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Abstract
Physical activity and exercise training are underutilized by much of Westernized society, and physical inactivity may be the greatest threat to health
in the 21st century. Many studies have shown a linear relationship between
ones activity level and heart health, leading to the conclusion that if some
exercise is good, more must be better. However, there is evolving evidence that high levels of exercise may produce similar or less overall cardiovascular (CV) benefits compared with those produced by lower doses of
exercise. Very high doses of exercise may be associated with increased risk
of atrial fibrillation, coronary artery disease, and malignant ventricular arrhythmias. These acute bouts of excessive exercise may lead to cardiac
dilatation, cardiac dysfunction, and release of troponin and brain natriuretic
peptide. The effects of too little and too much exercise on the heart are
reviewed in this article, along with recommendations to optimize the dose
of exercise to achieve heart health.
Introduction
Considerable evidence indicates the profound benefits of
physical activity (PA), exercise training (ET), and higher
levels of cardiorespiratory fitness (CRF) on lowering morbidity and mortality from heart disease (11,38,40). Recent
studies have focused on the fact that PA levels do not meet
national guidelines in a substantial percentage of the population in the United States, probably in 50% to 80% of the
population, and most of the world (11,38,40), and physical
inactivity may represent one of the greatest threats to health
in the 21st century (5).
Although excessive endurance exercise (EEE), defined as
ET 9 60 to 90 min per session, is not nearly as prevalent as
low levels of PA, occurring in 2% to 5% of the population,
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Figure 1: Proposed pathogenesis of cardiomyopathy in endurance athletes. BNP, B-type natriuretic peptide; CK-MB, creatine kinase MB. Reproduced with permission from OKeefe et al. (29).
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were more pronounced. In another study, those endurance athletes had a 12% prevalence of RV abnormalities by MRI (6).
Other studies also have confirmed the long-term adverse
effects on myocardial structure (18,27Y30,32), including one
study suggesting that the CAD event rate during 2-year followup was significantly higher in the athletes than that in controls (P G 0.0001) (6).
Impact of EEE on CAD
Recent studies have suggested that long distance runners
may have increased levels of atherosclerosis and CAD (18,37).
In a study 6 years ago, male marathon runners had paradoxically increased coronary artery calcification (CAC) as measured by computed tomography (CT) CAC scoring (21). A
very recent study of men who completed at least one marathon yearly for 25 consecutive years (n = 50) compared with
23 sedentary controls demonstrated increased total plaque
volume (P G 0.01), calcified plaque volume (P G 0.0001), and
noncalcified plaque volume (P = 0.04) compared with those
with EEE (Fig. 3) (37). Despite the fact that runners have
better overall CAD risk profiles, these results underscore the
potential for very heavy EEE to increase the severity of CAD
through mechanisms largely independent of the traditional
CAD risk factors.
A very recent study by Mohlenkamp et al. (22) assessed
108 marathon runners and 864 age-matched controls as well
as 216 age- and risk factor-matched controls. Recreational
marathon runners with myocardial fibrosis by MRI-LGE had
higher troponin release than those without LGE. Higher
CAC scores and LGE, as opposed to troponin release (which
was present in 37% of the marathoners), predicted subsequent
CAD events, which were overall similar between marathoners
and risk factor-matched nonmarathon controls.
Impact of ET on Risk of AF
We recently evaluated various risk factors, including
metabolic factors, for the risk of AF (19,20). Certainly
many epidemiologic and observational studies, although
not all (26), have reported a strong statistically significant
association between chronic high-intensity ET and elevated
risk of AF (1,19,20). The impact of habitual PA and ET on
the risk of AF appears to be nonlinear, with lower rates of
AF among moderately active individuals compared with
those among sedentary controls, whereas an increased risk
of AF was noted among individuals performing EEE or long
bouts of high-intensity ET (18,27Y30,32). The mechanism
of AF with high ET is uncertain, but this may involve acute
fluxes in cathecholamines and autonomic tone, atrial stretch,
and RV cardiomyopathy.
In a study of 44,410 Swedish men, intense ET of 95
hIwkj1 at age 30 years increased the risk of AF later in life,
whereas moderate-intensity PA reduced the risk of AF (7).
In a study of 5,446 older athletes (mean age, 73 years),
again low- and moderate-intensity PA progressively reduced
the risk of AF, whereas the rate slightly increased in those
with high-intensity PA (slightly more risk than light intensity but still lower than nonexercisers) (25). In nearly
53,000 long distance cross country skiers from Sweden, there
was more AF with the greater amount of cross-country races
and the fastest finishing times (2). However, with detraining
Exercise Dose and the Heart
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Figure 4: Central illustration: hazard ratios (HR) of all-cause and CV mortality by running characteristic (weekly running time, distance,
frequency, total amount, and speed). Participants were classified into six groups: nonrunners (reference group) and five quintiles of each running
characteristic. All HR were adjusted for baseline age (yr), sex, examination year, smoking status (never, former, or current), alcohol consumption
(heavy drinker or not), other physical activities except running (0, 1 to 499, or 500 METIminIwkj1), and parental history of CV disease (yes or no).
All P values for HR across running characteristics were G0.05 for all-cause and CV mortality except for running frequency of six times a week
(P = 0.11) and speed of G6.0 miles/hyperlipidemia (P = 0.10) for CV mortality. Reproduced with permission from Lee et al. (15).
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