The transition from rest to exercise includes a marked increase of muscle blood flow, a reduction of total peripheral resistance, but nevertheless increases in arterial blood pressure. This review will address to what extent these readjustments are altered after long-term inactivity, such as bedrest, or long-term absence of hydrostatic gradients in the head-to-feet direction, such as during and after space flight.

Rest: 

Resting subjects frequently show impaired orthostatic tolerance after bedrest and spaceflight. Although small but significant changes of the carotid-cardiac-chronotropic baroreflex sensitivity has been observed under such circumstances, the tachycardic response to orthostatic stress seems to be intact during stand tests. Rather, present data suggests that is vascular arm of the baroreflex that is impaired in non-finishers during stand tests after spaceflight.

Exercise: 

The cardiovascular response to isometric muscle activity is a commonly used model to study the effects of central command and peripheral muscle receptors during exercise. Using such a model, bedrest was found to be followed by marked decrements of heart rate (HR) and blood-pressure (BP) responses to isometric lower arm exercise (ISO). After spaceflight, however, only a modest impairment were seen of the HR response to ISO.

The ability to maintain BP during orthostatic challenges in subjects performing dynamic leg exercise, has been studied by our group: Blood pressure swings in response to sudden up- and down tilts during exercise were exaggerated after long-term bedrest. This was associated with reduced amplitudes of tilt-induced compensatory HR responses. Over-all, the impaired buffering of BP in exercising humans after bedrest is likely caused by a higher background sympathetic drive and reduced stroke volumes. In turn, reduced stroke volumes are likely caused by combination of hypovolemia and cardiac atrophy.