Several studies have indicated that a single bout of physical exercise induced a significant antihypertensive effect during the hours after the activity. However, little information is presently available on the underlying hemodynamic changes. We examined 13 essential hypertensive patients and nine nonnotensive subjects in a randomized, crossover study design during 3 hours after a 30-minute period of upright leg cycling at 50% of peak aerobic capacity and during 3 hours after a 30-minute control period of rest Blood pressure, heart rate, cardiac output, total peripheral resistance, and regional vascular resistance in the forearm as well as venous plasma catecholamine concentrations were measured repeatedly. After exercise, systolic (-11±2 mm Hg) and diastolic (-4±1 mm Hg) blood pressures, total peripheral resistance (-27±5%), forearm vascular resistance (-25±6%), and plasma norepinephrine levels (-21±7%) were significantly (p<0.05) decreased, and cardiac output was increased (+31 ±8%) compared with control in hypertensive subjects. In contrast, in normotensive subjects blood pressure, forearm vascular resistance, and plasma norepinephrine were unchanged, and systemic hemodynamics changed to a lesser extent than in hypertensive subjects after exercise. It is concluded that a decrease in regional vascular resistance in skeletal muscles and possibly in the skin in hypertensive patients may contribute importantly to the antihypertensive effect of prior exercise. A decreased sympathetic nervous activity, as seen from lower plasma norepinephrine levels, may be involved in this effect (Hypertension 1992;19:183-191)

Background. It is generally accepted that physical training decreases blood pressure in hypertensive subjects, but the importance of training intensity has not been established. This study compared the effects of endurance training at different intensities on ambulatory blood pressure and on blood pressure load (percentage of readings above 140/90 and 120/80 mm Hg during the waking and sleeping periods,

The mechanisms underlying the antihypertensive period following a bout of exercise are not well understood. We examined the aftereffects of exercise on the linear relationship between forearm vascular resistance (FVR) and estimated central venous pressure (CVP) during leg raising and lower body negative pressure to determine whether an alteration of the baroreflex control of FVR was associated with the decreased blood pressure. Blood pressure, forearm blood flow (FBF), and estimated CVP were obtained in 13 hypertensive and 9 normotensive subjects evaluated in a randomized crossover fashion after 30 min of cycle ergometer exercise and after a nonexercise control period. In hypertensive subjects, the reduced blood pressure was accompanied by an increased baseline FBF after exercise. This resulted in a downward shift of the FVR-CVP relationship, while the slope was unchanged. In normotensive subjects, blood pressure and baroreflex control of FVR were unaffected by prior exercise. Four of the hypertensive subjects performed an additional study in which forearm skin was vasodilated with local heating to FVR levels similar to those observed after exercise. Results suggested that the aftereffects of exercise could not be attributed to changes in cutaneous blood flow. We speculate that modulation of the baroreflex control of FVR after exercise contributes to its antihypertensive effect.

A 6-month reduction in blood pressure under quinapril treatment was associated with decreases in left ventricular hypertrophy and in minimal vascular resistance in the forearm of elderly hypertensive patients. Absence of structural changes in leg vasculature could be related to the greater arterial pressure prevalent in the lower limbs while patients stood upright and, consequently, a proportionately smaller decrease in blood pressure, as well as greater structural changes and fibrous damage than those of the upper limbs.

Background-The information that insulin sensitivity and glycogen synthesis are reduced in hypertension arises primarily from studies using insulin infusions. Whether glycogen metabolism is actually altered in a physiological condition, such as during and after prolonged exercise, is currently unknown. Methods and Results-To examine this issue, 9 hypertensive and 11 normotensive subjects were evaluated on a rest day and after intense and prolonged exercise on a separate day. Insulin sensitivity and hemodynamic variables were measured on both days. On the exercise day, whole-body substrate utilization was assessed and muscle biopsies were taken in the leg at baseline, immediately after exercise, and 2.5 and 4 hours after exercise. Insulin sensitivity at rest was lower in hypertensive than normotensive subjects (PϽ0.05) and increased after exercise in normotensive (PϽ0.01) but not in hypertensive (PϭNS) subjects. Leg blood flow increased after exercise in both groups but to a lesser extent in hypertensive than normotensive subjects. Baseline glycogen content and maximal glycogen synthase activity were higher in hypertensive than normotensive subjects (PϽ0.001). Glycogen concentration decreased relatively less (Ϫ35 versus Ϫ66%) and returned to baseline levels faster in hypertensive subjects after exercise. Hypertensive subjects used Ϸ40% less carbohydrates during exercise (PϽ0.001) at the expense of greater free fatty acid oxidation. Conclusions-It is concluded that increased intramuscular glycogen storage and resynthesis in hypertension are independent of blood flow and may represent compensatory mechanisms for the reduced insulin sensitivity and carbohydrate metabolism in this condition.