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Abstract-Physiological hypertrophy represents the adaptive changes of the heart required for supporting the increased hemodynamic load in regularly trained healthy subjects. Mechanisms responsible for the athlete's hypertrophy still remain unknown. In 15 trained competitive soccer players and in 15 healthy men not engaged in sporting activities (sedentary control subjects) of equivalent age, we investigated the relationship among cardiac growth factor formation, cardiac sympathetic activity, and left ventricular morphology and function. Cardiac formation of insulin-like growth factor (IGF)-I, endothelin (ET)-1, big ET-1, and angiotensin (Ang) II was investigated at rest by measuring artery-coronary sinus concentration gradients. Cardiac sympathetic activity was studied by [ 3 H]norepinephrine (NE) kinetics. Cardiac IGF-I, but not ET-1, big ET-1, and Ang II, formation was higher in athletes than in control subjects (PϽ0.01). NE levels in arterial and peripheral venous blood did not differ between groups. In contrast, coronary sinus NE concentration was higher in athletes than in control subjects (PϽ0.01). Cardiac, but not total systemic, NE spillover was also increased in athletes (PϽ0.01), whereas cardiac [ 3 H]NE reuptake and clearance were not different. Echocardiographic modifications indicated a volume overload-induced hypertrophy associated with increased myocardial contractility. Multivariate stepwise analysis 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 heart appear to be responsible for the physiological hypertrophy in athletes performing predominantly isotonic exercise. Key Words: insulin-like growth factor-I Ⅲ norepinephrine Ⅲ sympathetic nervous system Ⅲ exercise Ⅲ hypertrophy, left ventricular T he heart sustains an increased hemodynamic load by adjusting its mass independently of whether the enhanced workload is due to physiological activity or to pathological alterations in the cardiovascular system. There is much evidence that the development of myocardial hypertrophy results from the interaction of mechanical forces (the increased workload) and cardiac growth factors. The hemodynamic overload leads to myocardial cellular stretch and strain that in turn induce gene expression of cardiac growth factors. 1,2 In regularly trained healthy subjects, both isotonic and isometric exercise cause cardiac changes resulting in modifications of the ventricular chambers and in a notable enhancement of heart performance. These modifications, called physiological hypertrophy or athlete's hypertrophy, are required for sustaining the tremendous increase in cardiac output during exercise. Cardiac growth factors involved in the development of physiological hypertrophy in humans are still unknown, and their knowledge might also be relevant for better understanding the mech...

Right ventricular pacing worsens LV function in patients with and without LV dysfunction unless the RV pacing site is optimized. Left ventricular and BiV pacing preserve LV function in patients with EF >40% and improve function in patients with EF <40% despite no clinical indication for BiV pacing.

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