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Astronauts who are occupied with prelaunch schedules may have to limit their regular physical exercise routines. To assess a potential effect on blood pressure control, carotid baroreceptor-cardiac reflex responses of 16 men were evaluated before and after two weeks of exercise detraining that followed ten weeks of regular scheduled exercise (30 min/d, 4 d/week at 75 percent V(O2) max). After detraining, the baroreflex stimulus-response relationship had a reduced slope 0.4 msec/mmHg and range of response. In addition, there was a resetting of the relationship on the R-R interval axis. Both the minimum and maximum R-R interval responses to the stimulus were significantly reduced after detraining. Baseline systolic pressure did not change with detraining, and the carotid baroreceptor-cardiac response relationship did not shift on the pressure axis. These results suggest that detraining from regular exercise can compromise vagally-mediated mechanisms of blood pressure regulation.

The effect of a spaceflight on the vagally mediated baroreceptor-cardiac reflex responses of humans were investigated by measuring the responses (provoked by neck pressure changes) in supine position and the heart rate and blood pressure in the supine and standing positions in 16 astronauts before and after 4- to 5-day long Space Shuttle missions. The results showed that exposures to spaceflight resulted in reduced baseline levels of the vagal-cardiac outflow and the vagally mediated responses to changes of the arterial baroreceptor input and that these changes contribute to postflight reductions of astronauts' ability to maintain standing arterial pressures.

Impaired cardiovascular function, characterized by orthostatic intolerance and reduced exercise capacity, is a result of space travel. We hypothesized that postflight baroreflex dysfunction may contribute. We studied the vagally mediated carotid baroreceptor-cardiac reflex response of 6 astronauts before, during, and after the ten day SLS-l mission. A series of R-waves triggered pressure and suction steps (from 40 to minus 65 mmHg) were delivered to a neck chamber during held expirtation. Resulting R-R interval changes were plotted against carotid distending pressure (systolic - neck pressure), and curve parameters calculated. After an initial rise, the operational point declined consistently during the flight and reached a nadir on landing day, but had recovered to preflight levels by L + 4. Slope and range of the response declined throughout the flight, were slightly recovered by the time measurements were made on landing day, but still were reduced on L + 4. These data indicate that space flight results in a significant impairment of the carotid baroreceptor cardiac reflex response.

A new system is described that delivers precise, stereotyped pressure changes to the human neck and elicits neurally-mediated heart rate changes. The centerpiece of this system is a Silastic chamber that is strapped to the anterior neck. This chamber is connected to a stepping-motor-controlled bellows assembly. A strain-gauge transducer measures the intensity of pressure changes. The entire system is controlled by microprocessors, and both stimuli and responses are displayed on a digital oscilloscope. The end-product of this system is a reproducible baroreceptor stimulus-cardiac response relation that can be recorded rapidly and safely in astronauts in space.

Valsalva's maneuver, voluntary forced expiration against a closed glottis, is a well-characterized research tool, used to assess the integrity of human autonomic cardiovascular control. Valsalva straining provokes a stereotyped succession of alternating positive and negative arterial pressure and heart rate changes mediated in part by arterial baroreceptors. Arterial pressure changes result primarily from fluctuating levels of venous return to the heart and changes of sympathetic nerve activity. Muscle sympathetic activity was measured directly in nine volunteers to explore quantitatively the relation between arterial pressure and human sympathetic outflow during pressure transients provoked by controlled graded Valsalva maneuvers. Our results underscore several properties of sympathetic regulation during Valsalva straining. First, muscle sympathetic nerve activity changes as a mirror image of changes in arterial pressure. Second, the magnitude of sympathetic augmentation during Valsalva straining predicts phase 4 arterial pressure elevations. Third, post-Valsalva sympathetic inhibition persists beyond the return of arterial and right atrial pressures to baseline levels which reflects an alteration of the normal relation between arterial pressure and muscle sympathetic activity. Therefore, Valsalva straining may have some utility for investigating changes of reflex control of sympathetic activity after space flight; however, measurement of beat-to-beat arterial pressure is essential for this use. The utility of this technique in microgravity can not be determined from these data. Further investigations are necessary to determine whether these relations are affected by the expansion of intrathoracic blood volume associated with microgravity.

The hypothesis that baroreflex malfunction contributes to orthostatic hypotension in microgravity was tested by studying vagally mediated carotid baroreceptor-cardiac reflexes in healthy human subjects before, during, and after 30 days of 6-deg head-down bed rest. The baroreflex response relationships were provoked with ramped neck pressure-suction sequences comprising pressure elevations to 40 mm Hg followed by serial R-wave-triggered 15-mm Hg reductions to -65 mm0 Hg; each R-R interval was plotted as a function of systolic pressure minus the neck chamber pressure applied during the interval. It is shown that head-down bed rest led to an impairment of vagal baroreflex function and that it was associated with an impairment of hemodynamic adjustments to standing, indicating that baroreflex impairment may contribute to orthostatic hypotension observed in spacecrews after a flight.