Editors and ContributorsPer Aagaard Team Denmark Test Center, Sports Medicine Research Unit, University of Copenhagen, Bispebjerg Steven Abramowitch Musculoskeletal Research Center, Depa
Trang 2Savio L-Y Woo
Trang 4Textbook of Sports Medicine
Trang 6Savio L-Y Woo
Trang 7© by Blackwell Science Ltd
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Trang 8Editors and Contributors, ix
Preface, xv
Introduction,
Part 1: Basic Science of Physical Activity and Sports Injuries: Principles of Training
. Cardiovascular and respiratory aspects of exercise —endurance training,
Sigmund B Strømme, Robert Boushel, Bjørn Ekblom, Heikki Huikuri, Mikko P Tulppo & Norman L Jones
. Metabolism during exercise —energy expenditure and hormonal changes,
Jan Henriksson & Kent Sahlin
. Skeletal muscle: physiology, training and repair after injury,
Michael Kjær, Hannu Kalimo & Bengt Saltin
. Neuromuscular aspects of exercise —adaptive responses evoked by strength training,
Per Aagaard & Alf Thorstensson
. Biomechanics of locomotion,
Erik B Simonsen & Paavo V Komi
. Connective tissue in ligaments, tendon and muscle: physiology and repair, and musculoskeletal
flexibility,
Peter Magnusson, Timo Takala, Steven D Abramowitch, John C Loh & Savio L.-Y Woo
. Cartilage tissue —loading and overloading,
Karola Messner, Jack Lewis, Ted Oegema & Heikki J Helminen
. Bone tissue —bone training,
Peter Schwarz, Erik Fink Eriksen & Kim Thorsen
Part 2: Aspects of Human Performance
. Recovery after training —inflammation, metabolism, tissue repair and overtraining,
Jan Fridén, Richard L Lieber, Mark Hargreaves & Axel Urhausen
. Principles of rehabilitation following sports injuries: sports-specific performance testing,
Malachy McHugh, Jens Bangsbo & Jan Lexell
v
Trang 9vi Contents
. Physical activity and environment,
Peter Bärtsch, Bodil Nielsen Johannsen & Juhani Leppäluoto
. Nutrition and fluid intake with training,
Leif Hambræus, Stefan Branth & Anne Raben
. Ergogenic aids (doping) and phamacological injury treatment,
Ulrich Fredberg, Timo Säppälä, Rasmus Damsgaard & Michael Kjær
Part 3: Physical activity: Health Achievements vs Sports Injury
. Epidemiology and prevention of sports injuries,
Roald Bahr, Pekka Kannus & Willem van Mechelen
. Exercise as disease prevention,
Ilkka Vuori & Lars Bo Andersen
. Physical activity in the elderly,
Stephen Harridge & Harri Suominen
. Exercise in healthy and chronically diseased children,
Helge Hebestreit, Oded Bar-Or & Jørn Müller
. Disabled individuals and exercise,
Fin Biering-Sørensen & Nils Hjeltnes
Part 4: Exercise in Acute and Chronic Medical Diseases
. Cardiovascular and peripheral vessel diseases,
Mats Jensen-Urstad & Kerstin Jensen-Urstad
. Exercise and infectious diseases,
Bente Klarlund Pedersen, Göran Friman & Lars Wesslén
. Osteoarthritis,
L Stefan Lohmander & Harald P Roos
. Exercise in the treatment of type and diabetes,
Hannele Yki-Järvinen & Flemming Dela
. Asthma and chronic airway disease,
Malcolm Sue-Chu & Leif Bjermer
. Amenorrhea, osteoporosis, and eating disorders in athletes,
Michelle P Warren, Jorun Sundgot-Borgen & Joanna L Fried
Trang 10Contents vii
. Physical activity and obesity,
Pertti Mustajoki, Per Björntorp & Arne Astrup
. Gastrointestinal considerations,
Frank Moses
Part 5: Imaging in Sports Medicine
. Imaging of sports injuries,
Inge-Lis Kanstrup, Hollis G Potter & Wayne Gibbon
Part 6: Sports Injury: Regional Considerations Diagnosis and Treatment
. Lower leg, ankle and foot,
Jon Karlsson, Christer Rolf & Sajkari Orava
. Knee,
Lars Engebretsen, Thomas Muellner, Robert LaPrade, Fred Wentorf, Rana Tariq, James H.-C Wang,
David Stone & Savio L.-Y Woo
. Hip, groin and pelvis,
Per Hölmich, Per A.F.H Renström & Tönu Saartok
Michael R Krogsgaard, Richard E Debski, Rolf Norlin & Lena Rydqvist
. Elbow, wrist and hand,
Nicholas B Bruggeman, Scott P Steinmann, William P Cooney & Michael R Krogsgaard
. Practical sports medicine,
Sverre Mæhlum, Henning Langberg & Inggard Lereim
. Multiple Choice Answers,
Index,
Trang 12Editors and Contributors
Per Aagaard Team Denmark Test Center, Sports Medicine Research Unit, University of Copenhagen, Bispebjerg
Steven Abramowitch Musculoskeletal Research Center, Department of Orthopaedic Surgery, University of
Lars Bo Anderson Institute of Exercise and Sports Science, University of Copenhagen, DK- N, Denmark
Arne Astrup Research Department of Human Nutrition, Royal Veterinarian and Agricultural University,
DK-F, Frederiksberg, Denmark
Roald Bahr The Norwegian University of Sport and Physical Education, Oslo, N- , Norway
Jens Bangsbo Laboratory for Human Physiology, August Krogh Institute, University of Copenhagen, DK- Ø, Denmark
Oded Bar-Or Children’s Exercise and Nutrition Centre, McMaster University, West Hamilton, Ontario,
Leif Bjermer Department of Lung Medicine, University Hospital, Norwegian University of Science and
Per Björntorp Department of Heart and Lung Diseases, University of Gothenburg, Sahlgrenska Hospital, SE-
, Sweden
Robert Boushel Department of Exercise Science, Concordia University, Montreal, Quebec, CAN-H B R, Canada
Stefan Brauth Department of Medical Sciences, Uppsala University Hospital, SE- , Sweden
Jens Ivar Brox Department of Orthopaedics, Section for Physical Medicine and Rehabilitation, Rikshhospitalet,
Nicholas Bruggeman Department of Orthopaedic Surgery, Mayo Clinic, Rochester, MN , USA
William P Cooney Department of Orthopaedic Surgery, Mayo Clinic, Rochester, MN , USA
Rasmus Damsgaard Copenhagen Muscle Research Centre, Rigshospitalet, Copenhagen, DK- Ø, Denmark
Richard E Debski Musculoskeletal Research Center, University of Pittsburgh Medical Center, Pittsburgh, PA
, USA
Flemming Dela Department of Medical Physiology, Panum Institute, University of Copenhagen, DK- N, Denmark
ix
Trang 13x Editors and Contributors
Bjorn Ekblom Department of Physiology and Pharmacology, Karolinska Institute, University of Stockholm,
SE-, Sweden
Lars Engebretsen Department of Orthopaedic Surgery, University of Oslo, Ullevål Hospital, NO- , Norway
Erik Fink Eriksen Department of Endocrinology, Aarlus University Hospital, DK- C, Denmark
Ulrich Fredberg Department of Medicine, Silkeborg Central Hospital, DK- , Denmark
Jan Fridén Department of Hand Surgery, Sahlgrenska University Hospital, SE- , Göteborg, Sweden
Joanna L Fried Department of Obstetrics and Gynaecology, Columbia University, New York, NY , USA
Göran Friman Department of Medical Services, Section of Infectious Diseases, Uppsala University Hospital,
SE-, Sweden
Wayne Gibbon Department of Sports Medicine, University of Leeds, LS NL, UK
Leif Hambraeus Department of Medical Sciences, Nutrition Unit, Uppsala University, SE- , Sweden
Mark Hargreaves Department of Exercise Physiology, School of Health Sciences, Deakin University, Burwood,
Steve Harridge Department of Physiology, Royal Free & University College Medical School, London, NW PF, UK
Helge Hebestreit Pneumologie/Sportsmedizin, Universitäts-Kinderklinik, Würzburg, DE- , Germany
Heikki Helminen Department of Anatomy, University of Kuopio, FIN- , Finland
Jan Henriksson Department of Physiology and Pharmacology, Karolinska Institute, University of Stockholm,
SE-, Sweden
Nils Hjeltness Department of Spinal Cord Injury, Sunnaas Hospital, Nesoddtangen, Norway
Per Hölmich Department of Orthopaedic Surgery, Amager Hospital, University of Copenhagen, DK- S, Denmark
Heikki V Huikuri Department of Medicine, Division of Cardiology, University of Oulo, FIN- , Finland
Kerstin Jensen-Urstad Department of Clinical Physiology, Karolinska Hospital, Stockholm, SE- , Sweden
Mats Jensen-Urstad Department of Cardiology, Karolinska Hospital, Stockholm, SE- , Sweden
Norman L Jones Department of Medicine, McMaster University, Hamilton, Ontario, CAN-L N Z, Canada
Hannu Kalimo Department of Pathology, Turko University Hospital, Turko, FIN- , Finland
Pekha Kannus Accident and Trauma Research Center, UKK Institute, Tampere, FIN- , Finland
Inge-Lis Kanstrup Department of Clinical Physiology, Herlev Hospital, University of Copenhagen, DK- , Denmark
Jon Karlsson Department of Orthopaedics, Sahlgrenska University Hospital/Östra, Gothenburg, SE- , Sweden
Albert I King Bioengineering Center, Wayne State University, Detroit, MI , USA
Trang 14Editors and Contributors xi Michael Kjær Sports Medicine Research Center, University of Copenhagen, Bispebjerg Hospital, Copenhagen,
Pavo Komi Department of Biology of Physical Activity, University of Jyväskylä, FIN- , Finland
Michael Krogsgaard Department of Orthopaedic Surgery, Bispebjerg Hospital, University of Copenhagen,
DK- NV, Denmark
Henning Langberg Sports Medicine Research Unit, Bispebjerg Hospital, Copenhagen, DK- NV, Denmark
Robert F La Prada,Sports Medicine and Shoulder Divisions, Department of Orthopaedic Surgery, University of
Juhani Leppäluoto Department of Physiology, University of Oulo, FIN- , Finland
Ingard Lerein Department of Orthopaedic Surgery, Region Hospital of Trondhjem, NO- , Norway
Jack Lens Department of Orthopaedic Surgery, University of Minnesota, MN , USA
Jan Lexell Brain Injury Unit, Neuromuscular Research Laboratory, Department of Rehabilitation, Lund
Richard L Lieber Department of Orthopaedics and Bioengineering, University of California and V.A Medical
John C Loh Musculoskeletal Research Center, Department of Orthopaedic Surgery, University of Pittsburgh ical Center, Pittsburgh, PA , USA
Med-Stefan Lohmander Department of Orthopaedics, University Hospital, Lund, SE- , Sweden
Sverre Mæhlum Norsk Idrettsmedisinsk Institutt (NIMI), University of Oslo, NO- , Norway
Peter Magnusson Team Denmark Test Center, Sports Medicine Research Unit, University of Copenhagen,
Willem van Mechelen Department of Social Medicine, Vreie Universität, Amsterdam, NL- , The Netherlands
Karola Messner Department of Neuroscience and Locomotion, Division of Sports Medicine, Faculty of Health
Malachy McHugh Nicholas Institute of Sports Medicine and Athletic Trauma, Lenox Hill Hospital, New York,
Frank Moses Gastroenterology Service, Walter Reed Army Medical Center, Washington DC, -, USA
Thomas Muellner Department of Orthopaedic Surgery, University of Vienna, Austria
Jørn Müller Department of Growth and Reproduction, Rigshospitalet, University of Copenhagen, DK- Ø, Denmark
Pertti Mustajoki Department of Medicine, Helsinki University Central Hospital, FIN- , Finland
Bodil Nielsen Johansen Institute of Exercise and Sports Science, August Krogh Institute, University of
Rolf Norlin Linköping Medical Center, SE- , Linköping, Sweden
Trang 15xii Editors and Contributors
Ted Oegena Department of Orthopaedic Surgery, University of Minnesota, MN , USA
Sakari Orava Tohturitalo Hospital, Turka, Fin- , Finland
Bente Klarlund Pedersen Finsencentret, Department of Infectious Diseases, University of Copenhagen,
DK-Ø, Denmark
Hollis Potter Department of Radiology and Imaging, Hospital for Special Surgery, New York, NY , USA
Anne Raben Research Department of Human Nutrition, Centre for Advanced Food Studies, Royal Veterinarian and
Per Renström Section of Sports Medicine, Department of Orthopaedics, Karolinska Hospital, Stockholm,
SE-, Sweden
Christer Rolf Centre of Sports Medicine, University of Sheffield, S TA, UK
Harald Roos Department of Orthopaedic Surgery, Helsingborg Hospital, Helsingborg, SE- , Sweden
Lena Rydqvist Linköping Medical Center, SE- , Linköping, Sweden
Kent Sahlin Department of Physiology and Pharmacology, Karolinska Institute, University of Stockholm,
Peter Schwartz Department of Endocrinology, Rigshospitalet, University of Copenhagen, DK- N, Denmark
Erik Simonsen Institute for Medical Anatomy, Panum Institute, University of Copenhagen, DK- N, Denmark
Scott Steinman Department of Orthopaedic Surgery, Mayo Clinic, Rochester, MN , USA
David Stone Musculoskeletal Research Center, Department of Orthopaedic Surgery, University of Pittsburgh ical Center, Pittsburgh, PA , USA
Med-Sigmund B Strømme The Norwegian University of Sport and Physical Education, Oslo, NO- , Norway
Malcolm Sue-Chu Department of Lung Medicine, University Hospital, Norwegian University of Science and
Jorun Sundgot-Borgen Norwegian University of Sport and Physical Education, Oslo, NO- , Norway
Harri Snominen Department of Health Sciences, University of Jyväskylä, FIN- , Finland
Timo Säppälä National Public Health Institute, Helsinki, FIN- , Finland
Timo Takala Department of Biology of Physical Activity, University of Jyväskylä, FIN- , Finland
Rana Tariq Department of Radiology, Ulleval University Hospital, Oslo, N- , Norway
Kim Thorsen Department for Sports Medicine, Norrland University Hospital, Umeå University, SE- , Sweden
Alf Thorstensson Department of Sport and Health Sciences, University College of Physical Education and
Trang 16Editors and Contributors xiii Mikko P Tulppo Merikoski Rehabilitation and Research Centre, University of Oulu, FIN- , Finland
Axel Urhausen Institute of Sports and Preventitive Medicine, Department of Clinical Medicine, University of
Ilkka Vuori UKK Institute for Health Promotion Research, Tampere, FIN- , Finland
James H.-C Wang Musculoskeletal Research Center, Department of Orthopaedic Surgery, University of
Michelle Warren Department of Obstetrics and Gynaecology, Colombia University, College of Physicians and
Fred Wentort Department of Orthopaedic Surgery, University of Minnesota, Minneapolis, MN , USA
Lars Wesslén Department of Medical Sciences, Section of Infectious Diseases, Uppsala University Hospital, Uppsala, Sweden
Savio L.-Y Woo Musculoskeletal Research Center, Department of Orthopaedic Surgery, University of Pittsburgh
King H Yang Bioengineering Center, Wayne State University, Detroit, Michigan, MI , USA
Hannele Yki-Järvinen Department of Medicine, University of Helsinki, FIN- , Helsinki, Finland
Liying Zhang Bioengineering Center, Wayne State University, Detroit, Michigan, MI , USA
Trang 18In past decades the number of exercising individuals and the area of sports medicine have grown considerably.Sports medicine has developed both in terms of its clinical importance with appropriate diagnosis and adequate re-habilitation following injury as well as its potential role in the promotion of health and prevention of life-style dis-eases in individuals of all ages Furthermore, lately the medical field has gained improved understanding of the use
of physical activity as a treatment modality in patients with a variety of chronic diseases and in rehabilitation afterdisabilities, injuries and diseases Common to these advancements is the fact that a certain amount of clinical expe-rience has to be coupled with sound research findings, both basic and applied, in order to provide the best possiblerecommendations and treatments for patients and for the population in general
There is a tradition in Scandinavia for an interaction between exercise physiology and clinical medicine and gery, and it is apparent that both areas have hypotheses, inspiration and possible solutions to offer each other It istherefore apparent that a textbook on sports medicine must attempt to incorporate all of these aspects to be com-prehensive A historical or classical reference has been selected as an introduction to each chapter to reflect the im-pact that a specific scientific work has had on that field Having several authors collaborating on each chapter in thebook ensures both diversity and a degree of consensus in the text, which will hopefully make the book usable as areference book, and as a textbook both at the pre- and postgraduate levels It has been our goal to address each topicwithin sports medicine in a scientific way, highlighting both where knowledge is well supported by research, as well
sur-as aresur-as where the scientific support is minimal or completely lacking It is the intention that the book will help thepeople who work clinically within the area of sports medicine in their daily practice, and that it will also provide thebasis for further research activity within all areas of sports medicine Moreover, we wish to highlight where knowl-edge and methodologies from different, and often distant, areas can interact to create a better understanding of, forexample, the mechanisms behind development of tissue injury and its healing
The editorial group has been delighted that some of the world’s leading experts have agreed to participate in thisproject, and they have all contributed with informative and very comprehensive chapters I greatly appreciate theircontribution and that of the editorial group who worked hard on the completion of the book Additionally, I wish
to acknowledge all other contributors who have helped with the practical procedures of this project Finally, I hopethe reader of this book will share the research dreams, the clinical interest, and the enthusiasm in relation to thesports medicine topics with that of the authors and the entire editorial group
Michael Kjaer
xv
Trang 20The exercising human: an
integrated machine
Physiological boundaries have fascinated man for a
long time, and achievements like climbing up to more
than m above sea level without oxygen supply or
diving down to more than m in water without
spe-cial diving equipment are at the limit of what textbook
knowledge tells us should be possible for humans
Likewise, athletes continue to set new standards
within sports performance, and patients with chronic
diseases master physical tasks of a very challenging
nature, like marathon running, that hitherto were
thought impossible
Muscles, tendons and bone are elegantly coupled
together to provide an efficient system for movement,
and together with joint cartilage and ligaments they
allow for physical activity of various kinds In order to
provide energy to contracting muscles, ventilation
often rises –-fold and cardiac pump function can
increase up to -fold during strenuous exercise in
well-trained individuals in the attempt to deliver sufficient
oxygen to allow for relevant oxidative processes that
can be initiated within seconds In addition, working
skeletal muscles can by training achieve substantial
in-creases in their capacity to both store energy and to
ex-tract and utilize oxygen With regards to endurance
capacity, humans are still left with the fact that the size
of the heart relative to the skeletal muscle is relatively
small — even in top-class runners — compared to
basi-cally all other animal species
To drive the human machinery, local as well as
dis-tant substrate stores provide fuel for energy tion, allowing for very prolonged exercise bouts Acontrolled interplay between exercise intensity, energymetabolism and regulatory hormones takes place, andintake of different food stores can cause the muscle toadjust its fuel combustion to a large degree The initia-tion of signals from motor centers to start voluntarymovement and afferent signals from contracting mus-cle interact to achieve this and several signalling path-ways for circulatory and metabolic control are nowidentified The brain can make the muscles move, andcan at the same time use substances for fuel that are re-leased from muscle Furthermore, intake of differentfood sources can cause the muscle to adjust its fuelcombustion to a large degree
combus-Training can cause major tissue and organ tion and it is well known that this to a large degree depends upon both genetic and trainable factors(Table) More recent studies on identical twins haveallowed for a discrimination of these two factors in re-lation to exercise and have shown that between and
adapta-% of the variation in parameters like maximal oxygen uptake or muscle strength are likely to be attributed to genetic factors Rather than discouragehumans from starting training on this background, it isfascinating to identify factors responsible for trainingimprovements in, for example, muscle tissue It is evi-dent that contractile force can elicit transcription andtranslation to produce relevant changes in the amount
of contractile or mitochondrial proteins, but the derlying mechanism in both muscle and connective
Trang 21 Introduction
tissue is not understood Interestingly, substances are
now being identified (e.g mitogenactivated protein
kinases) where subtypes are differentially activated by
either metabolic stress or by the degree of contractile
stress, to cause either increased cell oxidative capacity
or muscle cell hypertrophy, respectively We are
there-fore at a point where we can begin to master the study of
the adaptation of the human body not only to acute
ex-ercise, but also to loading and overloading, and this will
provide us with prerequisites for study of the ultimate
adaptation potential that the human organism achieves,
and thereby better describe also on an individual level
why tissue becomes overloaded and injured
The delicate balance between training
adaptation and injury — the dilemma
of rehabilitation
It is important for the clinician who treats the
recre-ational or elite athlete to have a thorough
understand-ing of the injury, and also the ability of the affected
tissue to adapt to immobilization, remobilization and
training One example is the considerable plasticitythat skeletal muscle tissue displays While strength islost (up to %) rapidly within a few weeks of immobi-lization, it can be regained over the next couple ofmonths, and strength can be augmented up to -foldwith training for extended periods (months/year).Bone loss also (up to %) occurs rapidly within weeks
of immobilization and is subsequently regained in thefollowing months of rehabilitation However, some-what in contrast to muscle, extended training periodshave a relatively modest impact on bone tissue aug-mentation Connective tissue loss in tendon is alsocomparable to muscle and bone; however, in contrast,its slower metabolism requires perhaps up to months or more before complete tissue recovery from
an injury and subsequent inactivity Thus, an injurythat demands a limb to be immobilized for a givenlength of time may require different time periods forthe various tissues to return to their preinjury levels
In this context it is important for the clinician to notethat the cardiovascular system recovers the fastest after
Table The capacity of various tissues and systems, and their ability to adapt to physical activity or inactivity.
Decrease in function Increase during single Improvement or maximal load bout of physical activity with training Time required for with 3–4 weeks of Function ultimate tensile strength (%) adaptation inactivity (%)
Trang 22Introduction
a period of relative inactivity, which may create a
dilemma: the athlete wants to take the rehabilitation
and training program to new and challenging
levels, but the different tissues may not be able to
withstand the associated loads, and re-injury or a
new so-called ‘overload injury’ may result Thus,
a thorough understanding of how tissues adapt to
physical activity or lack thereof is paramount for the
effective treatment and rehabilitation of the injured
person
While acute injury during exercise may intuitively
be somewhat easy to understand, it may be more
chal-lenging to grasp the insidious and frequent ‘overuse’
injuries that occur with training Some important
observations in the field of sports medicine have been
made in recent decades that have improved our
under-standing of these injuries An awareness of the
sub-ject’s loading pattern is important, of course The
recreational athlete who runs km/week may subject
each lower limb to approximately landings and
take-offs in that time period In contrast, the long
dis-tance runner who runs km/week may subject each
lower limb to approximately landings and
take-offs Clearly, a certain degree of appropriate tissue
adaptation has already taken place to withstand these
vastly different loads, but nevertheless, injuries may be
sustained by both the recreational and elite athlete and
therefore remains an enigma Interestingly, the weekly
loading of tissue induced by sports participation is
equivalent to that established by national authorities
as the upper limits for what is tolerable for manual
labour, suggesting that perhaps there is an inherent
tissue limitation to loading
Disadvantageous alignment, like severe pes planus
or genu valgus, for example, may be important factors
in determing who can withstand a given loading
pat-tern, although such internal factors cannot entirely
ex-plain overuse injury It has become generally accepted
that it takes appreciable time for tissues like connective
tissue to adapt to a new or increasing demand, even for
the most genetically fortuitous Therefore, any desired
progression or change in a training program should be
gradual However, more detailed information with
re-spect to the training frequency, duration and intensity
that is required to avoid an injury is currently
lack-ing, and thus preventative efforts in this respect remain
difficult At the same time, it is becoming increasingly
appreciated that tissues need restitution periods
to ‘adapt’ to the previous bout of physical activity This is put into practice, for example, by the tri-athletewho loads the cardiovascular system considerably
on a daily basis, but stresses the musculo-skeletal system alternately by training either cycling, running
or swimming, which may help to avoid injury It is during the restitution period that tissues are allowed
to recover, or further adapt to an increasing demand
by either expanding their quantity or improving theirquality It is likely that in years to come researchers will furnish new and improved measurement techniques that will yield important detailed informa-tion about tissue adaptation to physical activity andrestitution
Sports injuries and development of treatment: from recreational sports
to elite athletes
In many situations the transformation from overloadsymptoms to a sports injury is poorly defined and understood Intensified research in anatomy, bio-chemistry, physiology and mechanisms of tissue adaptation to mechanical loading is needed to providethe basic understanding of overload injury pathogene-sis Although this in itself represents a paramountchallenge, it seems even more difficult to understand
an individual’s disposition for developing symptoms.Why does one individual develop severe Achilles tendon pain in connection with a certain amount ofrunning, while others do not? Why are overhead activ-ities very painful for some athletes but not for others?Why is the functional stability of a cruciate ligamentdeficient knee or a mechanically unstable ankle jointdifferent between persons despite the same activitylevel? Obviously it would be essential to identify theweakest link in each individual case, but knowledge ofthe individual specific factors is very incomplete.Could there be physiologically different levels for initiation of symptoms in different individuals? It
is well known that persons with decreased sensory puts, for example caused by diabetic polyneuropathy,have a high rate of overload injuries like tendonitis
in-or stress fractures, simply because the natural alarmsystem is out of order If a physiological difference in,for example, the threshold of sensory inputs exists
in otherwise healthy people, the difference between a
Trang 23 Introduction
mechanical load that causes symptoms and one that
results in tissue damage would vary from person to
person
Treatment of sports injuries represents major
chal-lenges First, the aim to reduce symptoms is demanded
by the athlete, and several pharmacological treatments
will work well at rest, but will not provide pain relief
when the individual is exercising Secondly, when
surgical treatment is indicated to repair irreversible
changes of tissues (e.g rupture of anterior and
poste-rior cruciate ligaments of the knee) or to change
bio-mechanical inferior or insufficient movement patterns
(e.g multidirectional instability in the shoulder) the
procedures need to be minimally invasive in order to
leave the remaining tissue as intact as possible and to
allow for a quick regeneration process Thirdly, the
re-habilitation procedures and time allowed for recovery
will be challenged This is because athletes are eager to
return to their sports In this aspect, similarities can be
drawn to occupational and rehabilitation medicine,
which aims towards getting the patient back to the
functional level that is required to perform a certain
labour task
In contrast to the little which is known about the
in-dividual-based factors, there is increasing knowledge
about injury mechanisms in athletic performance
A number of specific pathological entities have been
recognized, especially during the past two decades, e.g
secondary impingement and internal impingement of
the shoulder in overhead athletes On the basis of
rec-ognizing certain common patterns of injury and
un-derstanding their pathogenesis, specific treatments —
surgical as well as nonsurgical — have been developed
Probably the first injury to be recognized as a specific
lesion connected to sports performance was the
Bankart lesion of the shoulder, described in , and
the way to repair the lesion was obvious once the
pathoanatomical background was established
Simi-larly, when the SLAP lesion of the labrum in the
shoul-der was described for the first time about years ago,
the surgical treatment options could be defined (for
further details see Chapter 6.5)
Arthroscopy, which was introduced for knee
disor-ders back in and developed for the treatment
of shoulder, elbow and ankle disorders in the s,
has made direct visualization of joint movement and
intra-articular structures possible, and has increased
the understanding of many intra-articular sports juries For the individual athlete it has resulted in amuch more specific diagnosis and treatment, and con-sequently rehabilitation has become faster and easierthan after open surgery Furthermore, the inventionand development of magnetic resonance imaging inthe early s, and the refinement and general avail-ability of ultrasound investigation during the late
in-s, has increased the spectrum of diagnostic toolssignificantly What still requires specific attention isthe relative use of these para-clinical supplements ascompared with a good clinical examination and judge-ment There is no doubt that the new ‘machine-tools’,developed to help the sports medicine practitioner,tend to be ‘over-used’ in the initial phase, which isoften followed by a more balanced phase in which it be-comes evident that patient history and clinical exami-nation can never be replaced by para-clinical tools, butthat the latter provides a fruitful supplement in theprocess of diagnosis in sports medicine
The collection of clinical information on matic conditions in athletes can lead to identification ofuniform patterns and logically based treatment modal-ities Series of treated patients can also give informa-tion about the success rate of certain treatments,whereas only randomized studies can identify the besttreatment strategy in a specific condition Unfortu-nately, there are very few randomized studies in sportsmedicine and especially within traumatology This isoften due to a high demand for treatment to ensure fastrecovery and return to sports participation, and it isunlikely that more than a small part of the surgical andnonsurgical treatment modalities will ever be evalu-ated by randomized studies Even though more than
sympto-anterior cruciate ligament (ACL) reconstructionsare performed every year in the USA, it is unknownwhich treatment strategy is the most advantageous.There are different factors influencing the decision toperform ACL reconstruction: the chance to get back tosports, prevention of secondary meniscus and carti-lage injury, prevention of giving-way or subluxationepisodes, risk for anterior knee pain or other operativecomplications, or timing of surgery There is no evi-dence for how these factors should be weighted, and it
is unknown if routine reconstruction in all patientsshortly after an ACL injury would reduce the risk oflate complications and increase activity level better
Trang 24Introduction than a more conservative approach with rehabilitation
as primary treatment It is very important to perform
randomized trials at the same time as new treatments
are introduced, as it is almost impossible to return to
such studies later
Most rehabilitation programs are based on
individ-ual, clinical experience and theoretical principles Just
as with surgical treatment, evidence is still lacking on
the effect of a number of general treatment principles
Rehabilitation is very costly, and it is desirable with
further development of evidence-based rehabilitation
strategies
New technologies will probably influence the
treat-ment of sports injuries in the near future Local
avail-ability of growth factors may reduce repair and
remodelling time after injury or surgery Scaffolds can
be used to introduce a specific architecture These
can be taken over by living tissue, and in combination
with controlled gene expression, injured tissue can
possibly be restored completely This will contribute to
an avoidance of reconstruction with replacement
tis-sue and accompanying suboptimal recovery, as well
as ensure the absence of scar tissue otherwise seen in
repair
In the recreational athlete, many overload
condi-tions are often self-limiting Nature’s alarm system
works: overloading of tissues often results in
symp-toms (pain) long before irreversible changes of the
tis-sue structures happen With a gradual reduction of
activity, symptoms and overloading disappears, and
the athlete can resume normal activity again Tennis
elbow is a good example of this mechanism During
one season about % of middle-aged persons
per-forming recreational racquet sports will experiencesymptoms of tennis elbow The majority of these casesresolve without specific treatment The interestingphenomenon is, why humans often carry on with exer-cise despite symptoms and signs of overuse Interest-ingly, inflammatory reactions within and aroundtendons are seen in humans and in a few animal speciesthat are forced to run like race-horses, whereas almostall other species (like mouse, rat or rabbit) do not showsigns of tendinitis or peritendinitis despite strenuousactivity regimens Elite athletes can be motivated tocontinue peak performance despite pain or othersymptoms, and it can be difficult or impossible for thenatural repair processes to take place Not enough isknown about tissue repair and rehabilitation to definethe maximum activity in each individual that is com-patible with a full and fast repair
The boundary between trivial, reversible conditionsand irreversible, disabling injuries still has to be de-fined in many sports As an example, there is an ongo-ing discussion about the risk for chronic brain damages
in boxing Furthermore, nearly nothing is knownabout the long-term effect of continued elite sports ac-tivity on degenerative changes in the knee after ACLreconstruction With this lack of evidence about physical consequences of sports injuries, ethical con-siderations have a central place in advice and planning.The influence of psychological factors such as compe-tition (matches only take up less than % of the activeplaying time in elite handball, more than % of theACL injuries happen there), self-confidence and ac-ceptance of personal limits have to be acknowledgedand further knowledge is warranted
Table Motivation and needs in different individuals with physical training.
Performance Disease-effect Prevention Guidelines for Tolerable amounts motivation motivation motivation training of training Patient + + (function) + + + + + + + + +
Recreational sports + – + + + + + + +
Elite athletes + + + (competition) – (+) + + + + + +
The motive for performing physical training can primarily be based upon a wish of increased performance either in sports or in everyday life,
or be related to a wish of increased health and disease prevention.All three groups of individuals display an individually varying degree of which for achieving mental well-being in relation to exercise.The tolerable amount of training depends on the ability of the body to
withstand loading and varies therefore significantly between athletes and patients, whereas both patients and athletes share a large request for specific guidelines in relation to the training they perform.
Trang 25 Introduction
Regular physical training: benefits
and drawbacks
For more than years, systematic exercise or sports
have been carried out worldwide, and one can easily
consider the average individual living today as being
much more inactive than they were in the past It is
be-coming more and more scientifically documented that
physical inactivity is a major risk factor for disease and
premature death, and that the magnitude of this lies on
the level of other risk factors like smoking, obesity or
drinking Studies have uniformly concluded that
being active or beginning physical activity even at an
advanced age, will positively influence risk factors for
development of inactivity-associated diseases In spite
of the fact that acute training is associated with a
tran-sient increased risk of cardiac arrest, taken in the
population as a group, as well as the costly treatment of
sports injuries, socio-economic calculation has found
that, for the recreational athlete, these drawbacks are
far outweighed by the cost-saving benefits of physical
training such as lower incidence of diseases, faster
hospital recovery after disease in general, as well as a
lower frequency of infection and time away from work
due to sickness The field of sports medicine is
there-fore facing a major challenge in improving the level
of physical activity in the general population, and for
setting up overall guidelines
Physical training and patients with
chronic diseases
Acute and chronic diseases are associated with both
organ specific manifestations as well as by more
gen-eral disturbances in function due to physical inactivity
and sometimes even additional hormonal and
cytokine-related catabolism In general, physical
training can counteract the general functional
distur-bances, and maybe even affect or prevent the primary
manifestations of disease It is important to note that
the motivational aspects, as well as the requirements
for supervision and guidelines, in the patient with a
present disease differ markedly from healthy
exercis-ing individuals (Table)
In principle, most diseases can be combined with a
certain degree of physical activity, but the amount of
restrictions put upon the patient differs considerably
between diseases (Table) Certain diseases have been
shown to be influenced greatly from physical activity
Table Effects of physical training upon different diseases.
Diseases in which physical training will act preventively in disease development and positively upon primary disease manifestations
Ischemic heart disease Recovery phase of acute myocardial infarction Hypertension
Type-2 diabetes Obesity (most pronounced with respect to prevention) Osteoporosis
Age-related loss of muscle mass (sarcopenia) Osteoarthritis (most likely only the prevention) Back pain
Cancer (prevention of colon and breast cancer) Depression and disturbed sleep pattern Infectious diseases (prevention of upper respiratory tract infection)
Diseases in which moderate or no direct effect can be demonstrated upon the primary disease manifestations, but where exercise will positively affect both health associated risk factors and the general disturbances in overall body function
Peripheral vascular diseases (arterial insufficiency) Type-1 diabetes
Bronchial asthma Chronic obstructive lung disease Chronic kidney disease Most forms of cancer Most acute and chronic liver diseases Rheumatoid arthritis
Organ transplanted individuals Spinal cord injured individuals Most neurological and mental diseases
Diseases in which much caution has to be taken or where exercise is to be discouraged, and where physical training often can have a worsening effect upon primary disease manifestations or may lead to complications
Myocarditis or perimyocarditis Acute heart conditions (e.g unstable angina, acute AMI, uncontrolled arrhythmia or third degree AV-block) Acute infectious diseases associated with fever (e.g upper respiratory tract infection)
Mononucleosis with manifest splenomegaly Aorta stenosis (chronic effect)
Acute severe condition of many diseases mentioned above (e.g severe hypertension, ketoacidosis in diabetes) Acute episodes of joint swelling (e.g rheumatoid arthritis) or severe muscle disease (e.g myositis)
Trang 26Introduction (e.g ischemic heart disease, type- diabetes), whereas
other diseases are known to be relatively insensitive to
exercise when it comes to primary disease
manifesta-tions (e.g chronic lung disease, type- diabetes) In the
later group of diseases, it should, however, be noted
that physical training can still have a beneficial effect on
health-related parameters that can be achieved by
indi-viduals in general This effect is achievable even in the
absence of any worsening of the primary chronic
dis-ease This emphasizes the importance of also
encour-aging individuals with chronic (and not necessarily
fatal) diseases to train on a regular basis from a general
health perspective In addition, almost all diseased
in-dividuals can exercise in order to counteract the
gener-al loss in function that their disease-related inactivity
has caused In very few cases, extreme caution has to be
taken when performing exercise (e.g acute infectious
diseases) (Table)
In spite of current knowledge of the effect of
physi-cal training on diseases, the exact mechanisms behind
this are still only partially described To find such
bio-chemical and physiological pathways will be tant not only for addressing which type and dose ofphysical training should be prescribed for the indivi-dual patient, but also for identifying more general
impor-‘health-pathways’ by which muscular contractions caninfluence the health status of the individual Especially
in relation to disease, the influence of training on suchpathways either by itself or in combination with phar-maceutical drugs will potentially play a role in treat-ment of disease and maintenance of health into old age.Specific identification of health-related pathways inour genes will furthermore provide insight into the ge-netic polymorphism and help to explain the interindi-vidual variation in training responses and health-related outcome of these Evidently, this will also openpossibilities for genetic treatment of inherited disor-ders with regards to tissue and organ adaptability totraining, and at the same time inadvertently provide opportunities for misuse of gene therapy in relation
to doping, a question that will challenge the sportsmedicine field ethically
Trang 28Part 1
Basic Science of Physical Activity and Sports Injuries: Principles of Training
Trang 30Classical reference
Krogh, A, Lindhard, J The regulation of respiration
and circulation during the initial stages of muscular
work J Physiol (Lond ) 1913; : –.
This paper demonstrated changes in respiration and
heart rate with the transition from rest to bicycle
exer-cise The investigators did experiments on themselves,
and Fig .. shows the changes in tidal air and heart
rate at the onset of exercise As will be noted, a very
rapid increase in both ventilation and heart rate was
observed, and this led to the conclusion that motor
center activity in parallel with activation of skeletal
muscle caused an increased stimulation of respiratory
centers as well as the heart This was called cortical
irradiation, and has later been referred to as central
command or feed-forward, and has become an
impor-tant topic in the discussion of respiratory, circulatory,
and hormonal changes during exercise
Cardiovascular adaptation
Cardiac output
The pumping capacity of the heart is a critical
deter-minant of endurance performance in exercise events
such as running, cycling, rowing, swimming, etc.,
where a large fraction of total body muscle mass is
con-tracting dynamically Because of the large dependence
on oxidative metabolism for the total energy turnover
in exercise activities sustained for longer than min,
performance level is, as will be discussed later, largelydependent on the capacity for O2delivery, and thus onthe magnitude of maximal cardiac output
Maximal aerobic power ( 2 max) is a classic ure of the capacity to perform endurance exercise, andmay be described physiologically as the product ofcardiac output and the extraction of O2by muscle Foralmost a century it has been recognized that a linear relationship exists between maximal oxygen uptakeand cardiac output, and this relationship is also observed in other species [–] It is estimated that
meas-–% of the interindividual difference in V˙ 2 maxis
˙
V
Chapter 1.1 Cardiovascular and Respiratory Aspects of Exercise — Endurance Training
S I G M U N D B S T R Ø M M E , RO B E RT B O U S H E L ,
B J Ø R N E K B LO M , H E I K K I H U I K U R I ,
M I K KO P T U L P P O & N O R M A N L J O N E S
Fig .. A recording of the tidal air on a spirometer
(constructed by Krogh) at rest and at the beginning of exercise.
Trang 31 Chapter .
attributable to the level of maximal cardiac output []
Looked at another way, during whole body exercise,
only ~–% of maximal mitochondrial respiratory
capacity is exploited because of the limits of O2
delivery [–] Endurance training augments skeletal
muscle oxidative capacity and O2extraction, but the
principal variant for improvements in 2 maxis
maxi-mal cardiac output [–] (Fig ..)
On the other hand, differences in athletic
perform-ance amongst competitive athletes with similar 2 max
are linked to peripheral mechanisms [], such as
running economy The basic question as to what limits
maximal aerobic power ( 2 max) will be discussed later
in this chapter
Cardiac structure
The increase in maximal cardiac output (Qmax)
follow-ing endurance trainfollow-ing results from a larger cardiac
stroke volume (SV), whereas maximal heart rate
(HRmax) is unchanged or even slightly reduced While
heart size is a function of total body size as well as
genetic factors, the higher SV achieved by endurance
training is attributed to enlargement of cardiac
cham-ber size and to expansion of total blood volume
[] On the basis of cross-sectional studies in both
There is a close relationship between cardiac volume and physical performance [] However, thecardiac hypertrophy is dependent on the type of sportcarried out There are two main types of myocardialhypertrophy In weight lifters and other strength-training athletes heart wall thickness is increased, withonly minor increases in heart cavity diameters, whileendurance athletes have increased heart volume andcavity diameter with a proportional increase in wallmuscle thickness [] The ratio of wall thickness
to cavity diameter is unchanged in the trained individual but increased as a result of strengthtraining []
The left ventricular hypertrophy in the trained individual is due to volume overload (‘eccen-tric’ hypertrophy), while the hypertrophy due tostrength training develops as a consequence of pres-sure overload (‘concentric’ hypertrophy) Rowing, for
Fig .. Relationship between increases
in cardiac output and maximal oxygen uptake in heart failure patients (circles), healthy males after days’ bedrest (squares), the same subjects before bedrest (inverted triangle), the same subjects after endurance training (upright triangle), and endurance athletes (diamonds).
Trang 32Cardiovascular and Respiratory Responses to Exercise instance, represents a mixture of volume and pressure
overloading In the former sarcomeres are added in
series to increase cavity diameter, while in the latter
sarcomeres are mainly added in parallel, causing wall
thickening [] Both these are reversible processes
since deconditioning from elite sport reduces cardiac
size and volume towards what is normal for age
and gender [] The cardiac morphology of the
female athlete heart is the same as in men but the
dimensions are in general smaller [] Structural and
functional echocardiographic indices characterizing
the normal limits of the athletic heart are shown in
Table ..
Whether or not cardiac hypertrophy (‘athlete’s
heart’) predisposes the athlete to future cardiac
prob-lems has been discussed for many years [,]
How-ever, the number and severity of cardiac arrhythmias
seem to be the same in young athletes compared to
un-trained individuals of the same age and gender [],
but increased in active elderly athletes [] However,
a fast regression of ventricular hypertrophy through
physical inactivity may cause some temporary increase
in the number of arrhythmias []
Functional adaptations
In addition to structural adaptations, endurance ing produces functional improvements in cardiac per-formance during exercise [] Most notable is a morerapid early and peak ventricular filling rate during diastole An enlarged blood volume, together withgreater ventricular compliance and distensibility, and afaster and more complete ventricular relaxation areimportant factors allowing stroke volume to increaseeven at high heart rates during exercise [,] Im-proved myocardial relaxation allows for a more rapidlowering of ventricular pressure, optimizing the leftatrial/ventricular pressure gradient for enhanced fill-ing [] At the same time, the cardiac output is distrib-uted more selectively to activated regions of skeletalmuscle, from where the muscle pump facilitates ve-nous return As a result of an enlarged end-diastolicvolume, left ventricular systolic performance is improved mainly by way of the Frank–Starling mechanism []
train-During submaximal exercise, myocardial work and
O2consumption are reduced in those who are durance trained due to a lower heart rate at a given cardiac output as well as a reduced afterload attributa-ble to lower peripheral resistance [] The enhanceddiastolic filling and reduced afterload ensure thatstroke volume is maintained or even progressively in-creased from submaximal to maximal exercise [], ascompared to the sedentary person whose stroke vol-ume plateaus at submaximal intensities and may fall asmaximal exertion is approached []
en-Myocardial vascularization and perfusion
In a comparison of the cross-sectional area of proximalcoronary arteries from endurance-trained and seden-tary humans it has been suggested that coronary vascu-lar volume may be increased by training [] Itremains unresolved whether in humans endurancetraining increases coronary vascular dimensions be-yond the vascular proliferation that accompanies normal training-induced cardiac hypertrophy On thebasis of studies in rats, endurance training has beenshown to increase myocardial capillary density ex-pressed as capillary/fiber ratio [] However, in largeranimals, there is little evidence for increased capillaryproliferation per fiber, nor is there evidence for proli-
Table .. The upper normal healthy limits of cardiac
dimensions associated with exercise training From Urhausen
& Kindermann, Sports Med; : –.
Men Women
LV mass/V·O2 max(g.min/L) 80 80
flow velocity
Left atrium thickness (mm) 43 (47a) 43 (45a)
*Hypertrophic index (%) = septum + LV thickness (mm)/LVED
diameter (mm).
Trang 33 Chapter .
feration of collateral coronary vessels in the healthy
non-ischemic heart
Commensurate with the reduction in myocardial
work and O2consumption at rest and during
submaxi-mal exercise after endurance training, coronary blood
flow per unit myocardial mass is reduced []
How-ever, studies in animals have shown that endurance
training can increase maximal coronary perfusion per
unit mass of the myocardium [] There are only
modest increases in myocardial O2extraction from rest
to maximal exercise since extraction is very high even
in the untrained state However, there is evidence that
exercise training elicits changes in vascular tone
lead-ing to an optimized distribution of blood flow, whereby
more capillaries are recruited without a change in
cap-illary density [,] This is probably due to specific
endothelium-mediated vasodilatation Results from
animal studies suggest that increased endothelial cell
nitric oxide synthase, an enzyme that synthesizes
nitric oxide from -arginine, contributes to such an
adaptation [,]
Heart rate
At the beginning of dynamic exercise, heart rate
in-creases rapidly due to the inhibition of
parasympa-thetic tone If the exercise is light (heart rate <
beats/min), the sympathetic activity applied to the
heart and the vasculature does not increase and
tachy-cardia occurs solely due to the reduction in
parasympa-thetic tone [] As the workload increases, heart rate
increases due to further vagal withdrawal and
con-comitant sympathetic activation (Fig ..) []
The increase in sympathetic activation may be due
to arterial baroreflex resetting, the muscle
metabore-flex or muscle mechanoreceptor activation []
Dur-ing heavy exercise, parasympathetic activity wanes and
sympathetic activity increases in such a way that, at a
workload corresponding to maximal oxygen
consump-tion, little or no parasympathetic tone remains []
The analysis of heart rate variability (HRV) has
be-come a frequently used tool for providing information
on cardiovascular autonomic regulation at various
phases of exercise, and also on the effects of physical
training on cardiovascular autonomic regulation The
most commonly used HRV methods are time and
frequency domain analysis techniques The standard
deviation of all normal-to-normal R–R intervals over
an entire recording (SDNN) is a simple time domainmethod This variable is considered to reflect bothparasympathetic and sympathetic influences on theheart The power spectrum of R–R intervals reflectsthe amplitude of heart rate fluctuations present at different oscillation frequencies The different powerspectral bands reveal different physiologic regulatorymechanisms; e.g an efferent vagal activity is a majorcontributor to the high frequency component (see Fig
..)
A distinct cardiovascular adaptation to endurancetraining is a lowering of the heart rate at rest and during submaximal exercise Maximal heart rate is unchanged or in some cases may be slightly reduced.The lowering of resting and submaximal heart rate ismediated by alterations in the autonomic nervous sys-tem, and by changes in the intrinsic automaticity of thesinus node and right atrial myocytes [,]
Both cross-sectional and longitudinal studies involving pharmacologic autonomic blockade andanalysis of HRV indicate that increases in cardiacparasympathetic (vagal) tone make an important con-tribution to resting bradycardia [,] The chronicincrease in parasympathetic tone occurs within a fewweeks after beginning regular training and this occursindependently of a lower intrinsic heart rate In cross-sectional studies, aerobic fitness and/or long-term
Sympathetic ef
fect
Fig .. Schematic diagram showing the relative
contributions of the sympathetic and parasympathetic systems
to cardioacceleration at various levels of exercise Comparisons are between the control state (broken line) and parasympathetic
or sympathetic blockade (Modified from [ ].)
Trang 34Cardiovascular and Respiratory Responses to Exercise
aerobic training have been suggested to be associated
with increased HRV, especially with vagally mediated
respiratory sinus arrhythmia, at rest [,] Some
studies, however, have failed to show such an
association [,] The results from most
longitudi-nal studies reveal decreased resting heart rate and
in-creased vagal activity at rest after aerobic training
[,]
During exercise in the trained, a given increase in
cardiac output requires less increase in heart rate due
to the maintenance of a larger stroke volume Studies
focusing on autonomic and endocrine responses to
training indicate that heart rate is reduced during
sub-maximal exercise (absolute load) in the trained due to a
lower intrinsic heart rate, a reduction in sympathetic
activity and circulating catecholamines, and a greater
parasympathetic influence [,,] Tulppo and
col-leagues [] found that higher levels of physical fitness
were associated with an augmentation of cardiac vagal
function during exercise, whereas aging resulted in
more evident impairment of vagal function at rest
The lower sympathetic activity to the heart at a given
submaximal work rate stems in part from diminished
reflex signals originating from skeletal muscle due to
less metabolite accumulation and attenuated discharge
of metaboreceptors []
The mechanisms underlying the training-inducedincrease in vagal tone are thought to be greater activa-tion of the cardiac baroreceptors in response to the enlargement of blood volume and ventricular filling[,], as well as changes in opioid [] and dopamin-ergic modulation of parasympathetic activity [] It isnot fully resolved whether a lowering of intrinsic heartrate is a true adaptation to endurance training, but itappears that an intensive and lengthy training periodmay be necessary for this adaptation [] Primateswith larger hearts have lower intrinsic heart rates and ithas therefore been hypothesized that training-inducedcardiac enlargement accounts for the lower intrinsicheart rate with training A plausible mechanism for reduced intrinsic heart rate is that atrial enlargementreduces the stretch–depolarization stimulus, andthereby alters resting automaticity
Blood pressure
There is general agreement that endurance trainingelicits small reductions in resting blood pressure[,] In addition, long-term exercise training hasthe beneficial effect of preventing the normal age-related increase in blood pressure A pressure-lowering effect of endurance training has been shown
to occur within days after initiating an exercise
Fig .. Representative examples of
R–R interval tachogram (a) and
corresponding power spectra (b) and
two-dimensional vector analyses of
Poincaré plot (c) at rest ( min
recording).
Trang 35 Chapter .
program [] Reduced adrenal medullary
cate-cholamine output during exercise at a given absolute
work rate may be of importance for the blood pressure
lowering effect of training, as well as changes in
sym-pathetic and renal dopaminergic activity
The reduction in resting diastolic blood pressure
with training is significantly related to the increase in
exercise capacity, which suggests that high-intensity
training may be important Attention is currently
fo-cused on determining the effectiveness of various
training regimens which induce both reductions in
resting blood pressure and significant improvements
in functional capacity During exercise at a given
sub-maximal load, blood pressure and vascular resistance
are reduced after endurance training This adaptation
is associated with reduced sympathetic activation and
lower circulating catecholamines At high exercise
in-tensities and at maximal exercise, blood pressure is
generally similar before and after training Yet a given
blood pressure is achieved by a lower vascular
resist-ance and a higher cardiac output in the endurresist-ance
trained
Blood volume
Blood volume (BV) is kept remarkably constant in
many different situations and hyper- and hypovolemia
are corrected fairly rapidly through the mechanism of
renal absorption of sodium Cross-sectional studies
show that there is a close relationship between 2 max
on the one hand and BV and total amount of
hemoglo-bin (but not the hemoglohemoglo-bin concentration [Hb]) on
the other Exercise training increases blood volume
Plasma volume usually increases after a few days of
training, while the expansion of erythrocyte volume
takes longer []
The central venous compartment of blood volume
is an important factor for cardiac output The
in-creased blood volume with physical training is
regarded as a requisite for increased Qmax, although it
may be that the blood volume increases in parallel with
the increased 2 max
Acute plasma volume expansion (using
Macrodex®) increases SV during submaximal and
maximal exercise in well-trained individuals [,]
The explanation is that the enhanced BV causes an
enhanced diastolic filling pressure (preload), which
through a direct Frank–Starling mechanism increases
and arterial oxygen content (Ca2), so that the 2 maxismainly unchanged compared to control experiments.However, in untrained or moderately trained individ-uals a corresponding plasma volume expansion may
increase Qmaxby a greater amount than that needed tocompensate for the reduction of [Hb] during maximalexercise and, thus, increase 2 max[]
Peripheral vascular adaptations
Regular physical activity results in peripheral vascularadaptations which enhance perfusion and flow capa-city Thus it has been shown that total leg blood flowduring strenuous exercise increases in parallel with therise in maximal aerobic power In addition, the musclearteriovenous oxygen difference is significantlygreater after conditioning Such adaptations may arisefrom structural modifications of the vasculature andalterations in the control of vascular tone [,].The increase in capillary density of the muscleseems to be the major factor responsible for the rise inmaximal oxygen extraction Both cross-sectional andlongitudinal studies have shown greater muscle capil-lary density in trained than in untrained individuals,and that physical inactivity is associated with reducedcapillary density [,,] Both capillary density andblood flow seem to increase in proportion with the rise
in maximal aerobic power during long-term physicalconditioning [,]
The rise in peak muscle blood flow appears to beachieved by enhanced endothelium-dependent dilatation (EDD) in the muscle which increases its vasodilator capacity in parallel with expanded oxida-tive capacity Accordingly, the rise in cardiac outputcan occur without any rise in arterial pressure An en-hanced peak hyperemic blood flow appears to be anearly adaptation to regular exercise [,] A near
% increase in flow-mediated EDD of the brachialartery after weeks of aerobic and anaerobic training
was shown by Clarkson et al [] Furthermore, a highcorrelation between maximal aerobic power and peripheral vasodilator capacity, measured by vascularconductance, has been demonstrated [,] King-
˙
V
˙
V
Trang 36Cardiovascular and Respiratory Responses to Exercise
well et al [] found a near % greater reduction in
forearm vascular resistance to an
endothelium-dependent stimulus in endurance athletes as compared
to sedentary subjects This reduction was directly
re-lated to maximal aerobic power In endurance-trained
older people a significantly greater EDD, as compared
with age-matched sedentary subjects, has also been
ob-served [] Additionally, Rinder etal [] found that
abnormal EDD discovered in older, otherwise healthy
individuals could be improved with long-term
en-durance training They also noted a significant and
reasonably good correlation between maximal aerobic
power and EDD
The mechanisms behind the enhanced endothelial
function associated with physical training may involve
exercise-induced increases in shear stress and pulsatile
flow According to Niebaur and Cooke [] chronic
in-creases in blood flow induced by training may exert
their effect on EDD by modulating the expression of
endothelial cell nitric oxide synthase (NOS) It has
been shown that endothelium-derived nitric oxide
(NO) may influence vascular tone in the periods
be-tween exercise bouts In animal studies, reactivity to
stimuli which mediate their effects via NO is increased
by training in coronary circulation, as mentioned
pre-viously in this chapter [,] Human studies have
produced evidence for a role of NO in the regulation
of muscle blood flow [,] NOS exists in several
isoforms Consequently, endothelial NOS is named
eNOS Another isoform, called neuronal NOS
(nNOS), is located in the sarcolemma and cytosol of
human skeletal muscle fibers, in apparent association
with mitochondria [] Frandsen and coworkers []
have shown that endurance training may increase the
amount of eNOS in parallel with an increase in
capil-laries in human muscle, while the nNOS levels remain
unaltered
Respiratory adaptation
As there are many variables that contribute to the
achievement of 2 max, it may be difficult to identify
which mechanism is ‘limiting’ This applies
particu-larly to respiratory responses, which are generally
considered as non-limiting or ‘submaximal’ during
maximal exercise Ventilation at maximal exercise is
not as high as the maximal achievable ventilation
(MAV), but MAV (or maximal breathing capacity,
˙
V
MBC) is usually measured over –s, and falls progressively by about % after –min Thus whilst some athletes may achieve an MAV of –
L/min, their sustainable maximal ventilation is
–L/min, a value frequently achieved duringmaximal exercise Of course, such values are accompa-nied by severe dyspnea, and it may be more helpful tounderstand factors contributing to limiting dyspnea,than to judge whether a ‘limiting’ ventilation has beenreached Trained individuals experience much lessdyspnea than the untrained Indeed, early in their ex-perience of exercise, athletes may sense that they areable to exercise with much less dyspnea than theirstruggling peers, leading them to take up their sport in
a serious way
The study and quantitative measurement of the tensity of dyspnea had to wait firstly for the introduc-tion of the field of psychophysics by Stevens [], andsecondly for the development of appropriate psy-chophysical techniques by Borg and Noble [] Theapplication of these techniques has allowed the assess-ment of the separate contributions of many factors todyspnea during exercise in health and disease, and pro-vided some answers as to why the sense of effort inbreathing is so much less in trained than in untrainedindividuals
in-Studies employing neurophysiologic techniqueshave suggested that the sense of dyspnea representsthe conscious appreciation of the central outgoingcommand to the respiratory muscles [] Thus, con-sideration of all the factors contributing to the sensa-tion spans the metabolic demands for ventilation;mechanical capacity to meet the demand; adopted patterns of breathing; pulmonary gas exchange ef-ficiency; central control of breathing; respiratory mus-cle function; and sensory mechanisms by which theeffort of breathing is appreciated Furthermore, allthese physiologic links are interdependent and capable
of adaptation, apparently with the overall objective ofminimizing discomfort and thereby enhancing performance
Ventilatory demands of exercise
The major demand on ventilation is CO2production
(V2); although this is closely related to metabolicoxygen consumption and pulmonary intake, manystudies have dissociated the two and shown close corre-
Trang 37 Chapter .
lation between V2and ventilation (VE) At a given
power or ATP turnover, V2is quantitatively related
to the balance between fat and carbohydrate as fuels,
and the amount of lactate accumulating in the blood;
increases in fat oxidation [] and reductions in lactate
accumulation [,] may account for as much as a
halving of VE at a given power in trained as against
un-trained subjects Higher activities of fat metabolizing
enzymes [], greater mitochondrial surface area []
and more efficient oxygen delivery mechanisms [] all
contribute to the metabolic changes
Training-related reductions in VE closely parallel
reductions in both V2(Fig ..) and plasma lactate
concentrations [,,] Thus, at a given power
out-put, an increase of% in fat utilization will reduce
ventilation by approximately %, and a reduction in
plasma lactate concentration ofmmol/L will be
ac-companied by a further, up to %, reduction In some
athletes changes may be much larger; moreover, when
accompanied by the other changes described below,
such small effects are magnified, so that ventilation in
some athletes may be half that observed in untrained
subjects exercising at comparable power []
Ventilatory capacity
In terms of dimensions, the maximal breathing
capac-ity is a function of the total lung volume and the
maxi-mal flow rates in inspiration and expiration; volume isrelated to thoracic volume, and flow rates to airwaycross-sectional area For a given stature and weightboth volume and maximal flow tend to be larger in athletes, but studies in twins suggest that this has a genetic basis, and that training has little influence [].Within these constraints, athletes employ a larger vol-ume, by being able to achieve both a smaller end-expiratory and larger end-inspiratory volume Theyalso employ larger flow rates in both inspiration andexpiration; indeed some athletes are capable of usingvirtually all their maximal flow-volume loop duringexercise [,] It seems likely that this is because ofstronger and more fatigue-resistant respiratory mus-cles (see below) In older subjects there is a loss of elas-tic recoil; this reduces flow at low lung volumes andprevents them from achieving a reduction in end-expiratory volume, and contributes to an increase inrespiratory effort in older athletes []
Pulmonary gas exchange
Pulmonary gas exchange efficiency is broadly related
to ventilation–perfusion (V/Q) matching in the lungs,and to diffusion across the alveolar capillary mem-brane In general, in healthy subjects larger lungsimply greater alveolar volume and surface area andlarger pulmonary capillary volume The range of V/Qratios extends from zero (representing anatomic path-ways between the right and left sides of the heart, or
‘shunt’) to infinity (representing anatomic airway deadspace); areas in the lungs with a low V/Q ratio con-
tribute to the alveolar–arterial P2 difference (A–
a D2), and those with high V/Q to physiologic dead
space (VD/VT) Both A–a D2and VD/VTare mized by increases in tidal volume However, healthyuntrained subjects as well as athletes appear to reachsimilar minimal values for both, and at higher levels of
mini-2there is no further reduction [,]
This phenomenon has been carefully studied,
espe-cially for A–a D2; in some athletes very wide A–a D2
have been observed, leading to arterial P2values aslow as mmHg (Fig ..) []
When associated with a ‘rightward shift’ of the oxygen dissociation curve due to low arterial pH, such
low Pa2values translate into arterial O2saturations of
% or less The cause of this ‘arterial desaturation’and ‘failure of gas exchange’ has been debated, but
Fig .. Reductions in ventilation at two power outputs in five
subjects, before and after training; reductions in VE are closely
related to reductions in V 2(there was no change in V · 2at
either power output) [ ] Open and filled symbols denote
before and after training, respectively.
Trang 38Cardiovascular and Respiratory Responses to Exercise
remains unresolved [] There is no doubt that it
oc-curs especially in elite athletes exercising at high 2,
leading to theories that include relatively high venous
P2, low venous O2contents and very short
pul-monary capillary transit times (Fig ..)
contribut-ing to incomplete O2diffusion Interstitial pulmonary
edema occurs in animal models of exercise but has
never been shown in humans
Other possible factors include incomplete
equili-bration for CO2in blood traversing the lung []
com-bined with low blood pH, leading to incomplete
oxygenation of hemoglobin The limiting process in
CO2equilibration appears to be the erythrocyte
chlo-ride exchanger which has a half-equilibration time that
is in excess of pulmonary capillary transit time in heavy
exercise [,]
Pattern of breathing
Athletes breathe more slowly and deeply than
non-athletes, and a slower breathing rate is one of the effects
˙
V
of training The volumes and flows determine the tidalvolume and frequency of breathing during exercise; allother matters being equal, larger tidal volumes andslower frequencies lead to greater efficiency in breath-
ing with lower values for the VD/VTratio Some jects entrain breathing frequency with their pedaling
sub-or running cadence [], but there is scope for widevariation in such responses ( strides/breath vs strides/breath, for example), so that the entrainmentnever dominates the pattern Although the use of agiven pattern of breathing is often assumed to be a self-optimizing response to minimize the oxygen cost ofbreathing, it seems more likely that patterns are adopted consciously or unconsciously to minimize thesense of effort in breathing []
Control of breathing
Whilst the mechanisms responsible for the control ofbreathing during exercise remain a topic of continuingresearch [] beyond the scope of the present chapter,there is general agreement that increases in ventilationare a closely related function of the body’s CO2production
Many have studied the ventilatory responses to
increases in arterial P2(VE/P2), in athletes anduntrained subjects The findings may be summarized
Fig .. Arterial blood gases and pH at rest and during
submaximal and maximal treadmill exercise in a group of
untrained [*] and three groups of trained subjects One group of
trained subjects (l) showed a significant fall in arterial P 2 ,
associated with higher P 2 at maximal exercise From
Dempsey [ ].
'Mas' pulmonary capillary blood volume
0 0.2 0.4 0.6 0.8 1.0 1.2
(Transit time)
(Pulmonary capillary blood volume)
Pulmonary capillary blood volume (mL)
80 100 150 200 250
Pulmonary blood flow (L/min)
Fig .. Increasing exercise is associated with progressive
increases in pulmonary blood flow; pulmonary capillary blood volume increases to a maximum of mL Capillary mean transit time falls, and at maximum exercise approaches values as short as .s From Dempsey [].
Trang 39 Chapter .
There is a wide range in both VE/P2 (.–
.L/mmHg) and VE/V2(–L/L) in trained
and untrained individuals [,]
There is a relationship between the two indices: low
responders to P2have a low response to exercise
One might interpret these findings as indicating no
influence of ventilatory control on performance
How-ever, the effect of the variations in VE/V2is
sub-stantial, even when associated with the normal range of
variation in arterial P2 At an exercise power
accom-panied by a V2of.L/min, ventilation may range
from to L/min in normal subjects [], with a
corresponding variation in breathing effort A child
taking up competitive swimming is presumably more
likely to persist if she experiences little breathlessness
compared to her panting friends
The ventilatory responses to hypoxia and P2are
closely correlated []; this fact may contribute to
the lack of response to a falling P2, but also may be
im-portant in athletes at high altitude A low ventilatory
responsiveness might be seen to predispose to
danger-ous hypoxia; however, what has emerged from studies
simulating the ascent of Mount Everest is that low
re-sponders are more likely to reach the summit and are
less likely to suffer the deleterious cerebral and
pul-monary effects of altitude []; these effects appear to
be mediated by reductions in arterial P2and
associ-ated alkalosis In athletes who because of their sport
have to breath hold for long periods of time, such as
synchronized swimmers, the ventilatory response to
hypoxia is blunted and breath hold times prolonged
[]
The respiratory muscles
As first systematically studied by Ringqvist [], the
respiratory muscles show considerable variation in
strength and endurance, in relation to stature, age and
sex, with fairly obvious implications for the capacity to
achieve and maintain ventilation during exercise [],
and also for the sense of effort experienced in
breath-ing Subjects with stronger respiratory muscles
achieve higher tidal volumes (and thus lower breathing
frequencies), and experience less dyspnea than thosewith weaker muscles []
The actions of the respiratory muscles differ; ratory flow is mainly dependent on the elastic recoil ofthe respiratory system with only a minor contributionfrom expiratory muscle contraction until very high ex-piratory flows are recruited Expiratory muscle con-traction mainly acts to reduce end-expiratory lungvolume and thus recruit the inspiratory recoil of thethorax and increase the precontraction length of theinspiratory muscles; in this way, they tend to ‘unload’the inspiratory muscles [] The latter have to gener-ate inspiratory flow against the lung recoil pressure,and thus carry the major responsibility for ventilatorywork Inspiratory muscle training mainly accompaniesother aspects of endurance training, but resistive train-ing is known to improve inspiratory muscle strengthand endurance [] These considerations have im-portant implications in aging athletes in whom there isthe normal decline in lung elasticity; end-expiratorylung volume cannot be reduced to the same extent as inthe young, forcing the inspiratory muscle to carry agreater proportion of the respiratory work during ex-ercise [] Johnson etal [] found that reductions
expi-in elastic recoil and expi-increases expi-in end-expiratory volumeparalleled reductions in 2 maxin a group of older (± years) people; such subjects are likely to havebeen limited by dyspnea
Because exercise is a voluntary activity, conscioushumans stop exercise when the sensation of excessiveeffort and weakness in exercising muscle or of dyspneabecomes intolerable A number of sensations related tobreathing can be discriminated and scaled [], in-cluding inspiratory muscle tension and displacement,
a sense of ‘satiety’ or appropriateness related to
in-creases in arterial P2[,], and a sense of effortrelated mainly to central outgoing command [](Fig ..)
Both effort and dyspnea are less in trained compared
˙
V
Trang 40Cardiovascular and Respiratory Responses to Exercise
to untrained individuals, enabling them to maintain
higher power for longer The factors accounting for
these differences are numerous and interactive For
dyspnea the reasons are mainly that the pressure
gen-erated by the respiratory muscles is relatively less in
subjects with large lungs (due to lower elastance and
resistance), and strong respiratory muscles (Fig
maximizing P2, through lower VE/V2;
reducing VD/VT, by increasing VT, a function oflung volume; and
increasing inspiratory muscle strength.
At an oxygen consumption of L/min, the firstthree factors could theoretically account for a differ-ence in ventilation from L/min in an unfit individ-ual to L/min in an elite endurance runner As the
Central motor drive Respiratory muscle tension Effective intrapulmonary pressure Impedance (elastance, resistance) Thoracic expansion Ventilation, gas exchange CONTROL
Sense of APPROPRIATENESS Sense of EFFORT Sense of TENSION
Fig .. Mechanisms contributing to
sensations related to breathing during
exercise Whilst the changes in tension
developed and displacement of
inspiratory muscles can be discriminated
and scaled, contributors to the sense of
effort include difficulty in breathing
(sense of impedance), sufficiency of the
ventilatory response (‘satiety’), and the
outgoing central motor command [ ].
Maximal 10 9 8 7 6 5 4 3 2 1
0 0 0.5
Very, very severe
Very severe
Severe Somewhat severe Moderate Slight Very slight Just noticeable Nothing at all
Power output (kpm/min)
Very weak Weak
StrongVery Strong
Fig .. Sense of dyspnea during exercise
in healthy subjects, grouped according to
strength of inspiratory muscles (measured
as maximal inspiratory pressure, MIP), into
four groups: very weak, MIP <%
predicted; weak, –%; strong,
–%; very strong, >% From
Hamilton et al [].