Exercise training enhances cardiac function in response to an afterload stress in older men.

Abstract

This study was designed to characterize cardiac adaptations to endurance exercise training in older healthy men by evaluation of changes in left ventricular function in response to an afterload stress in the presence of cardiac muscarinic receptor blockade. Eight men 65 +/- 2 (SE) yr old underwent 9 mo of endurance exercise training. Maximal O2 uptake (V(O2 max)) was determined during treadmill exercise. Left ventricular function was assessed with two-dimensional echocardiography and pulsed Doppler transmitral flow velocity profile at baseline, after an intravenous bolus of atropine and during infusion of graded doses of phenylephrine. V(O2 max) was increased by 29% in response to training (28.9 +/- 1 to 37.3 +/- 1 ml x kg(-1) x min(-1)). Baseline end-diastolic diameter (EDD) was increased, with no change in left ventricular wall thickness-to-radius ratio, after training, suggestive of eccentric left ventricular hypertrophy. EDD, end-systolic dimension, and end-systolic wall stress (sigma(es)) increased similarly in response to phenylephrine before and after training. Fractional shortening (FS) decreased in response to phenylephrine before but not after training. When the changes in FS (delta FS) during phenylephrine infusion were plotted as a function of changes in sigma(es), delta FS were significantly higher after than before training (P = 0.003) at comparable increases in sigma(es), indicative of improved contractile function. This adaptive response was preload independent, because EDD did not differ between the trained and untrained states during phenylephrine infusion. Heart rate responses to phenylephrine were similar before and after training. Exercise training resulted in a higher (P = 0.028) early-to-late transmitral diastolic flow velocity ratio at virtually identical heart rates, suggestive of improved diastolic filling. The results suggest that endurance exercise training induces an enhancement of left ventricular systolic function in response to an afterload stress in older healthy men.