Increased cardiac sympathetic activity and insulin-like growth factor-I formation are associated with physiological hypertrophy in athletes

Physiological hypertrophy represents the adaptive changes of the heart requ ired for supporting the increased hemodynamic load in regularly trained hea lthy subjects. Mechanisms responsible for the athlete's hypertrophy still r emain unknown. In 15 trained competitive soccer players and in 15 healthy m en not engaged in sporting activities (sedentary control subjects) of equiv alent age, we investigated the relationship among cardiac growth factor for mation, cardiac sympathetic activity, and left ventricular morphology and f unction. Cardiac formation of insulin-like growth factor (IGF)-I, endotheli n (ET)-1, big ET-1, and angiotensin (Ang) I was investigated at rest by mea suring artery-coronary sinus concentration gradients. Cardiac sympathetic a ctivity was studied by [H-3]norepinephrine (NE) kinetics. Cardiac IGF-I, bu t not ET-1, big ET-1, and Ang II, formation was higher in athletes than in control subjects (P<0.01). NE levels in arterial and peripheral venous bloo d did not differ between groups. In contrast, coronary sinus NE concentrati on was higher in athletes than in control subjects (P<0.01). Cardiac, but n ot total system ic, NE spillover was also increased in athletes (P<0.01), w hereas cardiac [H-3]NE reuptake and clearance were not different. Echocardi ographic modifications indicated a volume overload-induced hypertrophy asso ciated with increased myocardial contractility. Multivariate stepwise analy sis selected left ventricular mass index as the most predictive independent variable for cardiac IGF-I formation and velocity of circumferential fiber shortening for cardiac NE spillover. In conclusion, increased cardiac IGF- I formation and enhanced sympathetic activity selectively confined to the h eart appear to be responsible for the physiological hypertrophy in athletes performing predominantly isotonic exercise.