REVIEW ARTICLE
Cardiac Risk of Extreme Exercise
Zarina Sharalaya, MD and Dermot Phelan, MD, PhD
Abstract: Habitual moderate intensity exercise is a vital component
of a healthy lifestyle. For most of the population, increasing exercise
duration and intensity beyond current recommendations appears to
impart additional cardiovascular benefits; however, recent data has
raised the possibility of an inflection point after which additional
exercise no longer imparts benefit and may even result in negative
cardiovascular outcomes. Exercise at the extremes of human
Downloaded from http://journals.lww.com/sportsmedarthro by BhDMf5ePHKbH4TTImqenVPVWEjt0ik0+CmQ/g95MGUz7bYt5bv9cyqkrZlRBpT+AVUsf9hZAQZ4= on 01/08/2019
endurance places a large hemodynamic stress on the heart and
results in occasionally profound cardiac remodeling in order to
accommodate the huge increases in cardiac output demanded by
such endeavors. These changes have the potential to become mal-
adaptive and heighten the risk of various arrhythmias, influence the
rate of coronary atherosclerosis, and alter the risk of sudden cardiac
death. Herein, we will discuss the potential negative impact of
extreme exercise on cardiovascular risk.
Key Words: athlete, cardiac, athlete’s heart, sports cardiology
(Sports Med Arthrosc Rev 2019;27:e1–e7)
T he long-term health benefits of regular moderate exercise
has been documented in multiple large-scale epidemio-
logic studies. As a result, governing health organizations
throughout the world are unanimous in encouraging the
general population to engage in regular exercise. Partic-
ipation in organized sporting activity continues to rise. It is
estimated that over 50 million Americans under the age of
35 years participate in regular, organized sporting
activities.1 Perhaps the most rapidly expanding population
of sporting enthusiasts are the over 35 year age group par-
ticipating in endurance sports such as the marathon and
triathlons.2,3
Unfortunately, for those with subclinical cardiac dis-
ease the risk of an adverse cardiac event during strenuous
exercise is heightened. This usually occurs in the context of
an unrecognized congenital cardiomyopathy or channelop-
athy or as a result of an unrecognized acquired cardiac
insult such as myocarditis. This causal association between
strenuous exercise and sudden cardiac death (SCD) in those
with underlying cardiac disease has been recognized for
many years and has resulted in large-scale efforts to reduce
the risk of SCD in athletes through the implementation of
preparticipation screening and eligibility/disqualification
guidelines. However, more recently, concern has been raised
about the potential adverse effect of long term, strenuous
exercise on the cardiac structure and function of otherwise
normal hearts. Herein, we will discuss the current available
literature on the impact of extreme exercise on cardiac risk.
From the Department of Cardiovascular Medicine, Sports Cardiology
Center, Cleveland Clinic, Cleveland, OH.
The authors declare no conflict of interest.
Reprints: Dermot Phelan, MD, PhD, Desk J1-5, Cleveland Clinic, 9500
Euclid Avenue, Cleveland, OH, 44195.
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Sports Med Arthrosc Rev  Volume 27, Number 1, March 2019
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EXTREME EXERCISE AND NORMAL CARDIAC
ADAPTATION
Regular intense exercise results in a variety of struc-
tural, functional, and electrical adaptations specific to the
cardiovascular system. Cardiac output increases on the
order of 3- to 6-fold to meet the heightened oxygen demands
during exercise via increased heart rate, stroke volume, and
peripheral vasodilation. The resultant increase in preload
and wall stress results in an adaptive increase in size of all 4
chambers of the heart and a balanced increase in left ven-
tricular (LV) wall thickness known as eccentric hypertrophy
(Fig. 1). The heart becomes increasingly compliant to allow
more efficient filling during exercise. Cardiac enlargement
and structural remodeling can begin as soon as 90 days after
starting a fixed and intense exercise regimen.4 Electrical
remodeling is also expected with regular intense exercise
training which can manifest in numerous ways on the resting
electrocardiogram (ECG) (Fig. 2). These changes are a
result of a combination of the structural cardiac changes
described above along with an altered balance within the
autonomic system, specifically heightened parasympathetic
or vagal tone and lower sympathetic tone. As extreme
exercise can induce these expected cardiac changes, it is
important to be able to distinguish normal adaptation from
underlying pathologic disease.
EXERCISE AND SCD IN ATHLETES WITH
UNDERLYING CARDIAC PATHOLOGY
It is well recognized that, despite the long-term benefits
of exercise, participation in sporting activity can transiently
increase the risk of an adverse cardiac event, particularly in
those with certain underlying cardiac pathologies. This
phenomenon is known as the “sporting paradox.” The
incidence of sports-related SCD is difficult to truly define
and has ranged from 0.12 to 13 per 100,000 person-years in
past studies.5 Mohananey et al5 conducted a recent meta-
analysis, including 21 studies encompassing 1994 SCDs over
437,156,081 person-years of study, ultimately revealing a
fairly low incidence of SCD in athletes of 1 per 138,889
person-years. The etiology of SCD does vary greatly with
age. For those under the age of 35, the most common eti-
ologies of SCD in athletes are inherited cardiomyopathies or
channelopathies. The most common cause of sports-related
SCD in the older athlete, traditionally defined as over the
age of 35, is coronary artery disease (CAD), involved in
> 80% of cases.6 Sports-related SCD is also higher in men
compared with women, black compared with white race and
increases with age. There have been a number of studies
looking at the incidence of SCD in extreme endurance
events. A study of 10.9 million marathon runners revealed
an incidence of SCD of 1 per 259,000 participants with
hypertrophic cardiomyopathy or possible hypertrophic
cardiomyopathy being the most common cause.7 The inci-
dence of SCD was 1.45 per 100,000 person-years in partic-
ipants of triathlon events over the course of 31 years. In this
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Sharalaya and Phelan Sports Med Arthrosc Rev  Volume 27, Number 1, March 2019

FIGURE 1. Serial cMR images in an endurance athlete showing the dramatic effects of training on left ventricular size. Images are steady-
state free precession images taken at the level of the base of the left ventricle from the short axis stack. The athlete was training for the
Ironman event in Kona at the time of the cMR in August 2016 which shows a severely dilated left ventricle (left ventricular end diastolic
diameter of 73 mm). The images from January and December were preseason and postseason when training duration and intensity was
significantly reduced (left ventricular end diastolic diameter of 63 mm). cMR indicates cardiac magnetic resonance imaging.

study atherosclerotic coronary disease was the most frequent
cause of SCD.
The tragic, unexpected death of an athlete during a
sporting event has a particularly profound emotional effect
on, not only the athlete’s family and friends, but society at
large. This has resulted in attempts to perform large-scale
screening of athletes in attempts to identify subclinical car-
diac abnormalities before participation in extreme exercise.
There remains debate as to the optimal means of screening
athletes. Pelliccia et al8 used a very comprehensive screening
strategy which included an ECG, exercise stress test, and an
echocardiogram to examine the presence of cardiac abnor-
malities in a group of 2352 Olympic athletes under age 35.
The prevalence of cardiovascular abnormalities was found
to be 3.9%. Therefore, the rate of detection/existence of
cardiovascular abnormalities is incrementally higher than
the risk of SCD.
The question then arises: what is the risk of partic-
ipating in extreme exercise with a known cardiac abnor-
mality? Eligibility/disqualification guidelines have been
devised largely predicated on the assumption that exercise is
a modifiable risk factor for SCD. For most cardiac con-
ditions, this assumption has been largely unproven and
based on expert opinion. As newer and more robust data
have become available these guidelines have altered over
time. For example, a large registry of young athletes who
continued to compete with an implantable cardioverter
defibrillator in situ demonstrated no increased risk of SCD
resulting in modification of the guidelines with removal of
the global disqualification of such athletes.9 Similarly,
patients with long QT syndrome were previously dis-
qualified from most competitive sporting activities until
convincing data demonstrated very low risk of cardiac
events in those who are asymptomatic receiving adequate
treatment.10,11 In contrast, certain pathologies have clear
evidence that continued exercise will result in progression of
the disease along with increased risk of SCD. Robust animal
and clinical/epidemiologic studies have proven the sig-
nificant adverse effect of exercise on the natural history of
arrhythmogenic right ventricular cardiomyopathy (ARVC).
Therefore, it would appear justified and in the best interest
of the athlete with ARVC to recommend significant exercise

FIGURE 2. Representative electrocardiogram of an elite endurance athlete showing typical findings in this cohort including profound
sinus bradycardia, borderline first degree heart block and early repolarization.

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Sports Med Arthrosc Rev  Volume 27, Number 1, March 2019
restrictions. In those athletes with preexisting CAD, guide-
lines recommend regular moderate or vigorous exercise to
improve physical fitness for secondary prevention.12 How-
ever, vigorous exercise has been shown to increase the risk of
a cardiac event acutely;13 several studies have explored the
impact of extreme exercise in patients with underlying CAD.
For example, Williams and Thompson14 reported an
incremental reduction in CVD-related mortality with
increasing levels of physical activity up to a certain point,
though above some level (30 mile/wk runs) there is a sig-
nificant increase in CVD mortality (P = 0.009). Another
study of over 1000 patients with CAD revealed an inverse
J-shaped association between physical activity and car-
diovascular mortality, with increased cardiovascular mor-
tality in patients who undertook daily strenuous physical
activity.15
It is clear that the risk of exercising with underlying
cardiac disease is dependent on the type and severity of the
condition and that recommendation with regard to exercise
activity in such athletes is nuanced and often requires shared
decision making.
EXTREME EXERCISE AS THE ETIOLOGY FOR THE
DEVELOPMENT OF CARDIAC PATHOLOGY
Although the holistic benefits of regular moderate
intensity exercise are well defined, recently, there has been
some concern with regard to the potential adverse cardiac
effects of extreme exercise (Fig. 3). Vigorous exercise has
been associated with higher levels of coronary artery
FIGURE 3. Proposed cardiovascular risks of extreme exercise. AF
indicates atrial fibrillation; OR, odds ratio; RV, right ventricle; VF,
ventricular fibrillation; VT, ventricular tachycardia.
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Cardiac Risk of Extreme Exercise
calcification (CAC)16 and may accelerate plaque formation
in athletes with established CAD, possibly through
increased arterial shear stress in coronary arteries with
existing plaque along with increased oxidative stress and
inflammation with intense exercise.17 Long-term endurance
training has been associated with higher risk of a variety of
conduction disturbances, atrial fibrillation (AF) most
commonly.18,19 Structural remodeling due to extreme exer-
cise can also present itself in the form of maladaptive RV
remodeling20 causing RV hypertrophy and fibrosis, which
can subsequently lead to higher risk of ventricular
arrhythmias.21 The rate of diagnosis of ARVC has been
growing in athletes and it is possible that the higher work-
load of exercise would worsen RV function.22 Extreme
exercise may cause aortic root remodeling due to repetitive
hemodynamic overload in the longer term.
Conduction Disease and AF
Risk of AF in Different Populations of Athletes
AF is commonly associated with other cardiovascular
disease states such as hypertension, valvular disease, and
coronary disease among others, but can also occur in
healthy individuals. The influence of exercise on the inci-
dence of AF is complex (Fig. 4). There is increasing recog-
nition that long term, endurance athletes are at higher risk
for the development of AF. It has been proposed that elite
athletes who perform years of regular exercise as well as
nonelite athletes who partake in a high volume of endurance
exercise have higher rates of AF.18 A study of 252 male
marathon runners revealed that they had a higher risk of AF
[hazard ratio (HR), 8.8] compared with a sedentary control
group over 11 year follow-up.24 Andersen and colleagues
examined the association between endurance exercise and
incidence of arrhythmias in a group of skiers competing in
the 90-km cross-country event in Sweden, Vasaloppet. Data
were compiled over 10 years yielding 52,755 participants
(90% male; mean age, 38.5 y) without known cardiovascular
disease. Arrhythmias were noted in 17.9% of all competitors
—a higher incidence of arrhythmias was noted with
increasing number of races [HR, 1.30; 95% confidence
interval (CI), 1.08-1.58; for ≥ 5 vs. 1 completed race] and by
faster finishing time (HR, 1.30; 95% CI, 1.04-1.62; for 100%-
160% vs. > 240% of winning time). AF was the most
common arrhythmia occurring in 681 skiers (13.2%; 95%
CI, 12.3-14.3/10000 person-years at risk). Another study of
cross-country skiers (age 65 years and older) who participate
in the Norwegian Birkebeiner race revealed a prevalence of
AF in skiers of 13% compared with 9.8% in the general
population, after excluding those patients with CAD.25
Furthermore, it was determined that AF increases with
years of endurance training; skiers had an odds ratio (OR)
of 1.16 for AF per 10 years of experience in comparison with
a sedentary population.25 Another study examining 78 male
skiers in the race showed AF prevalence of 12.8% compared
with the general population.26 Aizer et al27 analyzed data
from the Physicians’ Health Study and described an
increased risk of AF in those who exercised vigorously (7 d/
wk) compared with all other groups. Finally, a meta-anal-
ysis revealed that the risk of AF in endurance athletes was 5
times higher than in nonathletes (OR, 5.29; 95% CI, 3.57-
7.85).18
In contrast to the higher rates of AF noted in endur-
ance athletes, population-based studies in those who engage
in regular light-moderate physical activity have revealed
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Sharalaya and Phelan Sports Med Arthrosc Rev  Volume 27, Number 1, March 2019

FIGURE 4. The relative risk of AF as related to increasing level of physical activity23—permission was obtained from the publisher to
reprint this figure. AF indicates atrial fibrillation. Copyright Sage Publications, Newbury Park. All permission requests for this image should
be made to the copyright holder.

lower rates of AF compared with sedentary controls
(Fig. 1).18 The amount of activity necessary to decrease this
risk seems to be low recreational walking, cycling, or other
physical activity for > 4 hours per week which reduced the
risk of AF by 25%.23 Another study demonstrated that
walking for 20 minutes per day is protective against AF in
comparison with very sedentary people.28 A study of over
36,000 women (median age, 60 y) revealed that leisure-time
exercise of 1 to 4 hours per week or daily walking/bicycling
for at least 20 to 39 minutes per day was associated with a
lower risk of AF.29 Overall the literature supports a higher
risk of AF in athletes, while light and moderate physical
activity reduce AF risk; the mechanisms underlying AF in
these 2 populations may be different as will be discussed.18
Mechanisms of AF in Endurance Athletes
The mechanism behind higher rates of AF observed in
individuals undertaking vigorous exercise is not completely
understood. Suggested hypotheses include maladaptive left
atrial remodeling with fibrosis and enlargement, high
parasympathetic tone, oxidative stress, undiagnosed hyper-
tension, atrial ectopy, exercises-induced sympathetic nerv-
ous system surges, or the effect of alcohol or caffeine.7 Left
atrial size, an independent risk factor for AF, is usually
increased in athletes though cannot explain the association
between extreme exercise and AF entirely. A study of 107
patients partaking in moderate and heavy physical activity
had higher rates of AF even after controlling for LA size.30
Increased parasympathetic activity has been associated with
AF in people with structurally normal hearts,31 which is
likely a contributor to higher risk of AF in athletes.
Excessive exercise may lead to tissue injury, inflammation
and release of inflammatory cytokines which has also been
postulated to increase the risk of AF, as evidenced by higher
CRP and interleukins in those with paroxysmal and per-
sistent AF.32 The lower risk of AF in those who undertake
light-moderate physical activity may be influenced by
improvement of cardiovascular risk factors such as obesity,
hypertension, and diabetes which are also risk factors for
AF, though data are mixed.18
Conduction Disease in Athletes
Athletes can also be subject to conduction disease
leading to a variety of bradyarrhythimas, which have been
hypothesized to result from high vagal tone and possibly ion
channel remodeling within the sinus node.33 In the study of
cross-country skiers by Andersen et al,19 bradyarrhythmias
(mainly grade II and III AV block and sick sinus syndrome)
occurred in 2.3% of skiers (95% CI, 1.9-2.8/10000 person-
years at risk), and ventricular tachycardia/ventricular
fibrillation/cardiac arrest occurred in 90 participants but
notably there was no association with finishing time or
number of races as with the risk of AF. It is important to
consider if bradyarrhythmias persist in former athletes who
are now elderly. Baldesberger et al34 examined this issue in
62 former professional cyclists who were at least 60 years of
age and discovered that compared with age-matched con-
trols, the former athletes were more likely to have signs of

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Sports Med Arthrosc Rev  Volume 27, Number 1, March 2019
sinus node dysfunction with bradycardia <40 bpm, atrial
flutter, or prior pacemaker insertion for bradyarrhythmias
at a rate of 18% compared with 2% (P = 0.004). There was
also a trend toward more AF and ventricular arrhythmias in
the former athlete group compared with controls.
Extreme Exercise and Risk of CAD
Habitual exercise reduces the risk of developing CAD
and improves symptoms in those with established disease.
Encouraging people with CAD to be physically active is the
cornerstone of cardiac rehabilitation with demonstrable and
dramatic improvements in outcomes for those that
participate.35,36 In 2008 Mohlenkamp et al16 noted higher
coronary artery calcium scores in German marathon run-
ners than sedentary controls. Since the publication of this
study the hypothesis that exposure to intense, long-term
endurance exercise may hasten coronary atherosclerosis has
been hotly debated. Mechanisms that have been proposed to
support this idea are that regular exhaustive exercise may
induce oxidative stress due to a high-flow and high-pressure
state,37 and the release of inflammatory cytokines impairs
microvascular integrity and accelerates atherosclerosis.38
Although rare, SCD can certainly affect athletes and CAD
and coronary ischemia are the most common causes in this
population.39
CAC
A major topic of this discussion is CAC which is a quan-
titative manner of assessing plaque burden and has been well
correlated with cardiovascular disease.40 Data have been con-
tradictory; in a study of young individuals, over the course of
15 years those with moderate to high cardiorespiratory fitness
had OR of 0.8 and 0.59, respectively for having CAC as opposed
to those with low cardiorespiratory fitness.41 The most recent
studies on this topic are somewhat opposing in their results as
they relate to athletes. Merghani et al42 studied 152 competitive
cyclists and runners with an average age of 55 and compared
them with a control group without CAD or cardiovascular risk
factors. 60% of athletes and 63% of control subjects did not have
any CAC though very high CAC scores ( > 300 Agatston units)
or coronary artery luminal stenosis of ≥ 50% were only seen in
the athletic group (11.3% and 7.5%, respectively) both of which
were associated with years of training. It was interesting to note
that athletic men were more likely to have purely calcified pla-
ques as opposed to sedentary males with mixed morphology
plaques suggesting potentially differing mechanisms for plaque
formation in the 2 groups. It is widely held that calcified plaques
are more stable in nature and less prone to rupture than mixed
plaques which are lipid rich and more vulnerable to fissuring and
possible thrombosis.43 In a similar study of Dutch men in the
MARC study (Measuring Athletes Risk of Cardiovascular
Events), 53% of athletes in the highest exercise dose group had
CAC and were also noted to have higher CAC scores and more
calcific plaques than those who exercised less.44 The conclusion
of these 2 studies suggest that a large minority of long-term
endurance athletes will develop calcified atherosclerotic plaques
that are not easily attributable to traditional atherosclerotic risk
factors. It is unclear, however, whether these differences are
explained by their exercise habits or other confounding factors
that were not measured and may play a significant role in CAC
development such as genetics, illicit performance enhancing
drugs, anti-inflammatory medication use or poor dietary habits,
which are surprisingly frequently seen in such athletes. It is also
important to point out that no clinically relevant negative out-
comes of these findings have been demonstrated.
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Cardiac Risk of Extreme Exercise
Relevant to this issue is the impact of cardiorespiratory
fitness on risk of cardiovascular events particularly in patients
with high CAC, Radford et al45 conducted an interesting study
of 8425 men without clinical CVD attending a preventive
medicine clinic in the Cooper Center Longitudinal Study.
Treadmill testing was used to quantify cardiorespiratory fitness.
It should be acknowledged that this study was not conducted in
elite athletes; however, this was the first study to date to eval-
uate the interaction between CAC and fitness levels. After an
average of 8.4 years of follow-up they demonstrated that across
all levels of CAC, better fitness levels was associated with lower
risk of CVD that persisted even after controlling for traditional
CVD risk factors and use of statins.43 These data strongly
supports the benefits of high cardiorespiratory fitness across all
degrees of CAC to reduce adverse events.
Right Ventricular Remodeling
Exposed to the lower pressure pulmonary circulation,
the RV is a thin-walled structure and thus more susceptible
to the greater hemodynamic load imposed by strenuous
exercise.46 The RV dilates in response to exercise rather than
undergoing hypertrophy which usually occurs con-
comitantly with LV dilation—isolated RV dilation is usually
abnormal in athletes and should warrant further
investigation.47 Balanced RV dilation is common in endur-
ance athletes and usually does not require further evaluation
unless associated with systolic dysfunction or other struc-
tural abnormalities.48 Several studies have revealed acute
RV dilation following endurance exercise (cycling, mar-
athon running, triathlon) which is associated with cardiac
biomarker release, is transient and fully reversible after
recovery.49–51 On a more chronic timeline, a study of com-
petitive rowers revealed an increase in RV size after 90 days
of intense training.52 In comparison with the LV, the RV
appears to be more susceptible to sustained intense exercise
with greater degrees of RV hypertrophy and dilation com-
pared with the LV noted in studies of endurance
athletes.53,54
The question remains whether RV structural remodel-
ing leads to clinically significant myocardial damage and
fibrosis over time. Some authors have raised the possibility
of an “exercise-induced” ARVC phenotype based on a study
associating structural RV changes with higher risk of
inducible ventricular arrhythmias with left bundle branch
morphology (suggesting RV origin).55 Some magnetic res-
onance studies of endurance athletes have suggested in
increased prevalence of myocardial delayed gadolinium
enhancement (DGE), suggestive of myocardial fibrosis,
usually at the RV insertion point.49,56,57 The reason for this
nonischemic pattern of DGE has been proposed to be
related to mechanical stress on the RV during strenuous
exercise. The concern is that this could potentially be an
arrhythmogenic substrate. It should be noted that several
other studies have not found any significant correlation
between endurance exercise and DGE.58–60
RV dilation is also frequently associated with repolari-
zation abnormalities on the 12 lead ECG. In one study of 675
elite athletes in Britain, RV dilation sufficient to fulfill task
force criteria for ARVC was seen on ~50% of athletes. The
combination with ECG abnormalities and RV dilation can
make differentiating normal RV adaptation in elite athletes
from AVRC challenging; however, to meet task force criteria
for ARVC the RV dilation must be accompanied by regional
dyskinesia, akinesia, or aneurysm.
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Sharalaya and Phelan
Aortic Dilation
Because of the significant hemodynamic load placed on
the cardiovascular system by extreme exercise, it would be
reasonable to hypothesize that the aorta would undergo
remodeling and dilate. Indeed, a meta-analysis of young ath-
letes confirms that the aorta is larger in athletes when compared
with sedentary controls but still falls within established normal
limits for the general population.61 Ascending aortic dimen-
sions of > 40 mm are uncommon in this age group and should
warrant further evaluation.62,63 To examine this issue in an
older population, Gentry et al64 published a recent study of a
group of 206 middle-aged former National Football League
(NFL) players. In comparison with the control group, NFL
players had a mid-ascending aortic diameter of 38 ± 5 mm
compared with 34 ± 4 mm (P < 0.0001) and were twice as likely
to have a dilated aorta even after adjusting for parameters
known to be associated with aortic dilation. Ultimately, more
data are needed to identify which variables are most important
in influencing the development of aortic dilation in former
athletes and to assess whether this finding is a normal physio-
logical adaptation or translates to increased risk of aortic
complications.
CONCLUSIONS
In this manuscript we have reviewed recent data which
have raised concerns about the potential cardiovascular risks of
extreme exercise. These studies are generally small cross-sectional
studies with the inherent limitations of such work and should be
put in the context of much larger epidemiological data on the
relationship between exercise and mortality. It should be recog-
nized and emphasized that a sedentary lifestyle is associated with
a far higher risk of adverse cardiac outcomes compared with any
level of exertion. Evaluating 661,137 participants from pop-
ulation-based prospective cohort studies, Arem and colleagues
reported on the dose-response relationship between physical
activity and mortality. They concluded that the maximum lon-
gevity benefit was seen in those who exercise 3 to 5 times the
current recommended physical activity minimum proposed by
the federal government and there was no increased mortality for
those who exercise up to 10 times the recommended minimum
( > 75 MET h/wk).65 Elite athletes, including Tour De France
cyclists, Olympians and cross-country skiers, who have engaged
in vigorous physical activity for years have been consistently
found to have an increased life expectancy of 3 to 6 years when
compared with the general population.66–68 Although there may
be a small subsection of individuals who experience adverse
events related to extreme exercise the tremendous benefits of
habitual leisure-time physical activity have been well charac-
terized, and should be promoted for most individuals to improve
cardiovascular health and increase longevity.
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