Potential adverse cardiovascular effects from excessive endurance exercise

Abstract

A routine of regular exercise is highly effective for prevention and treatment of many common chronic diseases and improves cardiovascular (CV) health and longevity. However, long-term excessive endurance exercise may induce pathologic structural remodeling of the heart and large arteries. Emerging data suggest that chronic training for and competing in extreme endurance events such as marathons, ultramarathons, ironman distance triathlons, and very long distance bicycle races, can cause transient acute volume overload of the atria and right ventricle, with transient reductions in right ventricular ejection fraction and elevations of cardiac biomarkers, all of which return to normal within 1 week. Over months to years of repetitive injury, this process, in some individuals, may lead to patchy myocardial fibrosis, particularly in the atria, interventricular septum, and right ventricle, creating a substrate for atrial and ventricular arrhythmias. Additionally, long-term excessive sustained exercise may be associated with coronary artery calcification, diastolic dysfunction, and large-artery wall stiffening. However, this concept is still hypothetical and there is some inconsistency in the reported findings. Furthermore, lifelong vigorous exercisers generally have low mortality rates and excellent functional capacity. Notwithstanding, the hypothesis that long-term excessive endurance exercise may induce adverse CV remodeling warrants further investigation to identify at-risk individuals and formulate physical fitness regimens for conferring optimal CV health and longevity.

FIGURE 1

Relationship between dose of physical activity and reduction in all-cause mortality. The mortality benefits of exercise appear with even small amounts of daily exercise and peak at 50 to 60 minutes of vigorous exercise per day.

FIGURE 2

A, Picrosirius-stained photomicrographs of RV sections. By 16 weeks, the RVs of exercising rats show widespread interstitial collagen deposition with disarray of myocardial architecture (arrows). B, Mean ± standard error of the mean collagen content in RV FW, IVS, and LV FW. *P<.05 (exercising vs sedentary rats). FW = free wall; IVS = interventricular septum; LV = left ventricle; RV = right ventricle.

FIGURE 3

High-sensitivity cardiac troponin T (hs-cTnT) concentrations before, immediately after, and 24 and 72 hours after marathon race.

FIGURE 4

Duration-dependent effect of endurance events on right ventricular (RV) ejection fraction.

FIGURE 5

Differential effect of prolonged intense exercise on right and left ventricular volumes. Baseline volumes are shown on the left, and the changes in volume post-race are shown on the right. Right ventricular volumes increased in the post-race setting, whereas left ventricular volumes decreased, resulting in a decrease in right ventricular ejection fraction but not left ventricular ejection fraction.

FIGURE 6

Delayed gadolinium enhancement in 5 athletes. Images of 5 athletes in whom focal delayed gadolinium enhancement was identified in the interventricular septum (arrows), compared with a normal study in an athlete (top left).

FIGURE 7

Proposed pathogenesis of cardiomyopathy in endurance athletes. BNP = B-type natriuretic peptide; CK-MB = creatine kinase MB; LV = left ventricle; RA = right atrium; RV = right ventricle; SCD = sudden cardiac death.