PHYSICAL-TRAINING AND BARORECEPTOR CONTROL OF SYMPATHETIC-NERVE ACTIVITY IN HUMANS

In nine sedentary subjects (16.5+/-0.4 years, mean+/-SEM) we measured blood pressure (Finapres device), heart rate (electrocardiogram), and postganglionic muscle sympathetic nerve activity (microneurography from the peroneal nerve) at rest and during intravenous infusion of phenylephrine and nitroprusside. These measurements were performed before and after 10 weeks of endurance training (2 h/d, 5 d/wk) that increased maximum oxygen consumption from 34.8+/-2.1 to 40.4+/-1.8 mL/kg per minute (P<.02). Basal mean blood pressure and muscle sympathetic nerve activity were lower after than before endurance training (86.5+/-2.6 versus 97.5+/-1.8 mm Hg, P<.05, and 14.0+/-1.8 versus 21.2+/-2.3 bursts per minute, P<.02), and the changes in these variables were closely related (r=.95, P<.01), Similar mean blood pressure increases induced by phenylephrine caused greater reductions in heart rate and muscle sympathetic nerve activity after than before endurance training (-8.6+/-0.8 versus -6.1+/-1.1 beats per minute, P=NS, and -78.0+/-4.6% versus -53.6+/-4.8%, P<.05). Likewise, similar mean blood pressure reductions induced by nitroprusside caused greater increases in heart rate and muscle sympathetic nerve activity after than before endurance training (18.6+/-3.0 versus 12.4+/-2.4 beats per minute, P<.05, and 128.1+/-26% versus 63.2+/-11%, P<.02). No alteration in hemodynamics, oxygen consumption, muscle sympathetic nerve activity, and baroreceptor reflex sensitivity occurred in four other age-matched sedentary subjects studied before and after a 10-week observation period without endurance training. These data provide evidence that endurance training markedly lowers sympathetic nerve traffic. This is accompanied by potentiation of the baroreceptor-sympathetic reflex, and this effect is more evident than that on baroreceptor vagal cardiac control.