Clinical Significance of Cardiac Damage and

Changes in Function after Exercise

CLINICAL SCIENCES

GREGORY P. WHYTE
Research Institute for Sport and Exercise Science, Liverpool John Moores University, Liverpool, UNITED KINGDOM

ABSTRACT
WHYTE, G. P. Clinical Significance of Cardiac Damage and Changes in Function after Exercise. Med. Sci. Sports Exerc., Vol. 40,
No. 8, pp. 1416–1423, 2008. Acute bouts of ultraendurance exercise may result in the appearance of biomarkers of cardiac cell damage and
a transient reduction in left ventricular function. The clinical significance of these changes is not fully understood. There seems to be two
competing issues to be resolved. First, could prolonged endurance exercise produce a degree of cardiac stress and/or damage that results,
during the short or long term, in deleterious consequences for cardiac health. Second, there is a clear need to educate those responsible for the
medical care of endurance athletes about the possibility of a transient reduction in cardiac function and the appearance of cTnT/cTnI after an
exercise. Minor elevations in cardiac troponins are commonplace after an endurance exercise in elite and recreational athletes and may occur
alongside exercise-associated collapse. Misdiagnosis of myocardial injury and subsequent mismanagement can be unnecessarily expensive
and psychologically damaging to the athlete. Diagnosis of myocardial injury after prolonged exercise should be made on the basis of all
available information and not blood tests alone. The clinical significance of chronic exposure to endurance exercise is unknown. The
development of myocardial fibrosis has been suggested as a long-term outcome to chronic exposure to repetitive bouts of endurance exercise
and has been linked to an exercise-induced inflammatory process observed in an animal model. This hypothesis is supported by a limited
number of studies reporting postmortem studies in athletes and an increased prevalence of complex arrhythmia in veteran athletes. Care is
warranted in promoting this hypothesis without further detailed work, given the unequivocal link between exercise and mortality and
morbidity. It would seem erroneous, however, to assume that a linear relationship exists between exercise volume and cardiac health.
Key Words: MYOCARDIAL FIBROSIS, ARRHYTHMIA, TROPONINS, INFLAMMATION

R
ecent work from our laboratory, and others, has sug-
gested that acute bouts of ultraendurance exercise may
result in the appearance of biomarkers of cardiac cell
damage in the systemic circulation and a transient reduction in
the left ventricular (LV) function (9,23,27,36,49,50,56).
Establishing the clinical significance of changes in cardiac
biomarkers and function after acute and chronic endurance
exercise is important in the management of the endurance
athlete.
There seems to be two competing but equally important
issues that scientists and clinicians must resolve. First, could
prolonged endurance exercise produce a degree of cardiac
stress and/or damage that results, during the short or long term,
in deleterious consequences for the health of the heart. This
requires further analysis of the current cardiac biomarker liter-
ature, reflection on cohort, case study data related to topics
such as sudden cardiac death, and ongoing empirical data
Address for correspondence: Gregory P. Whyte, Ph.D., FACSM, Research
Institute for Sport and Exercise Science, Liverpool John Moores University,
Liverpool, L3 2ET, United Kingdom; E-mail: gregwhyte27@yahoo.co.uk.
Submitted for publication December 2007.
Accepted for publication March 2008.
0195-9131/08/4008-1416/0
MEDICINE & SCIENCE IN SPORTS & EXERCISEÒ
Copyright Ó 2008 by the American College of Sports Medicine
DOI: 10.1249/MSS.0b013e318172cefd
collection. Furthermore, this necessitates an evaluation
of broader aspects of cardiovascular health in the athlete with
a lifetime history of endurance exercise exposure. Clearly, in-
terpretation and speculation must adequately reflect a risk/
benefit analysis that includes the beneficial effects of moder-
ate physical activity in reducing cardiovascular mortality and
morbidity (12). Baseless speculation and scaremongering
could have a profoundly negative impact on the uptake of
physical activity in the general population. Second, there is a
clear need from a clinical perspective to educate those res-
ponsible for the medical care of endurance athletes about the
possibility of a transient reduction in cardiac function and the
appearance of cTnT/cTnI in the systemic circulation. Case
study evidence suggests that cTnT/cTnI detected in blood
samples after an event, associated with other signs and
symptoms of the athletic heart (mimicking cardiac disease),
may prompt significant medical intervention when, physio-
logically, these signs and symptoms may be entirely normal
and indeed common. A vivid example of the necessity for
raising awareness in this field is provided.
CLINICAL SIGNIFICANCE OF ACUTE ELEVATIONS
IN CARDIAC TROPONINS
Minor elevations in cardiac troponins are commonplace
after endurance exercise in elite and recreational athletes and
may occur alongside exercise-associated collapse after an
endurance exercise. The collapse of an athlete concomitant to

1416

Copyright @ 2008 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
minor elevations in cardiac troponins and ECG anomalies
commonly observed in athletes, particularly rapid uptake of
the ST segment (ST elevation), may lead to the inappropriate
provision of care. We recently described the inappropriate
provision of care in a triathlete immediately after the
successful completion of an Ironman triathlon (58). After a
postrace massage and prolonged standing in the heat, the
athlete reported presyncopal symptoms and collapsed with-
out syncope. Blood pressure was measured at 75/40 mm Hg,
and after fluid resuscitation, the athlete was referred to the
cardiology department of the local hospital. The athlete was
conscious and alert with normal core temperature, blood
glucose, and plasma sodium and was otherwise asympto-
matic. On admission, his ECG demonstrated minor ST
segment elevation in the anterior lateral and inferior leads,
and his cTnI was mildly elevated at 0.06 UILj1. Echocardio-
graphy was normal with mild, concentric left ventricular
hypertrophy (LVH). The athlete underwent diagnostic cardiac
catheterization, which demonstrated normal coronary arteries.
On the basis of the mildly elevated cTnI and minor ST segment
elevation, the athlete was diagnosed with mild myopericarditis
and advised to avoid exercise for 6 wk. On follow-up, 2 wk
after being discharged from hospital, the resting 12-lead ECG
demonstrated similar findings of marginal ST segment
elevation in anterior lateral and inferior leads. Echocardio-
graphy demonstrated mild concentric left ventricular hyper-
trophy (12 mm) in the presence of normal diastolic and systolic
function. There was no evidence of myocarditis or pericar-
ditis, and the athlete was immediately cleared for training and
competition.
It is entirely possible that acute elevations of cardiac tro-
ponins are likely to be physiological in nature because of their
rapid appearance and return to baseline (G24 h), the generally
low values observed, and the lack of other signs and symptoms
of cardiac disease. Therefore, they may, have little or no cli-
nical significance. Indeed, some authors have suggested that
their release may, in part, be related to the regulatory process
of cardiac adaptation to exercise (48). The appearance and
removal of cardiac troponins in athletes are normally in
contrast to the kinetics of cardiac troponin release observed
after myocardial infarction, where an initial release of un-
bound (cytosolic) troponin is followed by a continued release
of the structurally bound troponin as it degrades, resulting in
a sustained elevation in circulating troponin for many days
after infarction (37). Accordingly, the use of one-off mea-
sures of cardiac troponins should be viewed with caution
after prolonged exercise. Serial measures of cTnT/cTnI after
exercise may assist in the differentiation of underling phy-
siologic versus pathologic mechanisms, but this has rarely
been reported. Misdiagnosis of myocardial injury after ultra-
endurance exercise and subsequent mismanagement including
hospitalization and invasive intervention can be unnecessarily
expensive and psychologically damaging to the athlete.
Diagnosis of myocardial injury after prolonged exercise
should be made on the basis of all available information and
not blood tests alone.
CLINICAL SIGNIFICANCE OF CARDIAC DAMAGE
Copyright @ 2008 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
The underlying mechanism(s) responsible for exercise-
induced cTnT release is unknown. Furthermore, the long-
term impact and clinical significance of chronic exposure to
CLINICAL SCIENCES
elevations in cTnT on the heart is unclear. On this basis, we
cannot provide any strong conclusion as to the immediate or
short-term clinical significance of elevated cardiac tropo-
nins associated with bouts of prolonged exercise.
CLINICAL SIGNIFICANCE OF CHRONIC
EXPOSURE TO ENDURANCE EXERCISE
Endurance exercise and reactive scar tissue
formation. The ‘‘leap’’ from cardiac responses to indi-
vidual bouts of prolonged exercise to the consequences of
chronic exposure to such training is not straightforward, and
prospective data are limited. Despite this, the concept that
individual bouts of exercise, producing cTnT/cTnI release,
reflects minor but irreversible cardiomyocyte damage has
been proposed by many studies that have suggested that
endurance exercise may lead to scar tissue formation in the
myocardium (23,24,26,42,52,54,59). The development of
myocardial fibrosis has been linked to an exercise-induced
inflammatory process observed in an animal model (6). It is
pertinent to prompt some debate and further research to
inform current understanding of the clinical significance of
chronic exposure to endurance exercise.
Two hypotheses for the significance of the minor myocar-
dial injury, evidenced by elevated cardiac troponins, observed
after prolonged endurance exercise have been proposed in the
literature (24,44). Myocardial injury with exercise is rever-
sible and followed by repair and results in myocyte hyper-
trophy. This process is analogous to the process involved in
the response of skeletal muscle to training and is termed
‘‘supercompensation’’ (61). Thus, this hypothesis contends
that myocardial injury is a physiological signal for adaptation
leading to an enhanced structure and function. In contrast, a
second hypothesis (44) suggests that myocardial injury is
followed by scarring leading to fibrotic replacement of the
myocardium that is associated with an increased potential for
arrhythmia generation. This hypothesis contends that myo-
cardial damage leads to a pathologic process of myocardial
replacement that may be deleterious to the heart.
To provide more detail, Rowe (43) suggested that perm-
anent cardiac damage could develop in some endurance
athletes despite the absence of coronary atherosclerosis and
ventricular hypertrophy proposing two physiologic ‘‘vicious
cycles’’ that could lead to fibrotic replacement of the myo-
cardium: 1) severe ischemia and high catecholamines and
2) coronary vasospasm and endothelial injury. Other
suggested mechanisms with exercise included Mg2+ defi-
ciency, elevated free fatty acids, and elevated free radicals.
Of note, the author postulated that injury becomes permanent
if there is insufficient time between repeated bouts of exercise.
Evidence to support the notion of a pathologic process of
fibrotic infiltrate after exercise is limited. A small number of
Medicine & Science in Sports & Exercised 1417

CLINICAL SCIENCES
FIGURE 1—Representative hematoxylin–eosin-stained cross section of
LV. Damaged myocardial fibers and damaged intracellular areas are
shown by foci of inflammatory infiltrates consisting of neutrophils,
lymphocytes, and histiocytes (a) and vesicular nuclei-enlarged chro-
matin patterns (b) (6).
animal and human studies have reported findings from acute
and chronic exercise exposure that support this hypothesis.
Animal studies. Chen et al. (6) examined the heart of
rats after a forced swim for 3.5 or 5 h with 8% of body mass
attached to their tails. The rats were killed immediately after
exercise and histologic examination demonstrated localized
myocyte damage demonstrated by interstitial inflammatory
infiltrates consisting of neutrophils, lymphocytes, and
histiocytes (Fig. 1). Again, care is warranted in the in-
terpretation of this finding given the highly stressful
environment induced with survival in this model. It is
evident, however, that exercise per se is able to induce
inflammatory changes within the myocardium, which may
act as a substrate for fibrotic replacement of the myocardium.
Another study reported findings from the hearts of five horses
that died suddenly (22). Autopsy findings revealed foci of
myocardial fibrosis in the right atrium, interatrial septum,
interventricular septum, and the conduction system. The
authors postulated a relationship between sudden cardiac
death and fibrotic and/or fibroplastic lesions in the area of the
atrioventricular bundle and bundle branches associated with
exercise, regardless of age.
Human studies. Limited premortem evidence exists to
support the presence of cardiac fibrosis in athletes. A
recent study reported a biochemical evidence for cardiac
fibrosis in veteran endurance athletes (25). The authors
suggested that the incomplete reversal of cardiac hypertrophy
after cessation of exercise training observed in veteran
athletes (34) is because of the presence of cardiac fibrosis.
Using humeral collagen markers (TIMP-1, CITP, and PICP),
the authors demonstrated an association between LVH and
a disruption of the collagen equilibrium and suggested that
this would favor the development of cardiac fibrosis in
veteran athletes. Although interesting, care is warranted in
the interpretation of the cause and effect from such
relationships, and further studies are required to corroborate
the findings.
1418 Official Journal of the American College of Sports Medicine
Copyright @ 2008 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
A small number of studies have reported fibrotic in-
filtrate in the hearts of trained endurance athletes at autopsy.
Virmani et al. (52) reported autopsy findings in 30 joggers
who suffered sudden cardiac death. Of 30 athletes, 7 (25%)
had no identifiable cause of death at autopsy. Of these, three
of the hearts were hypertrophied and six had evidence of
myocytolysis and contraction band necrosis. The authors
hypothesized that coronary vasospasm, possibly induced
during the stress of exercise, leading to a cascade of ischemia,
necrosis, and fibrosis, was a possible mechanism responsible
for these findings.
In one of the most prolifically cited papers on the subject,
Rowe (42) reported on the death of a world-record
marathon runner (cause of death: lymphoma). Premortem,
the athlete had experienced episodes of angina, and in the
presence of normal coronaries, had been diagnosed with
circadian variation in the coronary vasospasm (Prinzmetal
angina). At autopsy, small, patchy nontransmural scar in the
LV posterior wall and focal fibrosis of the left papillary
muscles consistent with remote ischemic insult were observed
in the presence of normal coronaries and microvasculature.
The author suggested that ischemia associated with coronary
vasospasm was responsible for the observed scarring. The
mechanism underlying the proposed coronary vasospasm
remains unclear, although, exercise may play a critical role.
A recent highly publicized study reported on the sudden
cardiac death of 16 Swedish orienteers between the years
1979 and 1992 (7 occurring between 1989 and 1992) (54).
Of 16 athletes, 5 presented with active myocarditis and 4
with arrhythmogenic right ventricular cardiomyopathy
(ARVC)-like alterations in the right ventricle (RV). All
athletes had undergone medical examination including ECG
on entry to the Swedish military. Of the four athletes
presenting with ARVC-like changes, only one athlete had
received a follow-up evaluation after an episode of
tachycardia. In the other three athletes, no cardiac signs or
symptoms had been reported premortem. There was
no family history of sudden unexplained death in any of
the athletes. The etiology of the ARVC-like changes
observed in these athletes is unclear; however, the absence
of overt ARVC may suggest an exercise-mediated mecha-
nism. Care is warranted, however, because first-degree
relatives were not screened after the death of the athletes.
Furthermore, the disease may have been in the early
concealed phase of ARVC where identification is difficult
(51).
In a recent case study from our group, we reported on the
presence of idiopathic interstitial myocardial fibrosis and
idiopathic LVH (ILVH) at postmortem in the heart of an
athlete that died suddenly during a marathon race (59). The
deceased had been running for 20 yr, having completed
multiple marathons, with a personal best time of 2 h 30 min.
At autopsy, the weight of the heart was 480 g, which is
above that expected for a 75-kg male (upper limit of 431 g),
and there was widespread replacement fibrosis particularly in
the lateral and posterior ventricular walls as well as interstitial
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FIGURE 2—Widespread replacement fibrosis particularly in the
lateral and posterior ventricular walls as well as interstitial fibrosis in
the inner layer of the myocardium. Myocyte hypertrophy was observed
around the areas of scarring but no myocyte disarray indicative of
hypertrophic cardiomyopathy.
fibrosis in the inner layer of the myocardium (Fig. 2).
Premortem, the athlete was healthy and free from cardiovas-
cular disease, and there was no documented evidence of
diseases associated with widespread myocardial fibrosis. The
cardiac pathologic findings were consistent with a left
ventricular hypertrophy of indeterminate causation (also
known as ‘‘idiopathic left ventricular hypertrophy,’’ ILVH)
in the presence of idiopathic interstitial fibrosis. ILVH has
been previously documented in athletes at postmortem
associated with sudden cardiac death (45,47). In an early
study of 30 nontraumatic deaths, Virmani et al. (52) observed
ILVH with coexiting myocytolysis and contraction band
necrosis in three joggers. In addition, Maron and Roberts
(29) reported a 7.5% incidence of ILVH at autopsy in
athletes after sudden cardiac death.
In postulating a mechanism for the development of myo-
cardial fibrosis, it is important to exclude known patholog-
ical substrates for its development. Widespread myocardial
fibrosis is observed in healed myocarditis, dilated cardio-
myopathy (28), hypertrophic cardiomyopathy, noninfarcted
myocardium from hearts with ischemic scars (53), and
systemic hypertension (40) and is rarely linked to small
intramural coronary artery disease. An increased collagen
content after Sirius red FB3 staining of the myocardium is
also observed in the presence of inflammatory and amyloid
cells and as a result of myocarditis at autopsy. Fibrosis creates
a potential substrate for reentry, arrhythmia, and sudden
cardiac death. Importantly, it is not the density of fibrosis that
dictates the arrhythmia potential rather the position of fibrosis,
i.e., near the conduction system and the architecture of fibrosis
(19). Thus, a low density of patchy fibrosis may be sufficient
to propagate fatal arrhythmias.
The etiology of the fibrosis observed in the studies
presented is unclear. The potential relationship between the
CLINICAL SIGNIFICANCE OF CARDIAC DAMAGE
Copyright @ 2008 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
elevated levels of the humeral markers of cardiac myocyte
damage observed after acute bouts of prolonged exercise
might suggest that chronic exposure to repeated bouts of
CLINICAL SCIENCES
minimal cardiac damage may result in the development of
interstitial myocardial fibrosis in some individuals. Limited
evidence to support this hypothesis exists in the literature,
likely because of the absent histological examination of the
hearts of athletes postmortem. Long-term follow-up of
athletes and closer interrogation of veteran athletes may shed
light of the impact of prolonged repetitive bouts of endurance
exercise.
Arrhythmia and the athlete. Previous studies have
reported an increased incidence of supraventricular,
complex ventricular, and profound bradyarrhythmias in
veteran athletes (5,11,14–16,18,38). Although the
underlying mechanism for this increased arrhythmia
prevalence is not fully understood, it has been suggested that
structural changes of the electrical conduction system and the
myocardium including interstitial fibrosis may be responsible.
Heidbuchel et al. (13) reported findings from 46 well-
trained endurance athletes presenting with ventricular arrhyth-
mia (VA). Eighty percent of the arrhythmias had a left bundle
branch morphology and a RV arrhythmogenic involvement
was manifest in 59% of athletes and suggestive in 30%. The
prognosis for these athletes was poor with a sudden death
incidence of 25% (all cyclists) in a 4.7-yr follow-up. The
authors postulated that repeated RV insults may lead to
chronic RV dysfunction providing a substrate for arrhythmia.
Although the authors recognized that the pathophysiology of
arrhythmias in endurance athletes is poorly understood, they
hypothesized that long-lasting volume overload and a higher
tendency to resort to performance enhancing drugs may play
a role in revealing an underlying (genetic) substrate and/or in
promoting the development of VA. This concept is supported
by recent findings in a mouse model of ARVC. Kirchof et al.
(21) demonstrated that heterozygous plakoglobin-deficient
mice presented an accelerated development of RV dysfunc-
tion and arrhythmia in response to endurance training. Based
on these findings, the term ‘‘exercise-induced ventricular
dysplasia’’ was coined.
Ector et al. (10) examined 22 endurance athletes present-
ing with VA. Findings suggested an RV arrhythmogenic
origin in 82% of athletes with RV dysfunction as the pre-
disposing substrate. The authors concluded that endurance
exercise may act as a promoter for RV structural remodeling
and a resultant trigger for VA. Some care is warranted in the
interpretation of this finding. Several forms of idiopathic VA
have been identified in athletes that, by definition, originate
in hearts without structural abnormalities (2). The differ-
entiation of pathological VA and benign VA originating in
the RV is clinically important when discussing prognosis and
management options (39). This is of particular importance in
the differentiation of right ventricular outflow tract–ventricular
tachycardia and arrythmogenic right ventricular cardiomyop-
athy (ARVC) given the association of the latter with sudden
death in athletes (51). Long-standing VA can result in
Medicine & Science in Sports & Exercised 1419
 ventricular hypokinesis leading to dysfunction. It is im-
portant to note, however, that after cardioversion through
pharmacologic or nonpharmacologic means, a normal func-
CLINICAL SCIENCES
tion is often restored suggesting a nonpermanent cause of
VA (57).
The clinical significance of supraventricular, complex ven-
tricular, and profound bradyarrhythmias remains to be fully
elucidated. Evidence from Heidbuchel et al. (13) would sup-
port a potentially fatal outcome of complex VA in endurance
athletes. Postmortem evidence of arrhythmic death in the
absence of any other cause is difficult to collect, and very
few studies have proposed an arrhythmic substrate as the
cause of death. One study reporting the deaths of 60 squash
players suggested an arrhythmic cause in 2 players (38).
Unfortunately, the authors failed to describe how this
conclusion was reached. Further studies are required to
identify the underlying mechanisms of arrhythmia and their
clinical significance in athletic populations.
CLINICAL SIGNIFICANCE OF ACUTE CHANGES
IN CARDIAC FUNCTION AFTER
PROLONGED EXERCISE
A small and transient depression in cardiac function is
commonly observed after acute bouts of endurance exercise
(33). The nature of these changes seems dependent on
a number factors such as exercise duration (7,31,33,55).
Whether the changes represent global or regional responses
to the prolonged exercise is open to some debate (33), but
evidence of regional dyskinesis has been reported (9,24,
36,41). These findings offer some support for a ‘‘true,’’
load-independent depression in LV function, which requires
further investigation. The mechanisms underlying the
observed dysfunction remain elusive (56), and the clinical
consequences have yet to be fully evaluated. The time course
of change in cardiac function after prolonged exercise is such
that rapid recovery occurs normally within 24–48 h (7,31,33)
and again supports the suggestion that the changes observed
are physiological in nature. In this case, there may be limited
clinical significance of such changes.
A small number of studies have reported more prolonged
changes in function. Neilan et al. (36) reported the persistence
of diastolic changes 4 wk after a marathon in recreational
runners. La Gerche and Prior (24) noted sustained RV
dysfunction in one athlete at 7 d and 12 months after an
Ironman triathlon. Occasionally, there have been case reports
of a more profound acute impact of cardiac function. An
early study reported pulmonary edema in two highly trained
runners after an ultraendurance race. The authors suggested
that RV dysfunction may have resulted in pulmonary con-
gestion leading to pulmonary edema (32). This has prompted
some specific interest in the response of the RV to bouts of
prolonged exercise. The difficulty associated with imaging
the RV has led to a preponderance of studies examining the
left ventricle; however, the RV may be less able to compen-
sate for the sustained elevation in cardiac output and/or pul-
1420 Official Journal of the American College of Sports Medicine
Copyright @ 2008 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
monary hypertension during prolonged exercise. In an early
study, Douglas et al. (9) observed RV dilatation and seg-
mental wall motion abnormalities in triathletes immediately
after an Ironman triathlon. Davila-Roman et al. (8) examined
cardiac function in 14 well-trained runners after a high-
altitude ultraendurance run (163 km). Immediately after
exercise, 35% (5/14) of runners presented with RV dilatation
and dyskinesis. The authors concluded that an increased
pulmonary artery systolic pressure (PASP) i.e., pulmonary
hypertension was responsible for the observed changes. In a
recent study, La Gerche et al. (23) examined cardiac function
in 26 triathletes after an Ironman triathlon. The authors
reported RV dysfunction in all subjects in the absence of
change in PASP.
These data prompted further study; however, there is
some suggestion that some individuals have more marked
or more clinically relevant changes in cardiac function after
prolonged exercise. There may also be a genetic component
in the presence of cardiac troponins and the level of cardiac
dysfunction after an acute bout of endurance exercise (3).
At this stage, again, we do not know what the long-term
relevance of such changes are nor can we identify those
individuals at greater risk. The development of our under-
standing of the mechanism(s) underlying the changes in LV
and RV function after a single bout of endurance exercise
will likely aid the development of understanding related
to the notion that an acute bout of prolonged endurance
exercise could have a prolonged deleterious effect on car-
diac function.
FUTURE DIRECTIONS
Future studies should examine the cardiac response to, and
clinical significance of, repetitive bouts and lifelong partic-
ipation in endurance exercise. Cross-sectional and prospective
studies of veteran athletes engaged in lifelong endurance
exercise may be valuable in elucidating the impact of
repetitive cardiac insults imposed by endurance exercise.
Further studies are required to examine the potential rela-
tionship between minimal cardiac damage, inflammation, and
interstitial myocardial fibrosis. Within this quasiphysiologic
milieu, inflammation may be the precursor of the observed
fibrosis. Recently, cardiovascular magnetic resonance (CMR),
by the technique of delayed myocardial contrast hyperenhance-
ment, has been successfully used to visualize acute and chronic
myocardial infarction (4,20,60). This technique relies on the
difference between wash-in and wash-out kinetics and the
volume of distribution of gadolinium in edematous/fibrotic
myocardium. This technique shows promise in detecting
causes of myocardial fibrosis including sarcoid, systemic
sclerosis, hypertrophic cardiomyopathy, and dilated cardiomy-
opathy (30,35). In addition to the identification of interstitial
fibrosis, work from our group has demonstrated a role for late
gadolinium-enhanced CMR and STIR scans in the identi-
fication of myocardial inflammation (4). Future studies should
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FIGURE 3—Hypothetical relationship between exercise volume and incidence of cardiac events.
aim to investigate the potential inflammatory effects of en-
durance exercise on the heart of humans.
CONCLUSIONS
A burgeoning body of literature supports a positive impact
of moderate-intensity, moderate-duration exercise on mortal-
ity and morbidity. In contrast, little is known regarding the
upper limit of exercise volume (intensity, frequency, and
duration) for cardiac health. It would seem erroneous to
assume that a linear relationship exists between exercise
volume and cardiac health. A plateau or possible increased
risk may be present with very high exercise volumes (Fig. 3).
It is apparent from the literature that there exists the
potential for a clinically relevant or pathological response to
prolonged arduous exercise in a small number of individuals.
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CLINICAL SIGNIFICANCE OF CARDIAC DAMAGE
Copyright @ 2008 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
CLINICAL SCIENCES
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