Background: The age-associated decline in aerobic exercise capacity is partially reversible by endurance exercise training. Moderate-intensity endurance exercise training increases aerobic exercise capacity mediated, in part, by improvement of stroke volume and left ventricular performance in older men. The present study was designed to characterize the nature of cardiovascular adaptations to strenuous endurance exercise of long duration and to delineate the mechanisms underlying increased stroke volume and cardiac output in highly trained older endurance athletes.
Methods and results: Nine male master athletes (MA: 64 +/- 2 years old, mean +/- SEM) and 9 older sedentary healthy men (controls: 63 +/- 1 year) were studied. Left ventricular systolic function was evaluated with the use of cardiac blood pool imaging and echocardiography. Maximal O2 uptake (VO2max) was 50.4 +/- 1.7 mL.kg-1 x min-1 in the MA and 29.6 +/- 1.4 mL.kg-1 x min-1 (P = .0001) in controls. Systolic and mean blood pressures at rest and during exercise were not different in the two groups. Left ventricular systolic function at peak exercise was higher in the MA than in sedentary controls as evidenced by (1) a higher left ventricular functional reserve (delta EF: 12.4 +/- 2 versus 5.6 +/- 2.5, P = .05), (2) a large decrease in end-systolic volume during exercise (MA: 56 +/- 4 mL at rest and 42 +/- 5 mL at peak exercise, P = .007; controls: 43 +/- 2 mL at rest and 42 +/- 6 mL at peak exercise, P = .35) with no differences in systolic blood pressure, (3) a higher left ventricular fractional shortening at peak exercise (MA: 52 +/- 2.6%; controls: 45 +/- 1%, P = .046) at comparable values for end-systolic wall stress (MA: 56 +/- 12 g/cm2; controls: 53 +/- 7 g/cm2, P = .50), and (4) a greater decrease in end-systolic diameter at peak exercise in the MA than in controls (MA: -1.2 +/- 0.16 cm versus -0.57 +/- 0.13 cm, P = .014) despite no significant differences between the changes in end-systolic wall stress during exercise (MA: -15.5 +/- 7.5 g/cm2, controls: -11.0 +/- 9.0 g/cm2, P = .6). MA had a larger end-diastolic volume at rest (153 +/- 6 versus 132 +/- 4 mL, P = .009) with a normal wall thickness-to-radius ratio (0.34 +/- 0.02). Peak exercise stroke volume was higher (P = .023) in the MA (132 +/- 6 mL/min) than in the sedentary controls (111 +/- 6 mL/min). Changes in stroke volume correlated strongly with changes in ejection fraction in the MA (r = .80, P = .010) but not in sedentary controls (r = .59, P = .097). Further, changes in stroke volume from rest to exercise correlated strongly with changes in end-diastolic volume in both MA (r = .78, P = .013) and sedentary controls (r = .73, P = .026), suggestive of reliance of stroke volume on end-diastolic volume and preload. However, for a given increase in end-diastolic volume, the rise in stroke volume during exercise was significantly larger in the MA than in controls, which, in the absence of differences in mean blood pressures, indicates that enhanced left ventricular systolic function independent of preload plays an additional role in maintaining a higher stroke volume at peak exercise in the highly trained older men.
Conclusions: Cardiac adaptations in older endurance trained men are characterized by volume-overload left ventricular hypertrophy and enhancement of left ventricular systolic performance at peak exercise. These adaptive responses contribute to enhanced stroke volume at peak exercise in older endurance trained men.