Reproducibility and clinical significance of exercise-induced increases in cardiac troponins and N-terminal pro brain natriuretic peptide in endurance athletes

Abstract

Cardiac troponins I and T and brain natriuretic peptide are the accepted standards to serologically identify myocardial necrosis and elevated wall stress. In addition, they allow risk stratification in cardiovascular patients. The clinical significance of increases in cardiac markers after strenuous endurance exercise in obviously healthy athletes is unclear. We therefore examined the reproducibility and clinical significance of exercise-induced increases in cardiac troponins I and T and N-terminal pro brain natriuretic peptide after two standardized endurance exercise trials in healthy endurance athletes with prior competition-induced elevations of cardiac troponins (I, 0.08-1.93 mug/l; T, 0.01-0.56 mug/l). Twenty male athletes (36+/-7 years; VO2max: 60+/-5 ml/min per kg) completed a 1-h and a 3-h exercise study (exercise intensities 100 and 75%, respectively, of the individual anaerobic threshold) on two different days in randomized order to determine cardiac markers before, 30 min and 3 h after exercise. In addition to pre- and post-exercise echocardiography including tissue Doppler imaging, delayed enhancement magnetic-resonance-imaging was performed after a 3-h exercise study to detect myocardial necrosis. A marginal increase in cardiac troponin I was documented after both exercise trials (from 0.02 to 0.03 mug/l; P < 0.001). Cardiac troponin T remained without significant changes. N-terminal pro brain natriuretic peptide increased by 9 and 30 ng/l after 1-h and 3-h exercise studies, respectively (P < 0.001). In contrast to cardiac troponins, increases in N-terminal pro brain natriuretic peptide after competition correlated with those after 1-h exercise study (rho = 0.88) and 3-h exercise-study (rho = 0.82). No pathologies were demonstrated by echocardiography or delayed-enhancement magnetic resonance imaging. Due to the missing reproducibilty and evidence of myocardial damage, exercise-induced increases in cardiac troponins may represent a physiologic reaction under special conditions and seem to be without pathological significance in healthy athletes.