Are There Deleterious Cardiac Effects of Acute and Chronic Endurance Exercise?

Abstract

Multiple epidemiological studies document that habitual physical activity reduces the risk of atherosclerotic cardiovascular disease (ASCVD), and most demonstrate progressively lower rates of ASCVD with progressively more physical activity. Few studies have included individuals performing high-intensity, lifelong endurance exercise, however, and recent reports suggest that prodigious amounts of exercise may increase markers for, and even the incidence of, cardiovascular disease. This review examines the evidence that extremes of endurance exercise may increase cardiovascular disease risk by reviewing the causes and incidence of exercise-related cardiac events, and the acute effects of exercise on cardiovascular function, the effect of exercise on cardiac biomarkers, including "myocardial" creatine kinase, cardiac troponins, and cardiac natriuretic peptides. This review also examines the effect of exercise on coronary atherosclerosis and calcification, the frequency of atrial fibrillation in aging athletes, and the possibility that exercise may be deleterious in individuals genetically predisposed to such cardiac abnormalities as long QT syndrome, right ventricular cardiomyopathy, and hypertrophic cardiomyopathy. This review is to our knowledge unique because it addresses all known potentially adverse cardiovascular effects of endurance exercise. The best evidence remains that physical activity and exercise training benefit the population, but it is possible that prolonged exercise and exercise training can adversely affect cardiac function in some individuals. This hypothesis warrants further examination.

Histological evidence for reversible cardiomyocyte changes and serum cardiac troponin T elevation after exercise in rats

“…The clinical interpretation of postexercise cTn release is complex, but should be interpreted holistically with other clinical signs and symptoms of cardiovascular disease. Despite this, case reports of sudden cardiac death in athletes with adverse cardiac structural remodeling as well as reports of links between cTn elevation and depressed cardiac function (La Gerche 2013;Eijsvogels et al 2016) have prompted ongoing debate about the cardiovascular consequences of high levels of exercise exposure (Whyte et al 2009). Whether exercise-induced cTn release reflects reversible or irreversible changes in cardiomyocyte integrity is not clear and is currently the source of some debate (George et al 2011;Guasch and Nattel 2013;Eijsvogels et al 2016).…”

Cardiac troponin: more than meets the eye

“…The physiological mechanisms responsible for the release of cTn during exercise are still not fully understood 9–11. Benign reversible cardiomyocyte membrane damage is thought to be the main reason for this manifestation 14. Such damage following repetitive exposure to high-intensity endurance regimes may consequently give rise to myocardial fibrosis,15 with this phenomenon in relation to chronic endurance veteran athletes currently being explored 16.…”

Athlete's heart syndrome: A friend or foe?

“…Zato su Mičel (Mitchell) i saradnici (2005) predložili klasifikaciju sporta u devet grupa, na osnovu preovlađivanja dinamičke (u literaturi se mogu naći i termini: izdržljivost, aerobna i/ili izotonična aktivnost) i statičke (u literaturi se mogu naći i termini: trening sa otporom, anaerobna i/ili izometrijska aktivnost) komponente. Ova klasifikacija je napravljena u cilju uključivanja sportista sa kardiovaskularnim oboljenjima u sportske aktivnosti (9). Poslednjih godina se primenjuje i modifikovana Mičelova klasifikacija na četiri grupe, u skladu sa preovlađujućim karakteristikama treninga: veštine (engl.…”