Effects of exercise and inactivity on intravascular volume and cardiovascular control mechanisms

Abstract

Exercise, inactivity and confinement have been used as effective tools to assess the contributions of vascular volume and baroreflexes to orthostatic hypotension associated with exposure to microgravity. Prolonged exposure to bedrest, physical inactivity, or wheelchair confinement removes baroreceptor unloading caused by regular upright standing and induces attenuation of cardiovascular baroreflex responses. The magnitude of reduced baroreflex sensitivity following bedrest or wheelchair confinement is related to the degree of orthostatic hypotension. Reduction in vascular volume caused by bedrest or progressive hypovolemia does not affect carotid-cardiac baroreflex function. In contrast, intense exercise that increases arterial baroreceptor loading causes an acute increase in carotid baroreceptor sensitivity and has been associated with enhanced orthostatic stability following exposure to simulated microgravity. Endurance exercise training designed to enhance orthostatic stability was associated with increased blood volume and vasoconstrictive reserve, but no change in the carotid baroreflex response. Therefore, using models of exercise, inactivity and confinement, integrated and redundant roles for vascular volume and cardiovascular baroreflexes have been demonstrated as probable underlying mechanisms that contribute independently to the development of orthostatic hypotension following spaceflight. These data suggest that loading of arterial baroreceptors may be necessary to maintain baroreflex function.