It is assumed that the athlete’s heart represents a physiological adaptation to endurance exercise, caused by an increased volume load.¹ As a new cardiac biomarker, brain natriuretic peptide (BNP) allows us to serologically perceive myocardial wall stress. As elevated resting BNP concentrations reflect pathological ventricular overload, it was hypothesised that in case of a physiological hypertrophy BNP concentrations have to be similar in endurance athletes with athlete’s heart and healthy untrained control subjects.

In contrast to atrial natriuretic peptide, which refers to atrial stretch, BNP refers to ventricular strain. Synthesised by cardiomyocytes in response to ventricular overload and elevated myocardial wall stress,² resting concentrations of BNP and its cleaved precursor peptide N-terminal pro-BNP (NT-proBNP) have become useful markers to assess cardiac dysfunction, chronic heart failure, and left ventricular (LV) hypertrophy caused by hypertension or cardiomyopathy. In British Army recruits an association between the increase in LV mass and elevated resting BNP concentrations after a 10 week training period was demonstrated by Montgomery and colleagues³ However, in another study, BNP concentrations did not correlate with echocardiographically determined LV mass in a small group of eight cyclists with athlete’s heart.⁴

Therefore, we determined NT-proBNP in a subgroup of previously reported healthy male endurance athletes and healthy untrained control subjects, which were examined by cardiac magnetic resonance (CMR) imaging to determine LV and right ventricular (RV) mass, end diastolic volume (EDS), end systolic volume (ESV), and ejection fraction (EF).⁵ To confirm the assumption that the athlete’s heart represents a physiological adaptation to endurance exercise, …