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To test the hypothesis that reduced baroreflex sensitivity is a direct result of exercise, we measured forearm vascular conductance (FVC) responses to graded lower body negative pressure (LBNP) 2, 20, and 44 h after intense exercise. Eight 4-min bouts of exercise at 85% of maximum oxygen uptake produced 3.5 +/- 0.7 and 3.9 +/- 1.0% blood volume (BV) expansions at 20 and 44 h of recovery, respectively. BV was unchanged from control values 2 h after exercise. The reduction in FVC was significantly less than control values during 30 and 40 mmHg of LBNP at 2 and 20 h of recovery, respectively, whereas heart rate and cardiac stroke volume responses were unchanged. Thus, a reduced FVC response to LBNP preceded BV expansion, demonstrating that exercise itself can elicit an attenuation of baroreflex function. To test the hypothesis that volume sensitivity of renal function is attenuated by intense exercise, we measured cardiovascular variables, plasma hormone concentrations, and renal output. At 20 h of recovery, resting mean arterial blood pressure and cardiac output were increased by 6 +/- 1 mmHg and 0.6 +/- 0.2 l/min, respectively, but resting plasma aldosterone and overnight Na+ excretion rate were unchanged. At 44 h of recovery, plasma aldosterone was decreased by 26 +/- 9% and overnight Na+ excretion rate was increased by 51 +/- 26%. Thus, appropriate endocrine and renal responses to increased BV were delayed until 44 h of recovery. Our findings suggest that a postexercise attenuation of baroreflex function participates in the induction of BV expansion by intense exercise.

The purpose of this study was to compare the cardiovascular control mechanisms that defend arterial blood pressure against blood pooling between rest and moderate dynamic exercise. We studied ten physically active men during rest and five 12-min graded supine cycle ergometer exercise bouts with and without application of LBNP in 25 degrees C and 35 degrees C. Exercise intensities were 10, 50, and 100 watts (W), each for 4 min, and LBNP was applied at 0 (control), -20, -40, and -60 mm Hg in 25 degrees C and -40 mm Hg in 35 degrees C. At rest, cardiac stroke volume (SV) decreased from 120 +/- 5 ml during control to 94 +/- 6, 67 +/- 5 and 49 +/- 3 ml during -20, -40, and -60 mm Hg LBNP, respectively, and to 55 +/- 3 ml during -40 mm Hg at 35 degrees C. Exercise elevated SV toward the control level during LBNP due to muscle pumping action. Heart rate (HR) did not increase significantly during application of LBNP until SV decreased by 20-25 ml during LBNP, both during rest and exercise. The magnitude of HR increase per decrease in SV, once an increase in HR occurred, was similar between rest and exercise, regardless of exercise intensity. The change in total peripheral resistance (TPR) with respect to SV was linear, confirming that peripheral vascular adjustments were proportional to changes in the heart's preload. The slopes of the TPR-SV relation were similar during rest and exercise, although shifted to the left with increasing exercise intensity.(ABSTRACT TRUNCATED AT 250 WORDS)