Is exercise-induced myocardial injury self-abating?

Abstract

Dear Editor-in-Chief: A recent report has shown marked increases of cardiac troponin in healthy individuals after a prolonged bout of exercise (5). The release of cardiac troponin from exercise-induced myocardial injury is likely from localized minor, irreversible myocyte degeneration, suggestive of myocarditis (1). A variety of transitory abnormalities can cause minor degrees of myocardial injury that may be self-abating (2). For example, increases in biomarkers might occur with cardiotrophic viral infections, with only a small subset of patients progressing to overt myocarditis or heart failure (2). However, whether exercise-induced myocardial injury, as indicated by increased cardiac troponin concentrations, in healthy individuals as a result of physiologic stress has any long-term clinical or athletic consequence or relevance is unknown at present (3,4). Our own observations on 30 participants in an Alpine ultramarathon of 70 km found one 26-yr-old participant with increases in cardiac troponin T (cTnT) levels immediately (0.2 μg·L-1) and 2 h (0.2 μg·L-1) after the race. cTnT level was measured by immunoassay in strip format (Cardiac T Quantitative; Roche Diagnostics, Mannheim, Germany) with the Cardiac Reader (Roche Diagnostics); 24 h before the competition this individual had no detectable cTnT level. A physician reviewed the medical history and performed a physical examination including brachial artery blood pressure measurement, echocardiography, and electrocardiography. No cardiovascular abnormalities were identified. Two days after the run the physician repeated the cardiological examination of this individual. In addition, a blood sample was drawn in the morning after an overnight fast. The sample was analyzed for lipids, lipoproteins, and cTnT level. No cardiovascular abnormalities or cardiovascular disease risk factors were identified. cTnT was not detectable. The rapid increase and normalization of cTnT is in agreement with recent findings (1,3–5). The start and finish of this Alpine ultramarathon is in Gmunden (Upper Austria, Austria; 425 m above sea level); the highest point reached is the Traunstein, 1575 m above sea level. The athlete won the race (running-time was 7 h and 35 min). Two months after the ultramarathon this individual took part in an Alpine marathon of 42.3 km in Galtür (Tirol, Austria) (3). The athlete had no detectable cTnT levels before and after the marathon. A physician performed a cardiological examination including brachial artery blood pressure measurement, echocardiography, and electrocardiography 2 d after exercise. A blood sample was drawn in the morning after an overnight fast. The sample was analyzed for lipids, lipoproteins, and cTnT level. No cardiovascular abnormalities or cardiovascular disease risk factors were identified. cTnT was not detectable. The athlete finished third (running-time was 3 h and 17 min). This case report suggests that increases in troponin levels in a healthy individual as a result of a prolonged bout of exercise, such as a marathon, does not have any clinical or athletic consequence or relevance. Because exercise-induced myocardial injury may be self-abating, athletes should not be excluded from participating in sports predicated solely on the presence of increased marker proteins. Only, if a cause for a biomarker increase can be ascertained (a potentially lethal cardiovascular abnormality), athletes should be disqualified, ultimately for the purpose of protecting the health and welfare of sports participants. Arnold Koller, Ph.D. Stefan Mertelseder, M.Sc. Hans Moser, Ph.D.