Postexercise hypotension is mediated by reductions in sympathetic nerve activity.

Mean arterial pressure (MAP), the product of cardiac output (CO) and total peripheral resistance (TPR), is reduced below preexercise levels after a single bout of mild to moderate dynamic exercise. Thus acute, dynamic exercise may be used as a safe, therapeutic approach to reduce MAP. However, the mechanisms responsible for the postexercise hypotension (PEH) are unknown. We tested the hypothesis that PEH is associated with reductions in TPR and sympathetic nerve activity (SNA). Two experimental protocols were designed to test this hypothesis in male spontaneously hypertensive rats (SHR). In protocol 1 (n = 9), CO and TPR were determined before, during, and after exercise. In protocol 2 (n = 7), lumbar SNA (LSNA) was recorded before and after exercise. Rats in protocol 1 were chronically instrumented with left carotid arterial catheters and ascending aortic Doppler ultrasonic flow probes. Rats in protocol 2 were chronically instrumented with left carotid arterial catheters and electrodes around the lumbar sympathetic trunk. Dynamic treadmill exercise (9-12 m/min, 10% grade for 40 min) resulted in a postexercise reduction in MAP (from 143 +/- 5 to 128 +/- 4 mmHg, P < 0.05). Associated with the PEH was a reduction in TPR (from 28 +/- 3 to 19 +/- 2 mmHg/kHz; P < 0.05) and an elevation in CO (from 5.7 +/- 0.4 to 7.2 +/- 0.5 kHz; P < 0.05). The reductions in arterial pressure and TPR were associated with a decrease in LSNA (from 98 +/- 3 to 49 +/- 6%; P < 0.05). These results suggest that PEH is mediated by reductions in TPR and SNA.