scaffold proteins 179-180 scaling and scaling factors 47-50 allometry applications 44-45 for body size 43-44,48-50 children/adolescents 48,49 Fhax 45.45-47,46,47 VO2subrnax 47-48,48,49 definition 43 historical background 44-45 isometric 44 non-isometric (allometric) 44,50 principles 44-45 scars 472 school athletes, cardiovascular screening 671,672-673 Schwinn Air-Dyne 577,578 scientificstretching for sport (3s system) 476 screening see medical screening sculling 836 SDS-PAGE 34+341 sedatives 64M47 Seldinger technique 341 selenium 806407 self-efficacy, input to perception of effort 383 self-esteem 757,759 self-presentation theory 38-381 Selye’sstress reaction 32 sensation 374 sensorimotor systems 153 adaptive response 152-153 overloading 147-149 plasticity 1 4 reducing loading 144,146,149,151 see also motoneurones; sensory neurones Sensor-Medicsmetabolic cart 305 sensory disorders 584-586 sensory neurones 136-157 dorsal root ganglion 142-144 morphological/physiological properties 151 overloading effect 147-149 reduced loading (spaceflight)effect 151-152 soma size and enzyme activities 142-1443 143 septa1hypertrophy 710,712 serotonin (5-hydroxytryptamine) 205 agonists 499 branched-chain amino acids effect 655 elevated 205 melatonin synthesis from 639 overtraining marker 499


receptor 499 role in central fatigue 4x9 serotoninergic challenge, response 499 serotonin uptake inhibitors 574 sesamoids, stress fractures 771 sex hormone(s) 188,805 sex hormone-binding globulin, overtraining marker 493 sexual maturation, children 514 shielding, economy of movement and 254 shinty 926 shivering 28-29,260 shock absorption, by shoes 481 shoe orthotics see orthotics shoessee footwear shoulder, tennis 467,467 shoulder pads 479 shuttle run test 913 sickle cell disease 623 Siggard-Andersen nomogram 321 sign language systems 586 sinoatrial node 107 Siri equation 347,349 SI system of units 5,6 site visit, preliminary, for international competition 658 skating 847 classic skiing comparison 847,849 shielding from air resistance 254 work components 246,246 skeletal muscle see muscle skeletal muscle-specificcreatine kinase see creatine kinase skiing and skiers adaptation to training 854 aerobic metabolism 846 age, body size and physique 39,40 anaerobic metabolism 847 blood lactate 847 bodyfat 353 body mass 850,850 body position 849 classic technique 846,847,848,849 skating comparison 847,849 cold injury 855 competitions 844-846 cross-country 844-857 distance-velocity relationships 846 double pole techniques 847,848, 849-850 economy of movement 251 elite skiers, characteristics 850-852 energy yield 846447 ergometers 276,277 freestyle technique 847,848 heart rate 849 heat balance 855 improvement of endurance 8 4 , 845



skiing and skiers (continued) injuries 463 lifespan 760,760,761 maximal oxygen intake 400,847, 850,851,852 muscle adaptation 852,854 muscle fibres 851 oxygen costs 851 oxygen intake 849 performance 846 prediction 852,853 racetypes 844 racing course and terrain 844-845, 849 racing styles 846,8474450,854 roller-skiing training 854 slow-twitch muscle fibres 13 speeds in championships 844,845 stretchshortening cycle 248 sweating 855 training 852-855 amounts 854,854 poling techniques 854,855 types and benefits 852,854 velocity decrease with distance (males) 846 viscous work 5 4 work components 246,246 skin atrophy 807 blood flow see cutaneous blood flow cancer 758 thermal gradient and heat transfer 27 water vapour pressure 261 ski-walking 854 sleep adequacy 742 deprivation, jet lag 646 EEG 646 loss, effects 642,643 partial deprivation 642 sleepwake cycle 639,642,644 sliding filament theory 159 slow-twitch muscle fibres see muscle fibre types smoking 444-445 adverse effects 445 bodymass 757 carboxyhaemoglobin levels 635 cessation 760 nicotine effects 444-445 respiratory diseases 750 smooth muscle, vascular, relaxation 94,95196 Soccer ~ 3 0 , 9 0 8 , 9 0 9 , 9 4 5 anaerobic threshold 902903 backwards/sideways movements 907 blood lactate 905,905906, 906-907

categories of activity 901,902 clothing 905 dietary practices 908 distance covered per game 901, 901,903 dribbling ball, physiological responses 906,906 early selection 399 energy expenditure 903,906,907 training 908,908,909 environmental conditions 904305 fatigue 903-905 fitness measures 907 goalkeeper 902 goal scoring 904 groinpain 791 heart rate 905,908 immune system 90-09 low-intensity / high-intensity exercise 902 maximal oxygen intake 902-03, 905,907 mental fatigue 904 metabolic data 282 metabolic loading 905 oxidative enzymes 907 physiological demands/responses 9Oc-909 game-related activities 906-go7 match-play 905-906 roles of individual players 902 training and habitual activities 907909,908 intensity 907 tapering off phase 908 work-rates factors affecting 902303 profiles 9~0-902 social competence, training of children and 515 society, costs of injuries 458 sodium addition to drinks 420,421 high sodium solutions 606 imbalance, heat cramps and 593 renal loss 190 retention 190 see also hyponatraemia sodium cromolyn 571 sodium pump see Na+/K+pump softball, area equipment 463-464 soleus muscle 777 somatotype 37-38,38-40,41,232,233 Southern blot 341 soybeans 203 spaceflight 144,146,149,151 plasma volume reduction 683 spasticity, amyotrophic lateral sclerosis 582 speed 247 stride length and cadence 250-251 spinal cord injury 147,578-579

spinal fractures 718 spinal motoneurones 1 4 ~ 1 5 1 lack of adaptation 150 splanchnic circulation 103,106 elderly 548 reduction in exercise i04-i05,106, 107,112 splenic rupture 623 splints, plantar fasciitis 787 spondylolisthesis 467 spondylolysis 771 spondylosis 467 sports, classification 7 ’sports anaemia’ 190,424-425 sports drinks carbohydrate 200,201 exercise-associatedcollapse 607 see also carbohydrate beverages sports hernia 794-796 sports injury see injury, sports sports psychologists 370-371 sports surfaces injury prevention 462-463 overuse injuries 769,774,778,784 sportswear see clothing sprinting 902,918 squash, sudden cardiac death 79 3Ssystem 476 stabilization, spinal cord injuries 579 staleness 4,32,214 overtraining marker 497 standard international (SI)units 5,6 Starling effect 520,548,683 state-trait controversy 366,368-369, 370 statisticalmethods 44 statistical modelling, maximal oxygen intake 226 stature children and adolescents 41,42 for specific sports 38-40 see also body sue; height ’steal effect,’ of respiratory muscles 57-59,63 steroids Achilles tendon injuries 779 anabolic see anabolic-androgenic steroids (AAS) replacement therapy 7x9 see also corticosteroids; hormones Stevens’power law 374 stiffness, morning 786 stimulants adverse effects and injury 477 banned 439 caffeine 441 ephedrine 442-443 jet lag management 647 see also amphetamine stimulus intensity, input to perception of effort 382-383 strength, definition 7-8


strength athletes, left ventricle dimensions 76,77 strength events 7 strength training elderly 559-560 negative effect on flexibility 475 osteoporosis 576 stress exercise, menstrual disorders 723, 724-725 musculoskeletal adaptation 475 reduction by exercise 573 responses 184 training, effect on mood 213,214 stress (force),definition 768 stress fractures 753,767-774,794 aetiology 466,768769 anatomy 769 &-risk 77@77',773r 774 children 513 definition 767 diagnosis and examination 466, 769-770 differenhal diagnosis 71 incidence 767-768 investigation 771772 prevention 773-774 risk factors 466,773 sites 767,768 treatment 773 stress hormones 184,185 immune system and 735,740 see also cortisol stress hypothesis, menstrual disorders 723,724-725 stretchers 609 stretching Achilles tendon injury treatment 781 adductor longus injury treatment 793 in cool down period 474-475 dynamic and static 476 flexibility training 476 hamstring and calf 776 pre-exercise, hamstring injury prevention 791 stretch-shortening cycle 248-250 contributions, source 248-249 flexibility effect 471 muscle training to prevent injury 475 running and jumping 249 training and flexibility 249-250 stride length, speed and cadence 25c-251 stroke (cerebrovascular) 577-578,578 aetiology and risk factors 696 mortality reduced by exercise 697 risk reduction by exercise 696-698 stroke volume children 510,511,513

decrease, exercise in hot environment 263 high altitude 617 increase with cardiac hypertrophy 713 maximal aerobic power definition 259 maximum 1 2 pregnancy 531-532,533,534 triathlon 873 women 519,520 substrate availability input to perception of effort 379, 387 see also carbohydrateM; fatty acids succinate dehydrogenase 119,127, 129 dorsal root ganglion 142,143, 151-152 motoneurones and muscle fibres 148,148-149 swimming training interruption 831 ventral horn neurones 149 sudden cardiac death 69,77430, 667-681 cardiomyopathy see hypertrophic cardiomyopathy (HCM) causes 668,668-671,708,711712 disorders predisposing 653 exercise-related 77-78,711712 myocardial infarction, reduced by exercise 694 non-exercise-related 78 potential triggers 7 5 ~ 8 0 prevalence and scope 78,668,671 race and gender aspects 677-678, 678 screening see cardiovascular screening ventricular hypertrophy and 710 young athletes 654,667-681 sudden deaths 667,671 erythropoietin use 429 non-cardiac 670 sudden exercise, sudden death 79,80 sulphur dioxide 297,634-635 Super Bowl 915 'supramaximal' effort 311 supraspinal input, motor units recruitment 136-137 surface friction 246,246 surgery, tendon injuries 782, 79c-791,793 sustained distance training, women 518 sweat, evaporation 26c-261 sweat glands 261 sweating 261 cold environments 294 pregnancy 532 rates 419


skiers 855 threshold temperature for 108 sweat-suits, hyperthermia from 917 swimming and swimmers 824-835 aerobic metabolism 824,825 aerobic power due to workouts 824 aerodynamic clothing 253 age, body size and physique 38, 39t40.42 anaerobic events 8 3 anaerobic metabolism 824,825 as 'arm and upper body sport' 825 benefits in asthma 750 blood lactate 827,827-828 performance profile 828,829, 830,832 body fat 292-293,293,353 body weight in water and 826 channel swimmers 266,600 cold stress 265-266 critical swim speed 828-829 detraining and inactivity 831 drag forces 253 economy 824,884 endurance testing 826-829 endurance training 830 15:15 training method 831 aerobic exercise 8 3 controlled-intensity 830 effectiveness assessment 833 fast-speed 831 glycogen depletion 830 interval approach 830 low-speed 830,831 patterns for Soviet swimmers 833,833 risks 830-831 tapering phase 828,831-832 whole stroke 830 energy balance, negative 830-831 energy costs per unit of body mass 250 fatmass 350 heart rate 826-827,827 heat conductance 27 heat transfer coefficient 265 hypothermia 600 long-distance, training 830 lower extremity amputees 577 maximal oxygen intake 824,825, 826 land and hydrostatic weight comparison 826,826 mechanical power and economy 247 medals for East Germany 400,400 net efficiency 6 neuromuscular problems 831 overtraining 487,497,830 oxygen consumption 827 performance 829-830



swimming and swimmers (continued) periodization and 527 pregnancy 537 psychological response 213,213 tissue insulation in cold water 292-293,293 triathlon 829,872-873,874,884 twin, trained 271,273 work and energy expenditure 248 swimming flumes 277,277 sympathetic system 107,190,683 sympathoadrenal hormones 184-185 sympathomimetics +p-443,570,574 syncope 654 see also heat exhaustion (syncope) systemic vascular resistance 94 systolicblood pressure canoeists 896 elderly 549 ‘heat exhaustion‘ and 594 systolic function 70,75 systolic phase, duration 711 table tennis 945 tachycardia 320,594 tachypnoea 64,633 tachypnoeic drift 54 talent, identification and development 400 tape, medical 481 task aversion 33,374 task failure 158,166-167 Tcells 732 helper to suppressor ratio 656 mitogen-induced proliferative response 732,738 overtraining marker 495,656 proliferation, overtraining 495,496 team sports 9,669 telemetry 281 temazepam 646 temperature, body changes during exercise 262,263 circadian rhythm 640,640,644 core 26,32 see also rectal temperature effect on motivation 419 fatigue relationship 32,111,419 gradient during early exercise 260 heart rate relationship 110 heatstroke 595 increases 108,660 in infections 660 input to perception of effort 379, 380 low,fatigue 32 melatonin level changes 640,647 muscle, warm-up exercise 474 oral, avoidance 663 pregnancy 532 rectal see rectal temperature regulation see thermoregulation

skin 26 skin blood flow relationship 107-108,108 steady-state 262 upper limits 108,109 temperature, environmental 259267 drop with altitude 615 hypothermia due to 600 intolerance by elderly 548 wet bulb globe temperature (WBGT) 287 see also cold environment; hot environment tendinitis 778,780 see also patellar tendinitis tendinosis 778,780 paratenonitis with 778,780, 781-783 tendon benefit of exercise 751752 failure 778 injuries 779,805 classification 777-778 rupture, corticosteroid injections 809 strains, elderly athletes 468 structure 777 see also Achilles tendon tennis 945 early specialization 399 elderly 468 overuse injuries 463 racquet size/stringing and 463 tennis elbow 463,480 tennis shoulder 467 testosterone actions 511 analogues 443-444 cortisol ratio 493,656 free 492,493 levels at puberty 511 overtraining marker 492,493 reduced levels in athletes 723 response to exercise 188 as skeletal muscle pump 511 tetraplegia 578 theatre-goer’s sign 775 thermal conductivity 27,43 thermal gradient, skin to air 27 thermal pants 791 thermal sensors 262 thermodilution 341 thermodynamics 21,88 thermogenesis 7,26,108,260 shivering 260 thermography 772 thermoregulation 107-108,259262, 596 body surface area and 43 children 514 control 262

endurance exercise influence 110, 112,293 during exercise 262 exercise in obesity 575 hot environments 262,288 hyperhydration effects 290 influence on endurance exercise 110-111

pregnancy 532 ‘set point’ 110 triathlon 872-873 variations 108 water immersion 292 thermoregulatory centre 262 Thompson’s squeeze test 781 throwing, fat-free mass and performance 350 thyroid hormones 187,719,723 thyroxine (T,) 187 tibia anterior cortical fracture (’dreaded black line’) 770 internal rotation 468,778 stress fracture 768,770 tidal volume 53 time zones 639-650 adjustment and effect of direction 645 body temperature 645 jet lag adverse effects 643-644 light/dark adjustments 648 sleeping difficulty after crossing 642 see also circadian rhythm; jet lag tiredness 32 overtraining marker 499 see also fatigue tissue adaptation, mountaineering 935 tissue injury, exercise-induced causes 803-804 factors influencing 804-807 nutritional influences 806-807 prevention and treatment 807-809 process/reaction 801 training form and status affecting 804-805 see also inflammation toilet facilities 609,662 wheelchair athletes 662 total aerobic running capacity 403 total body mechanical power 246 total body water (TBW) 347 total lung capacity (TLC) 629 Tour de France druguse 439 energy expenditure 655 erythropoietin and 431 free fatty acids administration 655 training 860 tracer techniques 341-342 training 438


ACSM recommendations 554 acute fatigue 501 adaptation see adaptation($ after childbirth 539 American football 916-917 anaerobic metabolism response 312 Australian Rules football 919 children see children cold stress strategy 293-294 continuous vs interval 391 continuum with overtraining 501, 501

contraindications aneurysms 568-569 diabetics 573 elderly 551 diet see diet diffusive oxygen flux response 90-91 disabled persons see disability, persons with discontinuation, regression of adaptations after 130 ‘distress’signs 487 duration see duration of exercise/ training effect on athletes 405-406 elderly 552-555,554 E-endorphin response 189 enzyme adaptation induction mechanisms 131-133 errors 462,462,766-767 Achilles tendon injuries 778 patellar tendinitis 784 plantar fasciitis 786 tissue injury and inflammation 804-805 see also individual overuse injuries erythropoietin response 429-430 excitation-contraction coupling 178-179 Gaelic football 919 glucagon response 190 glycolyticenzymes after 127-129 goal 518 growth hormone response 187-188 heart rate recommendation 14 heterogeneity in response 227,229, 238 high altitude 12,296-297,321-322 high-intensity 180,231,232 high resistance 168,179 hill 403,407,407 hockey 925,926 imbalance see overtraining injury prevention see injury prevention insulin response 190 intensity see intensity of exercise/training

interval see interval training lung volumes 59-60 markers, running velocity (Vb4) 403-404 maximal oxygen intake response 14,227-228,406,406 menarche timing and 399 mitochondria1enzymes increase 90 mood disturbances 213-214 motivation maintenance 453 motor unit changes 147 mountaineering 937-939 muscle adaptation see muscle, adaptation muscle capillarization 122, 127-129,128,13O muscle contractile characteristics 130 muscle fibre types 127-129,147, 168 muscle sensitivity to epinephrine 130 muscle triglycerides 201 for muscular endurance 3x4 myofibrillar function/composition changes 167-169 myofibrillary plasticity 168 Na+/K+pump increase 176,179 need for recovery period after 501 objectives 767 optimal balance 486 optimum programmes 405-406 pace, women 519,521 perception of physical effort 33, 374-394 applications 389-391 see also perceived effort periodization 501,527 phases 767 physiological effects 406-408 pituitary-adrenal activation 186 prerace advice to athletes 608609 psychological response 212-214 pulmonary system response 59-61 regional blood flow capacity response 90-91 regression of adaptation after discontinuation 130 respiratory muscles response 60 rowers 842 rugby football 915 skiing 852-855 soccer 907-909 sport-specific,for injury prevention 476-477 stress hormone response 185 stretch-shortening cycle and 249-250 tempo (pace) 518 thyroid hormone response 187


tissue injury and inflammation 804-805 total aerobic running capacity and 403 ventricular performance response 69-70 women see women see also individual sports training cycle 767 training surfaces, overuse injuries 7693774,778,784 tranquillizers, minor 646 transdiaphragmatic pressure 57 transforming growth factor (TGF) 71 transmural pressure, muscle blood flowcontrol 96 transport chain 22 transversalis fascia, weakness 794 trauma see injury, sports travel fatigue 639 traveller‘s diarrhoea 659 treadmill 274 energy costs 813 external/internal locus of control 383 graded exercise test, disabled persons 565 maximal oxygen intake 12,304 in wind tunnel 279 triacylglycerol see triglycerides triage 602,604 mass participation events 663 triathlon and triathletes 872-887 acute effects of sequential exercise 874-875 aerobic power 880-882,881,882 air resistance 878-879 anaerobic threshold 883 backpain 877 body composition 879-880 body mass 878,879,879 cardiac output 873 characteristics of triathletes 877-885 physical 877-880 physiological 880-885 cycling 857,858,873,874,885 dehydration 873-874 demands 872-875 economy of movement 875, 884-885 fatigue 874,875 fractional utilization of VoZmax 882-884 ’heavy-weight’ 880 height 8774378,878 hyponatraemia 874 injury sites 876-877 Ironman 872,875-876 lactate threshold and performance 525 mixed ability 881



triathlon and triathletes (continued) muscle fatigue 874 overuse injuries 876,877 performance, training effect 875-876 running 874,883 stroke volume 873 swimming 829,872-873,874,884 swimsuits vs wetsuits 872-873 thermoregulation 872-873 training 875-877 BRICK 874 rating of perceived effort 390 training and performance in women 522 wetsuit 872473,885 tricarboxylicacid cycle see citric acid Webs) cycle triceps surae 777,781 ‘trigger hypothesis’ 510 triglycerides content of muscle, cyclists 864 medium-chain (MCTs) 202 metabolism/metabolites 28,312 reduction by exercise 698-699 stores 201 trochanteric bursitis 462 tropomyosin 160,164,165 structure and isoforms 164-165 troponin 160,164 troponinC 164 troponin I 164,669 troponinT 164 tryptophan branched chain amino acid relationship 499 circadian rhythm adjustment 646 transport 205 T tubules excitation-contraction coupling 170 Na+/K+pump 169,171-172 sarcoplasmic reticulum Ca2+ channel interface 173-174 sarcoplasmic reticulum coupling failure 176 terminal cisternae 172 ‘tube breathing’ 322,620 tumour necrosis factor-A (TNF-A) 738-739,801 tuning fork test 769770 turbulence, high altitude and 615 ’turf toe’ injury 771 twin studies maximal oxygen intake 225-227, 226 response to training 227-228,229 swimmers and training effect 271, 273 tyrosine, circadian rhythm 646 ultra-long distance events

emergency therapy of collapse 602 glycogen depletion and metabolism 313 muscle function 313 nutritional supplements 740 performance 7 plasma volume expansion for 432-433 ultrasound Achilles tendon injury 781 hamstring injuries 790 patellar tendinitis 785 plantar fasciitis 787 sports hernia 795 ultraviolet radiation high altitudes and 615,623 skin cancer risk 758 unconsciousness cerebral oedema 606 diagnostic steps 602-604 differential diagnosis 602-603 management protocols 604-606 underarousal 33 underwater athletes q,31 upper motor neurones, degeneration 582 upper respiratory tract infections (URTI) 731-732 overtraining association 494 prevention 742 urea serum levels, cycling 865,868 urine, concentrating ability, elderly 550


cardiovascular screening 672-673 year 2000 goals for exercise 701 uterine blood flow 107,535 uterine cancer, risk reduction 758 vaccination, recommended schedule 658 valine, supplements 204 valvular heart disease 676 vascular control models 94-98 see also muscle blood flow, regulation vascular resistance 104-105,105 increase 104 reduction 94,98,99 vasoconstriction ageing effect 107 cerebral, altitude acclimatization 617 cutaneous 10%109 graded responses in exercise 105-107 during hyperthermic exercise 111-112

peripheral 104-105 reflex response to exercise 104, 105-107 by respiratory muscles 57-58

renal 105,106 splanchnic see splanchnic circulation thermoregulatory-induced 110-111

vasodilatation cutaneous 108 factors causing 95-96 gastrointestinal circulation 105 impairment, congestive heart failure 91,92 intermittent exercise 9 muscle blood flow and 94,95,99, 104 vasodilators 567,578 vasomotor collapse 594 vasopressin (antidiuretic hormone) 1901432,447 vastus lateralis muscle, fibre area in cyclists 863 vastus medialis obliques (VMO)774, 7751 776 vegan diets 203 vegetarian diets 203,415 vegetarians 415,416 vehicular accidents 577 venous return 70,97 venous sampling, lactate 3x5 venous valves 97 ventilation (V,) air pollutants and 53 anaerobic threshold and 13 circadian rhythm 640,641 high altitude 296,936,936 increase with training 683 input to perception of effort 376-377 lactate relationship 60 mountaineering 932,932,938-939 oxygen costs 53-54 regulation 54 rowing 841 see also breathing ventilation curve, anaerobic threshold and 318-3iq ventilation-perfusion ratio (KO) 55 ventilatory drift 54 ventilatory threshold 13,318,319 estimationlmeasurement 304, 320 hockey 924 lactate threshold relationship 54 ventral horn neurones 149-151 ventricles dimensions 229,710 performance and training effects 69-70 see also left ventricle ventricular diastolic filling 548 ventricular fibrillation 306,696 ventricular hypertrophy 710,714 see also cardiac hypertrophy


ventricular performance 6 9 7 0 ventricular remodelling 69-70,77 ventricular wall tension 711 vertebral column decreased bone density 752-753 fractures 576 hypermobility 467,467 very low density lipoproteins (VLDL,) 201,574 veteran elite athletes, injuries 468 violent death 760 visceral blood flow, restriction 32 visual impairment 586 visualizations 215 vitamin B group 656 vitamin C 417,656,740 vitamin D, supplements 753 vitaminE 4x7 administration 656 increased requirement, high altitude 618 inflammation regulation 806 lipid peroxidation reduction 806 vitamins, fat-soluble, deficiency 202 volleyball 464,945 volume expanders 432,433 volume loading 432-434 antidiuretic hormone and 432 cardiac hypertrophy due to 70 detection 434-435 volume-regulating hormones 432-433 acute supplementation effects 433 levels and detection 434-435 walking energy costs 282 fast, elderly 559 speed, perceived effort 378 visual impairment and 586 walk/jogging (W/J) programme 558-559 walk-run programme, after overuse injuries 781,782,785,788 warm-up exercises elderly athletes 557 functions and importance 474 injury prevention 458,474,791 water excessive intake 662 in fat-free mass 346,348 ingestion, during exercise 200 loss 190 for mass participation events 661-662 pathogen transmission 658 purification/sterilization 658 requirements 419

temperature for biathlons 872-873 thermal conductivity 27,292 vapour pressure at skin 261 see also fluid water immersion 292 body fat and insulation 292-293, 293 heat conductance 292 heat transfer coefficient 265 hypothennia risk 261,266 survival time by temperature 292 see also swimming and swimmers watts 6 weight child athletes 514 energy expenditure importance 700 excess, injury risk 468 gain, maternal 538 hydrostatic 826 loss critical levels 362 exerciserole in obesity 574,698 risk of extreme leanness 362 weightlifting 350,409 weight training, elderly 560 Weil-Blakesley conchotome 342, 343 Western blotting 338,340 wet bulb globe temperature (WBGT) 287 wetsuit 872,873,885 wheelchair athletes adapted toilet facilities 662 ergometers 278,278 mass participation events 662 maximal oxygen intake 34 training 579 whitewater canoeing 888,889,893 wilderness trips 663-664 wind, velocity and skiing 855 wind chill 291-292,294 wind chill index (WCI) 291 wind resistance cycling speeds 279,280 at high altitudes 614-615 wind speed/direction 253,291 wind tunnel 279-284 W/J programme (walk/jog), elderly 558-559 Wolff-Parkinson-White syndrome 79,670 Wolff'slaw 768 women (athletes) 517-530 age, body size and physique 40 altitude training 526527 body composition 351 body fat, by sport type 353 body mass distribution 41


bone mineral density 355,357, 360-361,415,551 endurance sport needs 517-518 energy intake 202,205,410 exercise and benefits 693 fat-free mass 354-355,355 hockey 921,922924 injuries 465-466 intrinsic factors predisposing 465-466 iron losses 425 left ventricle size 7 5 7 6 nutritional modification 525-526 in Olympic Games 517 overtraining avoidance 527-528 overuse injuries 466 performance relationship 522-525 economy of movement 524 gender differences and 523 lactate threshold 524-525 maximal oxygen intake 522-524 resistance training 526 rowers 837-838 rugby football 909-910 stress fractures 767,769 stroke volume 519,520 sudden death 678 training aerobic interval 518-519 Pace 519 periodization 527 practices to enhance 525-528 requirements 518 sustained distance 518 techniques 518-519 training-induced physiological adaptations 519-522 economy of movement 521 lactate threshold 521-522 maximal oxygen intake 5q-520 triad of disorders 769,772,774 work 5-6 of breathing 58 components in different sports 246,246 energy expenditure 248 energy relationship 6 against gravity 246,246 viscous 5-6 World Health Organization (WHO), vaccination 658 'worldloppet' 844,851 wrestlers 217,452 young athletes see adolescents; children

Z disc 159,164 zinc oxide powder 663