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The dose-response association between physical activity and cardiovascular outcomes is well described (10). As little as 15 min·d−1 of moderate-intensity exercise significantly lowers the risk for cardiovascular morbidity and mortality. Greater volumes yield greater cardiovascular benefit. However, the impact of extreme volumes of exercise on cardiovascular health is under debate (9), because some studies present evidence of adverse clinical outcomes in endurance athletes who perform exercise volumes at the extreme upper end of the physical activity continuum. These observations raise the possibility that high doses of exercise have deleterious cardiac effects.Among the early evidence of adverse cardiac effects in athletes was the observation that joggers in Rhode Island had seven times higher risk of sudden cardiac death (SCD) during exercise compared with rest (26). Nevertheless, the relative risk (RR) of an exercise-induced SCD was significantly higher in men with low levels of habitual physical activity (RR, 56; 95% confidence interval [CI], 23–131) compared with men who perform the highest level of habitual activity (RR, 5; 95% CI, 2–14) (24). The incidence of cardiac arrest among athletes is considered low, and estimated at 1 per 200,000 during marathon running (12). The risk appears to be higher in men (0.9 per 100,000 runners) versus women (0.16 per 100,000 runners), and bystander cardiopulmonary resuscitation and a nonhypertrophic cardiomyopathy cause of SCD are significant predictors of survival in collapsed runners (12).SCD with exercise is rare, but exercise-induced increase of cardiac troponin concentrations is common (23). In fact, every runner participating in a Boston Marathon study demonstrated a postexercise increase in cardiac troponin subunit I, and 54% of the study population exceeded the cutpoint for diagnosing a myocardial infarction (8). Although an increase in cardiac troponin concentrations is associated with non-reversible cardiac damage in clinical populations, it is possible that this exercise-induced release does not represent cardiac damage (23). The observation that troponin concentrations return to baseline values below the clinical threshold within 24 to 72 h postexercise reinforces this hypothesis (21).Performance of endurance exercise also affects structure and function of the cardiac chambers. A study in triathletes found a reduction in left ventricular and left and right atrial sizes after the Hawaii Ironman Triathlon (6). Furthermore, significant reductions in left and right ventricular ejection fraction have been observed in athletes performing prolonged exercise (14,17), with larger decrements in the right heart. The greater vulnerability of the right ventricle is due to the exposure of a substantial exercise-induced increase in wall stress (≈125%) imposed on its thin wall compared with a moderate increase in wall stress (≈4%) of the thick wall of the left ventricle (15). All changes in cardiac function are believed to be transient, with a recovery to normal function within 24 to 48 h postexercise.The possibility that high volumes of lifelong exercise training may lead to adverse cardiac remodeling and subsequent development of cardiovascular diseases is known as the Too much exercise hypothesis. Although evidence is conflicting (7), some observations are noteworthy. For example, myocardial fibrosis (i.e., scarring of cardiac tissue) have been found in endurance athletes. A total of 14 studies used cardiac magnetic resonance imaging to assess the presence of cardiac scarring and found myocardial fibrosis in 30 of the 509 athletes (5.9%) (27). Interestingly, the prevalence of myocardial fibrosis varied between 2.1% and 50% of the study population. More years of exercise training and a greater number of completed marathons and ultramarathons were associated with the risk for myocardial fibrosis (28).