Ankle injuries in basketball: injury rate and risk factors G D McKay, P A Goldie, W R Payne, B W Oakes Abstract Objectives—To determine the rate of ankle injury and examine risk factors of ankle injuries in mainly recreational bas- ketball players. Methods—Injury observers sat courtside to determine the occurrence of ankle inju- ries in basketball. Ankle injured players and a group of non-injured basketball players completed a questionnaire. Results—A total of 10 393 basketball par- ticipations were observed and 40 ankle injuries documented. A group of non- injured players formed the control group (n = 360). The rate of ankle injury was 3.85 per 1000 participations, with almost half (45.9%) missing one week or more of com- petition and the most common mech- anism being landing (45%). Over half (56.8%) of the ankle injured basketball players did not seek professional treat- ment. Three risk factors for ankle injury were identified: (1) players with a history of ankle injury were almost five times more likely to sustain an ankle injury (odds ratio (OR) 4.94, 95% confidence interval (CI) 1.95 to 12.48); (2) players wearing shoes with air cells in the heel were 4.3 times more likely to injure an ankle than those wearing shoes without air cells (OR 4.34, 95% CI 1.51 to 12.40); (3) players who did not stretch before the game were 2.6 times more likely to injure an ankle than players who did (OR 2.62, 95% CI 1.01 to 6.34). There was also a trend toward ankle tape decreasing the risk of ankle injury in players with a history of ankle injury (p = 0.06). Conclusions—Ankle injuries occurred at a rate of 3.85 per 1000 participations. The three identified risk factors, and landing, should all be considered when preventive strategies for ankle injuries in basketball are being formulated. (Br J Sports Med 2001;35:103–108) Keywords: basketball; ankle; injury; risk; prevention In basketball, ankle injuries are among the most common injuries sustained and they are also amongst the most severe. 1–3 An Australian basketball study 2 determined that over half (53.7%) of the total time missed because of an injury in basketball was through an ankle injury. Ankle injuries may result in the player experiencing disability and residual symptoms, 4–6 the most common being pain, sense of instability, crepitus, and weakness. 5 However, arthroscopic surgery of 31 ankles 6 found that chondral lesions were evident in 95% of chronic ankle injuries and 89% of recently injured ankles. As ankle injury is a common occurrence, often with residual symp- toms aVecting performance and chondral lesions, preventive strategies need to be devel- oped, but risk factors associated with ankle injuries must first be identified and under- stood. Previous studies of risk factors for ankle injury have been carried out in either the labo- ratory, with emphasis on biomechanical assess- ment, or the sporting environment as a field/clinical study. Laboratory based studies examine the eVectiveness of a specific variable such as ankle tape or brace or cut of shoe on aspects of performance such as restriction of postural sway, 7 wobble board performance, 8 sporting activities such as jumping and running, 9–11 or aspects of body function such as amount of joint restriction provided, 12–15 pero- neal muscle activity, 16 and peroneal reaction time. 17 18 All of these authors have inferred how these factors may aVect the incidence of ankle injuries, without assessing the actual occur- rence of ankle injuries. On the other hand, field studies usually assess risk factors for ankle injury with respect to the actual incidence of ankle injuries. These field based studies may question the validity of the biomechanical studies in making inferences about the risk of ankle injury on the sports field. Therefore the aim of this study was to examine risk factors of ankle injuries, such as history of ankle injury 4 19 20 , ankle tape 15 16 and braces 12 13 , playing shoes 21 , warm up, 22 and position played 23 24 on the court, in the natural- istic environment of the basketball court. Subjects and method In Melbourne, Australia, an elite basketball competition and three recreational basketball competitions were observed to identify injuries prospectively. Injury observers were instructed to view games and note the occurrence of inju- ries during the game. At the end of a game, all players were asked about their injury status, and injured players completed a questionnaire. A control group was obtained by administering a questionnaire to entire teams of players who were not injured on a particular day but were from the same competition as the injured play- ers. All games observed were played indoors on wooden floors. Table 1 outlines the areas of questioning. The ankle injured players were telephoned to monitor the progress of their injury, to obtain information about time missed, treatment sought, and changes in shoes, protective equip- ment, and warm up on returning to play. Br J Sports Med 2001;35:103–108 103 School of Physiotherapy, La Trobe University, Victoria, Australia G D McKay P A Goldie School of Human Movement and Sport Sciences, University of Ballarat, Victoria, Australia W R Payne Department of Anatomy, Monash University, Victoria, Australia B W Oakes Correspondence to: Ms McKay, 339 Heidelberg Rd, Northcote, Victoria 3070, Australia alphsportsmed@ preston.hotkey.net.au Accepted 27 November 2000 www.bjsportmed.com group.bmj.com on May 9, 2011 - Published by bjsm.bmj.com Downloaded from
Transcript
Ankle injuries in basketball: injury rate and riskfactors
G D McKay, P A Goldie, W R Payne, B W Oakes
AbstractObjectives—To determine the rate ofankle injury and examine risk factors ofankle injuries in mainly recreational bas-ketball players.Methods—Injury observers sat courtsideto determine the occurrence of ankle inju-ries in basketball. Ankle injured playersand a group of non-injured basketballplayers completed a questionnaire.Results—A total of 10 393 basketball par-ticipations were observed and 40 ankleinjuries documented. A group of non-injured players formed the control group(n = 360). The rate of ankle injury was 3.85per 1000 participations, with almost half(45.9%) missing one week or more of com-petition and the most common mech-anism being landing (45%). Over half(56.8%) of the ankle injured basketballplayers did not seek professional treat-ment. Three risk factors for ankle injurywere identified: (1) players with a historyof ankle injury were almost five timesmore likely to sustain an ankle injury(odds ratio (OR) 4.94, 95% confidenceinterval (CI) 1.95 to 12.48); (2) playerswearing shoes with air cells in the heelwere 4.3 times more likely to injure anankle than those wearing shoes without aircells (OR 4.34, 95% CI 1.51 to 12.40); (3)players who did not stretch before thegame were 2.6 times more likely to injurean ankle than players who did (OR 2.62,95% CI 1.01 to 6.34). There was also atrend toward ankle tape decreasing therisk of ankle injury in players with ahistory of ankle injury (p = 0.06).Conclusions—Ankle injuries occurred at arate of 3.85 per 1000 participations. Thethree identified risk factors, and landing,should all be considered when preventivestrategies for ankle injuries in basketballare being formulated.(Br J Sports Med 2001;35:103–108)
In basketball, ankle injuries are among themost common injuries sustained and they arealso amongst the most severe.1–3 An Australianbasketball study2 determined that over half(53.7%) of the total time missed because of aninjury in basketball was through an ankleinjury. Ankle injuries may result in the playerexperiencing disability and residualsymptoms,4–6 the most common being pain,sense of instability, crepitus, and weakness.5
However, arthroscopic surgery of 31 ankles6
found that chondral lesions were evident in
95% of chronic ankle injuries and 89% ofrecently injured ankles. As ankle injury is acommon occurrence, often with residual symp-toms aVecting performance and chondrallesions, preventive strategies need to be devel-oped, but risk factors associated with ankleinjuries must first be identified and under-stood.
Previous studies of risk factors for ankleinjury have been carried out in either the labo-ratory, with emphasis on biomechanical assess-ment, or the sporting environment as afield/clinical study. Laboratory based studiesexamine the eVectiveness of a specific variablesuch as ankle tape or brace or cut of shoe onaspects of performance such as restriction ofpostural sway,7 wobble board performance,8
sporting activities such as jumping andrunning,9–11 or aspects of body function such asamount of joint restriction provided,12–15 pero-neal muscle activity,16 and peroneal reactiontime.17 18 All of these authors have inferred howthese factors may aVect the incidence of ankleinjuries, without assessing the actual occur-rence of ankle injuries.
On the other hand, field studies usuallyassess risk factors for ankle injury with respectto the actual incidence of ankle injuries. Thesefield based studies may question the validity ofthe biomechanical studies in making inferencesabout the risk of ankle injury on the sportsfield. Therefore the aim of this study was toexamine risk factors of ankle injuries, such ashistory of ankle injury4 19 20, ankle tape15 16 andbraces12 13, playing shoes21, warm up,22 andposition played23 24 on the court, in the natural-istic environment of the basketball court.
Subjects and methodIn Melbourne, Australia, an elite basketballcompetition and three recreational basketballcompetitions were observed to identify injuriesprospectively. Injury observers were instructedto view games and note the occurrence of inju-ries during the game. At the end of a game, allplayers were asked about their injury status,and injured players completed a questionnaire.A control group was obtained by administeringa questionnaire to entire teams of players whowere not injured on a particular day but werefrom the same competition as the injured play-ers. All games observed were played indoors onwooden floors.
Table 1 outlines the areas of questioning.The ankle injured players were telephoned tomonitor the progress of their injury, to obtaininformation about time missed, treatmentsought, and changes in shoes, protective equip-ment, and warm up on returning to play.
group.bmj.com on May 9, 2011 - Published by bjsm.bmj.comDownloaded from
Chronic traumatic brain injury or
chronic traumatic encephalopathy
(CTE) is considered by some au-
thorities to be the most serious health
problem in modern day boxing.1 The
condition is often referred to by a number
of names in the medical and non-medical
literature including dementia pugilistica
and “punch drunk” syndrome.
Whilst there exists great controversy
regarding the ethics of boxing, one of the
key medical issues is the risk of a boxer
developing CTE either during or after his
boxing career. Recent evidence suggests
that exposure to boxing alone is insuffi-
cient to cause this condition.
It is believed that CTE represents the
cumulative long term neurological con-
sequences of repetitive concussive and
sub concussive blows to the head.1–4 CTE
ismorecommoninprofessionalratherthan
amateur boxers, however, CTE has
been documented in other sports such as
AmericanFootball,icehockey,rugby,horse
racing, and soccer.5–7
CTE is clinically characterised by a
combination of speech and gait distur-
bance, pyramidal tract dysfunction,
memory impairment, extrapyramidal
features, behavior or personality
changes, and psychiatric disease.1–3 8 In
the early stages of this condition, the
symptoms are transient and reversible,
however, in the later stages they are
progressive.TheneurologyofCTEincludes
characteristic neuropathological features
of cerebral atrophy, septal fenestration,
cerebellar tonsillar scarring, cavum
septum pellucidum, loss of pigmented
cells, and prominent neurofibrillary
tangles.7
It is salient to review the original
paper discussing the neuropathology of
CTE. Although individual case reports
had been published of boxers with
chronic dementing illnesses, the seminal
paper discussing the association of neu-
ropathological findings in boxers was
published by the English pathologist,
John Corsellis.7 He studied the brains of15 retired boxers and retrospectivelystudied their fight histories. While anumber of characteristic changes werenoted in these brains, it is the boxers’histories that deserve specific note.Of thefighters studied, their exposure to boxingranged between 300 and 700 bouts in thecourseoftheircareers.Thiswasinadditionto sparring and other fight training thatwould have occurred.
The issue then that needs considera-tion is that in this day and age we wouldseldom see a fighter with such a record.Even the top professionals report fightcareers of 30–50 fights before retirement,an order of magnitude less than thatdescribed in Corsellis’ landmark study.
Recent research in boxers has alsosuggested that CTE in boxers may beassociated with a particular genetic pre-disposition. The apolipoprotein E e-4gene (ApoE), a susceptibility gene forlate onset familial and sporadicAlzheimer’s disease, may be associatedwith an increased risk of CTE inboxers.1 6 9
In a non-boxing population, ApoEpolymorphism was significantly associ-ated with death and adverse outcomesfollowing acute traumatic brain injury asseen in a neurosurgical unit.10 In arecent prospective study, ApoE genotypeswere tested for their ability to predict daysof unconsciousness and functionaloutcome after six months.11 There was astrongassociation demonstrated betweenthe ApoE allele and poor clinical outcome.
Furthermore, ApoE deficient (knock-out) mice have been shown to havememory deficits, neurochemicalchanges, and diminished recovery fromclosed head injury when compared tocontrols.12 It is suggested that ApoE playsan important role in both neuronal repairandantioxidantactivity resulting inApoEknockout mice exhibiting an impairedability to recover from closed head injury.
How then does this help the debate onthe risks of boxing? Firstly we need to
reconsider the original evidence on ex-posure as a risk factor for CTE. The sim-plistic assumption based on epidemio-logical data from previous studies thatCTE is a manifestation of the length of aboxer’s career and hence exposure topunches needs to be readdressed.
Similarly the development in under-standing of the genetic risk that a boxermay carry developing CTE means thatthis area may need to be re-examined inlight of current day research. This issuealso raises a number of ethical issues, if aboxer is found to be homozygous for theApoE e-4 phenotype should his boxingcareer be curtailed? At the very least,informed consent, and genetic coun-seling should be undertaken.
Whilst one may argue the ethics andmorality of boxing, it behooves us as sci-entists and clinicians to at least place themedical arguments regarding risk ofinjury on a scientific footing.
Br J Sports Med 2002;36:2
REFERENCES1 Jordan B, Relkin N, Ravdin L. Apolipoprotein
E epsilon 4 associated with chronic traumaticbrain injury in boxing. JAMA1997;278:136–40.
2 Jordan B. Genetic susceptibility to braininjury in sports: A role for genetic testing inathletes? Phys Sportsmed 1998;26:25–6.
3 Jordan B, ed. Medical aspects of boxing.Boca Raton: CRC Press, 1993.
4 Nicholl J, Coleman P, Williams B. Theepidemiology of sports and exercise relatedinjury in the United Kingdom. Br J Sports Med1995;29:232–8.
5 NH & MRC. Boxing Injuries. Canberra:Australian Government Publishing Service,1994.
6 Unterharnscheidt FJ. About boxing: reviewof historical and medical aspects. Tex Rep BiolMed 1970;28:421–95.
8 Unterharnscheidt FJ. Head injury afterboxing. Scand J Rehab Med 1972;4:77–84.
9 Corder E, Saunders A, Strittmatter W. Genedose of Apolipoprotein E type 4 allele and therisk of late onset Alzheimer’s disease infamilies. Science 1993;261:921–3.
10 Teasdale G, Nicol J, Murray G. Associationof Apolipoprotein E polymorphism withoutcome after head injury. Lancet1997;350:1069–71.
11 Friedman G, Froom P, Sazbon L, et al.Apolipoprotein E-epsilon 4 genotype predictsa poor outcome in survivors of traumatic braininjury. Neurology 1999;52:244–9.
12 Lomnitski L, Kohen R, Chen Y, et al. Reducedlevels of antioxidants in brains ofapolipoprotein E-deficient mice followingclosed head injury. Pharmacology,Biochemistry and Behaviour1997;56:669–73.
group.bmj.com on May 8, 2011 - Published by bjsm.bmj.comDownloaded from
Brain injury and heading in soccerHead to ball contact is unlikely to cause injury but head to head contact might
Whether repeated concussive or subconcus-sive blows cause permanent or cumulativebrain injury is a complex and controversial
question. Press coverage highlighted the case of JeffAstle, a former England international football player,where the coroner ruled the cause of his death as an“industrial disease”—suggesting that repeated headingof balls during his professional career was the cause ofhis subsequent neurological decline.1 This case was atodds with that of Billy MacPhail, a former GlasgowCeltic player, who in 1998 lost a legal battle to claimbenefits for dementia that he said was due to headingthe old style leather footballs. Concern has been raisedover whether heading in soccer may be the basis forinjury and cognitive impairment, and in the UnitedStates this has led to calls advocating the use of protec-tive headgear for soccer players.
Soccer players don’t just head the ball; their headscan collide with each other, and players in positionswhere heading is common are also more likely to havehead to head collisions more often. Although un-common, most concussive injuries seen in soccerderive from such head to head rather than ball to headcontact.2
Heading a soccer ball results in head accelerations ofless than 10 g (or less than 1000 rad/s2) whereas theminimum values for the development of sport relatedconcussion are 40-60 g (or 3500-5000 rad/s2).3 4 In con-trast, head to head contact can generate enough of theforces required to cause brain injury as in anyconventional head injury. Recent biomechanicalresearch has found that commercially available soft hel-mets fail to reduce even this degree of head trauma to asafe level, which implies that these helmets have only alimited protective role in this setting.5
There is no evidence that sustaining severalconcussions over a sporting career will necessarilyresult in permanent damage.6 Research on experimen-tal animals provides some supporting evidence againstthe concept that recurrent concussive injuries alonecause permanent damage. In studies of experimentalconcussion, animals have been subjected to repeatedconcussion 20-35 times in a two hour period. Despitethe unusually high number of injuries no residual orcumulative effect was shown.7
Can repeated subconcussive trauma such as mightbe seen in heading the ball cause a cumulative neuro-logical injury in this setting? Although this wasindicated by early retrospective studies, more recentstudies have not supported this idea.8–10
In a series of retrospective studies including retiredScandinavian soccer players, cognitive deficits werenoted.11 12 The results of these studies are flawed, withappreciable methodological problems. These prob-lems include the lack of pre-injury data, selection bias,failure to control for acute head injuries, lack of blind-ing of observers, and inadequate controls. The authorsconclude that the deficits noted in these former soccerplayers were explained by repetitive trauma such asheading the ball. However, the pattern of deficits seenis equally consistent with alcohol related brainimpairment—a confounding variable that was not con-trolled for.
Matser et al from the Netherlands have alsoimplicated both concussive injury and heading as acause of neuropsychological impairment in bothamateur and professional soccer players.2 13 Reanalysisof the data from these papers, however, indicates thatpurposeful heading may not be a risk factor forcognitive impairment.14
Prospective controlled studies using clinical exami-nation, neuroimaging, or neuropsychological testinghave failed to find any evidence of cognitiveimpairment in soccer players.8–10
We do not know for certain whether heading theball in soccer may result in chronic cognitiveimpairment. It seems unlikely that subconcussiveimpacts such as seen in head to ball contact will causechronic neurological injury. Although head to headcontact may cause concussive injury, it is both uncom-mon and unlikely to result in cumulative brain injury. Ithas been speculated from other sports that particulargenotypes may place athletes at heightened risk in
TO
BIA
SH
EY
ER
/DP
A/E
MP
ICS
Saturday 16 August 2003
BMJ
BMJ 2003;327:351–2
351BMJ VOLUME 327 16 AUGUST 2003 bmj.com
association with head trauma, although this is yet to bevalidated in other studies.15
For football players the avoidance of exposure tobrain injury is important, although currently there arefew means by which this may be achieved. Most head tohead contact is inadvertent, and coaching techniquesand visual perception training may help in a few casesbut are unlikely to eliminate this problem entirely. Softshell helmets or head protectors currently do not havethe biomechanical capability to prevent concussivetrauma and hence cannot be recommended.
Paul R McCrory research fellowCentre for Sports Medicine Research and Education, Brain ResearchInstitute, University of Melbourne, Parkville, Victoria 3054, Australia([email protected])
Competing interests: None declared.
1 Shaw P. Heading the ball killed England striker Jeff Astle. Independent2002 Nov 12.
2 Matser J, Kessels A, Jordan B, Lezak M, Troost J. Chronic traumatic braininjury in professional soccer players. Neurology 1998;51:791-6.
3 Naunheim RS, Standeven J, Richter C, Lewis LM. Comparison of impactdata in hockey, football, and soccer. J Trauma 2000;48:938-41.
4 McIntosh A, McCrory P. The dynamics of concussive head impacts inrugby and Australian rules football. Med Sci Sports Exerc 2000;32:1980-5.
5 McIntosh A, McCrory P. Impact energy attenuation performance of foot-ball headgear. Br J Sports Med 2000;34:337-42.
6 Johnston K, McCrory P, Mohtadi N, Meeuwisse W. Evidence based reviewof sport-related concussion—clinical science. Clin J Sport Med2001;11:150-60.
7 Parkinson D. Concussion is completely reversible; an hypothesis. MedHypotheses 1992;37:37-9.
8 Jordan BD. Acute and chronic brain injury in United States national teamsoccer players. Am J Sports Med 1996;24:704-5.
9 Putukian M, Echemendia R, Mackin S. The acute neuropsychologicaleffects of heading in soccer. Clin J Sports Med 2000;10:104-9.
10 Guskiewicz K, Maskell S, Broglio S, Cantu R, Kirkendall D. No evidence ofimpaired neurological performance in collegiate soccer players. Am JSports Med 2002;30:157-62.
11 Tysvaer A, Storli O, Bachen N. Soccer injuries to the brain: a neurologicand encephalographic study of former players. Acta Neurol Scand1989;80:151-6.
12 Tysvaer AT. Head and neck injuries in soccer. Impact of minor headtrauma. Sports Med 1992;14:200-13.
13 Matser J, Kessels A, Lezak M, Troost J. A dose-response relation of head-ers and concussions with cognitive impairment in professional soccerplayers. J Clin Exp Neuropsychol 2001;23:770-4.
14 Kirkendall D, Garrett W. Heading in soccer: Integral skill or grounds forcognitive dysfunction. J Athletic Training 2001;36:328-33.
15 Jordan BD, Relkin NR, Ravdin LD, Jacobs AR, Bennett A, Gandy S.Apolipoprotein E epsilon4 associated with chronic traumatic brain injuryin boxing. J Am Med Assoc 1997;278:136-40.
Self reports in research with non-English speakersThe challenge of language and culture is yet to be met
Assessment of the health and healthcare needs ofethnic minority populations, often relying onself reported data, is important in health and
social services.1 Major problems exist with the reliabilityof such information, particularly among recent andolder immigrants and refugees who may have little or nocompetency in English and may be at high risk of healthproblems. Approximately 23% of immigrants to Britainborn in China, Bangladesh, India, and Pakistan have nofunctional skill in English, and 70% cannot function fullyin an English speaking social environment.2
When a measure is probing differences within agroup it must be appropriate, valid, and reliable for thegroup concerned. However, if the data are to be used tomake comparisons between groups as in clinical trialsand most epidemiological studies, then the questionsmust be conceptually and functionally equivalent andappropriate for all the groups compared. Non-Englishspeakers are often excluded from clinical trials andepidemiological studies, for reasons including the lackof valid and reliable cross cultural measurements.3
In clinical and epidemiological studies questionsdeveloped for native English speakers are usuallytranslated into other languages. It is assumed that themodes of inquiry appropriate for native English speak-ers are applicable to other linguistic groups. Theseassumptions may reflect pragmatic issues relating totime and finance or lack of understanding of the com-plexities of language and culture. Translations, even byexperts, may fail to achieve questions that are compar-able to the original English in terms of appropriate-ness and meaning.4 It is therefore important toconsider conceptual matters, cultural relevance, andthe subtle connotations of words and phrases.
In multilingual studies, if each language istranslated and compared to the English, each may
resemble the English version, but the differentnon-English languages may differ in important ways,sometimes because it is impossible to find equivalenttranslations. For example the term “feeling blue,” usedin the original American version of the short formquestionnaire 36 (SF-36), has different connotations indifferent languages5 whereas the terms “check up” and“Pap smear” have no conceptual equivalent in anyChinese language.6
Research in our department, analysing the transla-tion of local and national health surveys, hasuncovered numerous potential problems—for exam-ple, asking Muslims whether they drink more atChristmas, and the use of terms such as “weekend” and“hangover” with questionable relevance to some ethnicgroups.7 Detailed examination of translations of theRose angina questionnaire into Punjabi and Canton-ese has highlighted subtle issues potentially explainingthe recently shown lesser validity of this instrument inSouth Asian populations.8
In face to face interviews complications arise wheredifferent forms of the same language are used—forexample, Bengali and the Sylheti variant of Bengali, thelatter having no written form. For some languages thewritten and spoken forms are not the same—for exam-ple, Arabic or Cantonese. At interview the questionsasked will not be the same as the questions written onthe questionnaire or interview schedule, with unknowneffects on data quality.
An alternative to seeking cross cultural equivalenceis to define issues as, firstly, salient and meaningfulwithin a culture, for example, chewing paan, and,secondly, concerns of salience between cultures, forexample, smoking tobacco. This strategy requires aparticipatory approach whereby monolingual andbilingual representatives of the target group(s) are
See end of article forauthors’ affiliations. . . . . . . . . . . . . . . . . . . . . . .
Correspondence to:M Saugy, SwissLaboratory for DopingAnalyses, Institute of LegalMedicine, Lausanne,Switzerland; [email protected]
. . . . . . . . . . . . . . . . . . . . . . .
Br J Sports Med 2006;40(Suppl I):i30–i34. doi: 10.1136/bjsm.2006.027532
Objective and method: To outline the direct and indirect approaches in the fight against blood doping insports, the different strategies that have been used and are currently being used to fight efficiently againstblood doping are presented and discussed.Results and conclusions: The paper outlines the different approaches and diagnostic tools that somefederations have to identify and target sportspeople demonstrating abnormal blood profiles. Originallyblood tests were introduced for medical reasons and for limiting misuse of recombinant humanerythropoietin (rHuEPO). In this way it became possible to prevent athletes with haematocrit levels wellabove normal, and potentially dangerous for their health, competing in sport. Today, with nearly a decadeof blood testing experience, sports authorities should be familiar with some of the limitations and speciallythe ability of blood tests performed prior to competitions to fight efficiently against the misuse of rHuEPO,blood transfusion, and artificial haemoglobin.
Erythropoiesis is part of the large process of haematopoi-
esis, which involves the production of mature cells found
in the blood and lymphoid organs.1 Haematopoiesis is
continuously required because of the normal turnover in the
cell populations in the blood and lymphoid organs. In the
normal adult human, the daily turnover of erythrocytes
exceeds 1011 cells. During periods of increased erythrocyte
loss, due to haemolysis or haemorrhage, the production of
erythrocytes increases rapidly and markedly. However, over-
production of erythrocytes does not occur, even after the
most severe loss of erythrocytes.
In haematopoiesis, a few pluripotent haematopoietic stem
cells in the bone marrow proliferate and differentiate to give
rise to all the cellular components of the blood and the
lymphoid system. During this process, an individual haema-
topoietic cell undergoes an apparently random process called
commitment. When a cell undergoes commitment, its
potential to proliferate becomes limited and its potential to
develop into multiple types of mature cell is also restricted.
Thus, these haematopoietic cells are termed committed,
lineage specific progenitor cells.
The major stages of differentiation in mammalian ery-
thropoiesis are as follows. The most immature stage of
committed erythroid progenitors is the burst forming unit-
erythroid (BFU-E). The next major stage of erythroid
progenitor cell development is the colony forming unit-
erythroid (CFU-E). A continuum of erythroid progenitor
stages exists between the BFU-E and CFU-E, with decreasing
proliferative potential as the progenitors approach the CFU-E
stage. The descendant cells of the CFU-E are termed erythroid
precursor cells. These erythroid precursors are proerythro-
See end of article forauthors’ affiliations. . . . . . . . . . . . . . . . . . . . . . .
Correspondence to:M Saugy, SwissLaboratory for DopingAnalyses, Institute of LegalMedicine, Lausanne,Switzerland; [email protected]
. . . . . . . . . . . . . . . . . . . . . . .
Br J Sports Med 2006;40(Suppl I):i35–i39. doi: 10.1136/bjsm.2006.027573
Background and objectives: Recombinant human growth hormone (rhGH) has been on the list offorbidden substances since availability of its recombinant form improved in the early 1990s. Although itseffectiveness in enhancing physical performance is still unproved, the compound is likely used for itspotential anabolic effect on the muscle growth, and also in combination with other products (androgens,erythropoietin, etc.). The degree of similarity between the endogenous and the recombinant forms, thepulsatile secretion and marked interindividual variability makes detection of doping difficult. Twoapproaches proposed to overcome this problem are: the indirect method, which measures a combinationof several factors in the biological cascade affected by administration of GH; and the direct method, whichmeasures the difference between the circulating and the recombinant (represented by the unique 22 kDmolecule) forms of GH. This article gives an overview of what is presently known about hGH in relation tosport. The available methods of detection are also evaluated.Methods: Review of the literature on GH in relation to exercise, and its adverse effects and methods ofdetection when used for doping.Results and conclusion: The main effects of exercise on hGH production and the use and effects of rhGH inathletes are discussed. Difficulties encountered by laboratories to prove misuse of this substance by bothindirect and direct analyses are emphasised. The direct method currently seems to have the best reliability,even though the time window of detection is too short. hGH doping is a major challenge in the fight againstdoping. The effect of exercise on hGH and its short half-life are still presenting difficulties during dopinganalysis. To date the most promising method appears to be the direct approach utilising immunoassays.
The human growth hormone (hGH) is a naturally
occurring peptide hormone secreted by the pituitary
gland.1 Although the hormone in the body is rather
heterogeneous, the major component is made up of 191
amino acids, stabilised by two disulphide bonds and reaching
a molecular weight of 22 kDa.2 3 Previously, the only source
of hGH was human cadavers, but the contamination that led
to Creutzfeldt–Jakob disease made this form of treatment
obsolete. In the late 1980s, recombinant hGH (rhGH) was
developed through genetic engineering and has been used
with good results in the treatment of patients with hGH
deficiency—allowing bone growth and impacting on the
patient’s final stature. This form of hGH has a sequence
identical to the naturally occurring 22 kDa hormone. Its
misuse has been suspected in sport because of its anabolic
properties. Athletes and bodybuilders claim that hGH
increases lean body mass and decreases the fat mass.
The use of hGH in sport today is not only based on its
anabolic properties, but also on its effect on carbohydrate and
fat metabolism. rhGH has been found in swimmers and also
in players taking part in major sports events. International
federations and the International Olympic Committee have
had hGH on the list of forbidden compounds since 1989,
when it became obvious that the development of biotechnol-
ogy products based on the recombination of DNA made hGH
much more easily available on the regular and black markets.
In the 2006 Prohibited List, hGH in listed under class S2 of
hormones and related substances. Erythropoietin (EPO) and
corticotrophin as well as insulin-like growth factor (IGF)-1
and insulin also belong to the same category of peptide
hormones. During the 2004 Olympics in Athens, for the first
time, the so-called direct method of Wu et al4 was used. None
of the positive serum samples were finally declared positive;
this was because of the too-short time window of detection of
the test and the short half-life of circulating GH (about
20 minutes).5 Studies have shown that GH concentrations
returned to baseline 8–16 hours after intramuscular injection
and 11–20 hours after subcutaneous injection.6
GROWTH HORMONE AND EXERCISEThe effect of acute exercise on production of GH in the body
has been widely described in the literature.7 The concentra-
tion of hGH in blood increases with time for a given work
intensity and can increase 10-fold during prolonged moder-
ate exercise. During more intensive exercise (with accumula-
tion of lactate at 70% VO2 max for a short term period such as
10–20 minutes) hGH will increase by 5–10-fold.8 With short
exercise durations, levels of GH will generally peak at 15–
30 minutes after the exercise. Furthermore, it appears that
hGH response is more closely related to the peak intensity of
exercise than the total work output.9 Endurance training
generally amplifies the pulsatile release of growth hormone,
elevating the GH amplitude. This appears evident when the
training is very hard and above the aerobic threshold.10
Apart from exercise related increase, hGH secretion can be
affected by other factors—for example, GH secretion is
increased in hypoglycaemia, increased temperature, and
stress, whereas it decreases in obesity, or with a carbohy-
drate-rich diet and intake of b2 adrenergic agonists. Thus, it is
hard to differentiate between the physiological increase in
hGH levels seen in exercise and what can be from external
hGH administration (as in doping). This problem makes the
purely quantitative approach of measuring directly the total
circulating GH not feasible in case of doping, except if the
conditions of collection of biological samples are well
Brit. J. Sports Med. - Vol. 18, No. 4, December 1984, pp. 288-292
R.....N cn..
R. Northcote
REDUCING THE PREVALENCE OF EXERCISE RELATED CARDIAC DEATH
R. J. NORTHCOTE, MRCP and D. BALLANTYNE, MD, FRCP (Glasg.)
Department of Medical Cardiology, The Victoria Infirmary, Glasgow, Scotland
INTRODUCTIONNon-traumatic sudden death during or immediatelyfollowing strenuous sporting activity is an event ofwhich most sportsmen are aware. The subject has beenthe concern of sportsmen, sports governing bodies andthe medical profession, and has often excited alarmistmedia reports.
Although there appears to be a statistically smallincreased risk of sudden death during strenuous exercise(Opie, 1975; Thompson et al, 1982), there remains anappreciable mortality (Northcote and Ballantyne, 1983,1984). The majority of sudden deaths are attributed tocardiovascular disease, particularly coronary heartdisease (CHD) and although a wide age range is affected,most subjects are over the age of 35 years (Northcoteand Ballantyne, 1983).
It is the intention of this article to examine ways inwhich the prevalence of sudden cardiac death in sportcan be reduced.
DEMOGRAPHIC DATAAt present, we are aware of 151 cases of sudden deathwhich have occurred in association with strenuous sportand have been documented in the medical literature
Address for correspondence:Dr. Robin J. Northcote,Department of Medical Cardiology,The Victoria Infirmary,Glasgow G42 9TY
(Northcote and Ballantyne, 1984). Only six non-cardiaccauses of death are recorded, four being attributed tointracranial haemorrhage, one to heat stroke, and one toan acute gastro-intestinal haemorrhage. Of the cardiaccauses, CHD accounted for 110 cases, followed bystructural cardiovascular abnormalities such as hyper-trophic obstructive cardiomyopathy (HOCM), coronaryartery anomalies and valvular heart disease. Asurprisingly small number (3) are attributed to myo-carditis. Most of the deaths occurred in association withrunning, field sports and squash. The subjects ranged inage from 16-66 years, but were mostly over the age of35 years (mean = 40 ± 9.1 years). Thirty-eight per centsuffered prodromal symptoms or conditions and 52% ofthose with CHD had documented risk factors for CHD.The prodromal symptoms included chest pain, dyspnoea,fatigue and gastrointestinal upsets. The most prevalentCHD risk factor was smoking.
In summary, it would appear from this data that mostsudden deaths are atrributed to cardiac disease, mostfrequently CHD, and a proportion of individuals may beat greater risk because of the presence of pre-morbidconditions and CHD risk factors.
Cardiovascular Effects of Strenuous SportSudden and excessive exercise is believed to be morelikely to precipitate "heart attacks" in the unfit(Shephard, 1974). In addition, competitive sports maybe more likely to precipitate sudden death than exercisetraining alone (Opie, 1975). It is probable, also, thataggressive individuals taking part in highly competitivesports are at greater risk.
288
D. Ballantyne
group.bmj.com on May 8, 2011 - Published by bjsm.bmj.comDownloaded from
A number of workers have reported the heart rate(HR) responses to various sports. In squash we haverecently confirmed HR responses of 80% of thepredicted maximum heart rate (PMHR), sustained for upto 40 minutes in healthy volunteers (Northcote et al,1983). Similar studies in tennis have reported HRresponse of 60-70% of PMHR for periods of rally playonly (Misner et al, 1980). Heart rate has been shown notto rise above 100 bpm in golf, bowls or cricket (Kozarand Himsicher, 1963).
Cardiac ArrhythmiasCardiac arrhythmias, including ventricular tachycardia,have been demonstrated in a group of healthy maleindividuals during squash (Northcote et al, 1983). Onecan assume, that such arrhythmias would be more likely
in the presence of CHD. Apart from myocardial ischaemia,a number of reasons exist which may explain thisphenomenon during or immediately after exercise.
Serum catecholamines rise during strenuous exerciseand may result in myocardial ischaemia and arrhythmiasin the presence of CHD (Raab et al, 1962). In theimmediate post-exercise period, serum concentrations ofcatecholamines and free fatty acids are known to beelevated (Dimsdale et al, 1984; Johnson et al, 1969).Both of these changes may be responsible for cardiacarrhythmias at this time (Northcote et al, 1983; Goochand McConnel, 1970). Other biochemical changes suchas exercise induced hyperkalaemia, may also contributeto the generation of arrhythmias (Lim et al, 1981).Likewise, environmental influences such as humidity andhigh temperature, are known to elevate heart rate andincrease cardiac ectopic activity (Taggart et al, 1972).Smoking is capable of stimulating both catecholaminerelease and an increase in free fatty acids in the serum(FFA's) (Ball and Turner, 1974; Kershbaum et al, 1961).
Heat StrokeHeat stroke, noted particularly in marathon running(Wyndham and Strydom, 1969), may result in haemo-concentration, which could make thrombus formationand subsequent coronary artery occlusion more likely. Ithas also been shown to cause patchy, subendocardialnecrosis (O'Donnel and Clowes, 1972).
The potentially hazardous effects of strenuousexercise outlined above are probably more harmful inthe presence of CHD or other cardiovascular abnor-mality. It is likely, that in the normal heart, theseinfluences are benign.
PREVENTIONRecognising the Problem
Study into the phenomena of sudden death duringvigorous exertion, is hindered by inadequate registrationand investigation of each case. At present, a death is
289
registered without information of the activity of thedeceased prior to death. Thus, the frequency of deathduring exercise is not known. There is a need for greaterrecognition of this problem in view of the growth inthe number of reported deaths and increasing age ofparticipants. Sports governing bodies can assist byattempting to document the extent and nature ofsudden death in their own sport. The Squash RacketsAssociation (SRA) is to be commended for its effortsin this way. They have gone as far as circulating somesensible suggestions to prospective players in an effortto reduce any complications occurring when playingsquash.
Which Sport?It is perhaps unfortunate, that squash has been subjectto much media coverage because of the prevalence ofsudden death. This may be a reflection of the individualsengaged in the sport. The SRA themselves, estimate thatthere may be 165,000 players over 45 years of ageplaying in the UK. As it is such a physically demandingsport, it may be wiser for individuals in the coronaryprone age group to consider more gentle forms ofexercise if taking up sport for the first time after someyears of inactivity. The present boom in marathonrunning is also potentially hazardous to the coronaryprone or those with undetected, overt, cardiovasculardisease. Only a few years ago, we would have questionedthe sanity of recommending a 26 mile run to a 50 yearold, but now this activity is encouraged! There is no evi-dence that such endeavours are more beneficial to thecardiovascular system, than other, more gentle forms ofexercise. Why has jogging a few miles a few times a weekbecome "unfashionable"? We would recommend thatindividuals should be encouraged to exercise, but toparticipate in sports which are suited to their age,physical ability and general health. Walking, jogging,swimming and cycling would be suitable in this respect.
EducationThere is a requirement for more adequate education andsupervision of the embryo sportsman. All sportsmenshould be aware of the small risks attached to vigorousexercise, and should be able to recognise warning symp-toms. Aggressive, competitive sportsmen have beennoted to deny prodromal symptoms (Opie, 1975;Northcote et al, 1984). Individuals should be encouragedto refrain from strenuous exercise if such symptomsoccur. It has been suggested that individuals should notexercise when suffering from an upper respiratory tractinfection or other pyrexial illness, as this can be accom-panied by a potentially lethal subdinical myocarditis(Kocnar and Rous, 1973). Although we have not beenable to implicate myocarditis as an important cause ofsudden death in sportsmen, we agree that vigorousexercise should be discouraged at this time. The medicalprofession and those concerned with the supervision ofsportsmen should be aware of the consequences of such
group.bmj.com on May 8, 2011 - Published by bjsm.bmj.comDownloaded from
prodromal symptoms and conditions. In a recent study(Northcote et al, 1984), of 30 sudden deaths in associa-tion with squash, we found that one third of theindividuals had hypertension documented on two ormore occasions, but this had been treated in only onesubject. Three subjects had hyperlipidaemia, three hadangina or previous myocardial infarction (Ml) and onesubject was known to have suffered a myocardial infarct10 years previously and also had aortic regurgitation,requiring regular review at a cardiology clinic. Thissubject had been told by his doctors that there was noharm in playing squash!
Pre-participation Medical ScreeningIndividuals such as those outlined above may benefitfrom medical screening which would detect overt cardio-vascular disease and would indicate a relatively increasedrisk. However, having been advised of this increasedrisk, it is of course the individual's decision whether hepersists in playing a particular sport.
The practicality of medical screening has been ques-tioned. However, often a simple interview and clinicalexamination would suffice. This would allow detectionof CHD risk factors, and overt, potentially lethal cardio-vascular disease. If a subject was found to have one ormore CHD risk factors or was symptomatic, we wouldadvocate screening using exercise electrocardiography.This policy has also been suggested elsewhere (Chung,1980; Levy, 1981; Nye, 1983).
The value of exercise electrocardiography in thisrespect is not solely related to the detection of CHD. Itcan be a useful investigation for predicting futurecoronary events. There is good evidence that it does so(Table 1). Bruce and McDonough (1969) studied 221asymptomatic men and found that those with an abnor-mal appearance on the exercise electrocardiogram had arelative risk of subsequent CHD, 13.6 times greater than
normal over the subsequent five years. Other workershave reported similar results ranging from a relative riskof 10-20 (Aronow, 1973; Forelicher et al, 1974;Cumming et al, 1975). We believe that the evidence ofthe exercise test result, when added to the other riskfactors assessed, would enable one to provide betteradvice to the subject contemplating strenuous sportingactivity. In the present state of knowledge, however, itwould not be justifiable to proceed from a positiveexercise test result in an asymptomatic subject to eitherthallium scintigraphy or coronary angiography.
We appreciate the potential cost of such a programme,but feel this could be minimised by screening the popu-lation at greatest risk, i.e. males> 35 years. Facilities forthis could perhaps be made available on a payment basiswithin the NHS or could be provided by individualsports centres.
Changes in individual sportsCertain sports could be made safer by alterations in theirrules. In boxing, title fights are now conducted over 12rounds instead of 15, and Olympic boxers now requireto wear "head guards". Possibly by improving theenvironment of some sports, a reduction in mortalitymay occur. Improved ventilation and temperaturecontrol on squash courts may be beneficial. Although itwould seem commercially unviable at the present,alterations in court design may be desirable. Variouschanges have recently been suggested such as removingthe back wall, or making the court bigger - both ofthese measures would reduce the length of rallies andperhaps place more emphasis on racquet head skill,rather than physical effort.
Useful PrecautionsAdequate warming-up and warming-down should beencouraged, this may reduce the number of dysrhythmicdeaths. Likewise the discouragement of smoking and
NBLE IFollow-up studies using maximal treadmill test to screen asymptomatic men for latent coronary heart disease.
Main investigator
Bruce and McDonough(221 su bjects)
Aronow (100 subjects)
Froelicher et al(1390 subjects)
No. (%) ofYears Exercise ST segment total
followed-up test used response population
5 Bruce test Abnormal(CB) Normal
2.5 Bruce test Abnormal(V) Normal
22 (10)199 (90)
13 (13)87 (87)
6.3 Balke test Abnormal 140 (10)(CC) Normal 1250 (90)
avoidance of a hot bath or shower may reduce the harm-ful effects of increased levels of catecholamines, freefatty acids and potassium after exercise. Because of therisk of hyperpyrexia and heat stroke, vigorous activityin extreme heat should be avoided. The BostonMarathon in 1973, in which one runner died of a myo-cardial infarct was run when the environmental temper-ature was between 3Oo-35oC (Sheehan, 1976). Fluid andelectrolyte loss should be compensated, particularlyduring endurance events such as marathon running.Although feeding stations are available at most marathonevents, not all runners utilise this service adequately.Hypothermia following cessation of activity, particularlyin marathon runners, should be avoided by preventingheat loss. However, the practice of supplying aluminiumfoil "space blankets" to finishing competitors is anexpensive and ineffective way to do this. It may be
better for competitors to have their tracksuits madeavailable at the finishing point.
CONCLUSIONSMany may take the view that the preventive measuresabove are unnecessary because of the low statistical riskof sudden death in sport. However, the extent of theproblem is probably grossly underestimated. We do notknow the prevalence of non-fatal coronary events duringexercise, and are dependent on media reports forinformation on sudden deaths. It has been estimated,that in squash alone, 27 deaths occur per annum in theUK (Fowler, 1980). If this is true then there are likelyto be a considerable number of deaths in other sports,all amounting to an appreciable mortality. Thesuggestions expressed in this paper may help reduce theoccurrence of sudden cardiac death in sport.
REFERENCES
Aronow, W. S., 1973 "Thirty-month follow-up of maximal treadmill stress test and double master's test in normal subjects". Circulation47: 287-290.
Ball, K. and Turner, R., 1974 "Smoking and the heart. The basis for action". Lancet 2: 822.
Bruce, R. A. and McDonough, J. R., 1969 "Stress testing in screening for cardiovascular disease". Bull.N.Y.Acad.Med.: 1288-1305.
Chung, E. K., 1980 "Exercise ECG testing: is it indicated for asymptomatic individuals before engaging in any exercise program?"Arch.lntern.Med. 140: 895-896.
Cumming, G. R., Samm, J. and Borysyk, L. et al, 1975 "Electrocardiographic changes during exercise in asymptomatic men: 3 yearfollow-up". Can.Med.Assoc.J. 112: 578-581.
Dimsdale, J. E., Hartley, H., Guiney, T., Ruskin, J. N. and Greenblatt, D., 1984 "Post-exercise period: plasma catecholamines andexercise". JAMA 251: 630-632.
Fowler, A. W., 1980 "Cause of death on squash courts.". On Call 14: 7.
Froelicher, V. F., Thomas, M., Pillor, C. et al, 1974 "An epidemiological study of asymptomatic men screened with exercise testing forlatent coronary heart disease". Am.J.Cardiol. 34: 770-776.
Gooch, A. S. and McConnel, D., 1970 "Analysis of transient arrhythmias and conduction disturbances occurring during submaximaltreadmill exercise testing". Proc.Cordiovasc.Dis. 13: 293-307.
Johnson, R. H., Walton, J. L., Krebs, H. A. and Williamson, D. M., 1969 "Metabolic fuels during and after severe exercise in athletes andnon-athletes". Lancet 2: 452-455.
Kershbaum, A., Bellet, S., Dickstein, E. R. and Feinberg, L. 4., 1969 "Effect of cigarette smoking and nicotine on serum free fatty acids,based on a study in the human subject and the experimental animal". Circ.Res. 9: 631-638.
Kocnar, K. and Rous, J., 1973 "Preventive approach to sudden death at sports performance". Brit.J.Sports Med. 7: 166-167.
Kozar, A. J. and Himsicher, P. A., 1973 "A study of telemetred heart rate during sports participation". J.Sports Med.Phys.Fitness 3:1-5.
Levy, R. I., 1981 "Exercise and your heart" (NIH publication 81-1677). Washington: US Department of Health and Human Sciences.
Lim, M., Linton, R. A. F. and Band, D. M., 1982 "Jqggers blQckade". BMJ 284: 826.
Misner, J. E., Boileau, R. A., Courvoisier, D., Slaughter, M. H. and Bloomfield, D. K., 1980 "Cardiovascular stress associated with therecreational tennis play of middle aged males". Amer.Corr.Ther.Jnl. 34: 4-8.
Northcote, R. J., MacFarlane, P. and Ballantyne, D., 1983 "Ambulatory electrocardiography in squash players. Brit.Heart J. 50: 372-377.
Northcote, R. J. and Ballantyne, D., 1983 "Sudden cardiac death in sport". BMJ 287: 1357-1359.
Northcote, R. J., Evans, A. D. B. and Ballantyne, D., 1984 "Sudden death in squash players". Lancet 1: 148-151.
group.bmj.com on May 8, 2011 - Published by bjsm.bmj.comDownloaded from
Northcote, R. J. and Ballantyne, D., 1984 "Sudden death in sport". Leading article. Sports Medicine 1: 181-186.
Nye, E. R., 1983 "Exercise and the middle-aged patient". National Heart Foundation of New Zealand. Technical Report Series. ReportNo. 37.
O'Donnel, T. F. Jr. and Clowes, G. M. A. Jr., 1972 "The circulatory abnormalities of heart stroke". N.Engl.J.Med. 287: 734-737.
Opie, L. H., 1975 "Sudden death in sport". Lancet 1: 263-266.
Raab, W., Van Lith, P., Lepesch in, E. and Herrlich, H. C., 1962 "Catecholamine induced myocardial hypoxia in the presence of impairedcoronary dilatability independent of external cardiac work". Am.J.Cardiol. 9: 455.470.
Sheehan, G., 1976 "Marathon racing and myocardial infarction". Annals of Intern.Med. 85: 392.
Shephard, R. J., 1974 "Sudden death - a significant hazard of exercise". Brit.J.Sports Med. 8: 101.
Taggart, P., Parkinson, P. and Carruthers, M., 1972 "Cardiac responses to thermal, physical and emotional stress". BMJ 3: 71-76.
Thompson, P. D., Funk, E., Carleton, R. A. and Sturner, W. Q., 1982 "Incidence of death during jogging in Rhode Island from 1975through 1980". JAMA 247: 2535-2538.
Wyndham, C. A. and Strydom, N. B., 1969 "The danger of an inadequate water intake during marathon running". S.Afr.Med.Jnl. 43:893-896.
EDINBURGH POST-GRADUATE BOARD FOR MEDICINE(The University of Edinburgh, The Royal College of Physicians of Edinburgh,
The Royal College of Surgeons of Edinburgh)Held in Lister Institute, Roxburgh Place, Edinburgh
Registration from 9 a.m. (2 sessions: £20: Section 63)
SPORTS MEDICINE1st February, 1985
Run by Drs. Donald MacLeod, FRCS and Elizabeth McSwan, MBChB, this one day course will deal with varied aspectsof sports medicine. It is intended for all doctors involved in the medical care of those participating in sport.
MARATHON MEDICINE MEETING20th April, 1985 (Saturday before London Marathon)
Held in The Royal Festival HallDetails from Dr. Dan Tunstall Pedoe, Cardiac Dept., St. Bartholomew's Hospital, London EC1A 2BE
INTERNATIONAL SYMPOSIUM ON SPORTS CARDIOLOGY10th-12th May, 1985
KnokkeDetails from Bekaert 1, Algemeen Ziekenhuis Sint-Jozef, Steenweg op Merksplas 44, 2300 Turnhout, Belgium
Tel. 014/41.04.51 ext. 3514
group.bmj.com on May 8, 2011 - Published by bjsm.bmj.comDownloaded from
