Effect of postural changes on cardiovascular responses to static exercise in hypertensive human beings

Objective In hypertensive patients, exaggerated increases in vascular resis tance and arterial blood pressure have been reported on changing posture fr om supine to upright. In this study we tested the hypothesis that in hypert ensive subjects, upright posture induces an increase in the vasoconstrictor and presser responses to physical exercise. Subjects and methods We studied 17 males with mild hypertension and 10 sex- and age-matched normotensives. Each performed three bouts of static handgr ip at 30% maximum voluntary contraction for 2 min after 10 min of supine re st and, in sequence, after 10 min of sitting and 10 min of standing. Arteri al pressure, heart rate and forearm vascular resistance were measured by Fi napres and plethysmography, respectively. Results Exercise posture did not affect the mean arterial pressure and hear t rate responses to static handgrip. No significant differences in these re sponses were observed between the hypertensives and the normotensives in an y posture. In the hypertensives (n = 12), forearm vascular resistance did n ot change significantly from resting values during supine and sitting stati c handgrip but increased significantly during standing static handgrip. In the normotensives, forearm vascular resistance did not change significantly from resting values during static handgrip in any posture. The forearm vas cular resistance response to the standing static handgrip was significantly greater in the hypertensives than the normotensives. The algebraic sum of forearm vascular resistance responses to postural change from sitting to st anding plus that induced by sitting static handgrip (i.e additive reflexes) was significantly less than the forearm vascular resistance response to th e standing static handgrip (i.e. combined relexes), indicating a facilitato ry interaction between exercise and orthostatic stimuli in hypertensives. I n contrast, the algebraic sum of the heart rate responses to postural chang e from sitting to standing plus that induced by sitting static handgrip was significantly greater than the response to standing static handgrip, indic ating an inhibitory interaction. Conclusions In hypertensive patients, physiological orthostasis causes an i ncreased vasoconstrictor response to static exercise, but this is opposed b y an inhibitory influence on the heart rate response, with the result that the presser response to static exercise is unaffected by upright posture. J Hypertens 1999, 17:99-105 (C) Lippincott Williams & Wilkins.