EXERCISE TRAINING ENHANCES CARDIAC-FUNCTION IN RESPONSE TO AN AFTERLOAD STRESS IN OLDER MEN

This study was designed to characterize cardiac adaptations to enduran ce exercise training in older healthy men by evaluation of changes in left ventricular function in response to an afterload stress in the pr esence of cardiac muscarinic receptor blockade. Eight men 65 +/- 2 (SE ) yr old underwent 9 mo of endurance exercise training. Maximal O-2 up take (Vo(2max)) was determined during treadmill exercise. Left ventric ular function was assessed with two-dimensional echocardiography and p ulsed Doppler transmitral flow velocity profile at baseline, after an intravenous bolus of atropine and during infusion of graded doses of p henylephrine. Vo(2max) was increased by 29% in response to training (2 8.9 +/- 1 to 37.3 +/- 1 ml . kg(-1). 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 lef t ventricular hypertrophy. EDD, end-systolic dimension, and end-systol ic wall stress (sigma(es)) increased similarly in response to phenylep hrine before and after training. Fractional shortening (FS) decreased in response to phenylephrine before but not after training. When the c hanges 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 sig ma(es), indicative of improved contractile function. This adaptive res ponse 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. Ex ercise training resulted in a higher (P = 0.028) early-to-late transmi tral diastolic flow velocity ratio at virtually identical heart rates, suggestive of improved diastolic filling. The results suggest that en durance exercise training induces an enhancement of left ventricular s ystolic function in response to an afterload stress in older healthy m en.