Postaerobic Exercise Blood Pressure Reduction in Very Old Persons With Hypertension :

1. The reduction in vascular resistance which accompanies acute dynamic exercise does not subside immediately during recovery, resulting in a post-exercise hypotension. This sustained vasodilatation suggests that sympathetic vascular regulation is altered after exercise. 2. Therefore, we assessed the baroreflex control of sympathetic outflow in response to arterial pressure changes, and transduction of sympathetic activity into vascular resistance during a sympatho-excitatory stimulus (isometric handgrip exercise) after either exercise (60 min cycling at 60% peak aerobic power (VO2,peak)) or sham treatment (60 min seated rest) in nine healthy subjects. 3. Both muscle sympathetic nerve activity and calf vascular resistance were reduced after exercise (-29.7 +/- 8.8 and -25.3 +/- 9.1%, both P < 0.05). The baroreflex relation between diastolic pressure and sympathetic outflow was shifted downward after exercise (post-exercise intercept, 218 +/- 38 total integrated activity (heartbeat)-1; post-sham intercept, 318 +/- 51 total integrated activity (heartbeat)-1, P < 0.05), indicating less sympathetic outflow across all diastolic pressures. Further, the relation between sympathetic activity and vascular resistance was attenuated after exercise (post-exercise slope, 0.0031 +/- 0.0007 units (total integrated activity)-1 min; post-sham slope, 0.0100 +/- 0.0033 units (total integrated activity)-1 min, P < 0.05), indicating less vasoconstriction with any increase in sympathetic activity. 4. Thus, both baroreflex control of sympathetic outflow and the transduction of sympathetic activity into vascular resistance are altered after dynamic exercise. We conclude that the vasodilation which underlies post-exercise hypotension results from both neural and vascular phenomena.

Blood pressure (BP) is immediately lowered after a session of dynamic exercise, e.g. postexercise hypotension (PEH). The optimal exercise intensity needed to evoke PEH has not been established. We examined the effect of light (LITE) and moderate (MOD) exercise intensity on PEH. Subjects were 49 men (mean +/- SEM, 43.8 +/- 1.4 years) with high normal to stage 1 hypertension (145.0 +/- 1.5/85.8 +/- 1.1 mmHg). Men randomly completed three blinded experiments: a control session and two cycle exercise bouts, one at 40% (LITE) and the other at 60% (MOD) of maximal oxygen consumption. Experiments began with a baseline period and were conducted at the same time of day and separated by >/= 2 days. Subjects wore an ambulatory BP monitor after the experiments. Repeated measure analysis of variance (ANOVA) tested if BP and heart rate differed over time and between experimental conditions. Multivariate regression tested factors related to the BP response. For 9 h after all experiments, average awake systolic blood pressure (SBP) increased and diastolic blood pressure (DBP) decreased compared with baseline (P < 0.001). Average awake SBP increased up to 6.9 mmHg less (P < 0.001) and DBP decreased 2.6 mmHg more (P < 0.05) after exercise versus control. For 5 h, PEH was greater after MOD; but over the course of 9 h, LITE was as effective as MOD in eliciting PEH. Baseline BP was the primary factor explaining the BP response (beta = -0.434 to -0.718, r = 0.096-0.295). LITE and MOD evoked PEH throughout the daytime hours. Lower intensity dynamic exercise such as walking, contributes to BP control in men with hypertension.

Recent investigations have demonstrated that there is a sustained reduction in arterial blood pressure after a single bout of exercise, ie, postexercise hypotension (PEH). The purpose of this discussion is to integrate the available information on this topic and to review studies using sustained stimulation of somatic afferents in experimental rats as a model to study the role of somatic afferents in PEH. PEH occurs in response to several types of large-muscle dynamic exercise (ie, walking, running, leg cycling, and swimming) at submaximal intensities greater than 40% of peak aerobic capacity and exercise durations generally between 20 and 60 minutes. PEH is observed in both normotensive and hypertensive humans and in spontaneously hypertensive rats but is generally greater in magnitude in hypertensive subjects. The maximal exercise-induced reductions in systolic and diastolic arterial blood pressures have been on average 18 to 20 and 7 to 9 mm Hg, respectively, in hypertensive humans and 8 to 10 and 3 to 5 mm Hg, respectively, in normotensive humans. PEH has been reported to persist for 2 to 4 hours under laboratory conditions. Whether PEH is sustained for a prolonged period of time under free-living conditions remains controversial, although the results of one study indicate that PEH can persist for up to 13 hours. Possible mechanisms involved in mediating postexercise and poststimulation reductions in arterial blood pressure include decreased stroke volume and cardiac output; reductions in limb vascular resistance, total peripheral resistance, and muscle sympathetic nerve discharge; group III somatic afferent activation; altered baroreceptor reflex circulatory control; reduced vascular responsiveness to alpha-adrenergic receptor-mediated stimulation; and activation of endogenous opioid and serotonergic systems. It appears that the magnitude of PEH in hypertensive subjects is clinically significant; however, more investigation is required to determine if the duration is sufficient under real-life conditions to contribute to the reduction in blood pressure observed with chronic exercise conditioning.