Key result
Cardiovascular changes during space flight LBNP testing reflect fluid deficit rather than altered autonomic processing.
Why the study?
Space travel causes post-flight orthostatic hypotension and it was assumed that autonomic cardiovascular control deteriorates in space.
Does lower body negative pressure stimulation reveal changes in autonomic cardiovascular control in crew-members during and after space flight?
Observational (n=6)
Does lower body negative pressure stimulation reveal changes in autonomic cardiovascular control in crew-members during and after space flight?
Cardiovascular changes observed during space flight are a consequence of fluid deficit rather than changes in autonomic signal processing.
Challenges assumption of autonomic deterioration in space; leaves open fluid-deficit mechanisms of post-flight orthostatic intolerance in larger cohorts.
BACKGROUND: It is well known that space travel cause post-flight orthostatic hypotension and it was assumed that autonomic cardiovascular control deteriorates in space. Lower body negative pressure (LBNP) was used to assess autonomic function of the cardiovascular system. METHODS: LBNP tests were performed on six crew-members before and on the first days post-flight in a series of three space missions. Additionally, two of the subjects performed LBNP tests in-flight. LBNP mimics fluid distribution of upright posture in a gravity independent way. It causes an artificial sequestration of blood, reduces preload, and filtrates plasma into the lower part of the body. Fluid distribution was assessed by bioelectrical impedance and anthropometric measurements. RESULTS: Heart rate, blood pressure, and total peripheral resistance increased significantly during LBNP experiments in-flight. The decrease in stroke volume, the increased pooling of blood, and the increased filtration of plasma into the lower limbs during LBNP indicated that a plasma volume reduction and a deficit of the interstitial volume of lower limbs rather than a change in cardiovascular control was responsible for the in-flight response. Post-flight LBNP showed no signs of cardiovascular deterioration. The still more pronounced haemodynamic changes during LBNP reflected the expected behaviour of cardiovascular control faced with less intravascular volume. In-flight, the status of an intra-and extravascular fluid deficit increases sympathetic activity, the release of vasoactive substances and consequently blood pressure. Post-flight, blood pressure decreases significantly below pre-flight values after restoration of volume deficits. CONCLUSION: We conclude that the cardiovascular changes in-flight are a consequence of a fluid deficit rather than a consequence of changes in autonomic signal processing.
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Baisch et al. (2000) conducted an observational in Post-flight orthostatic hypotension (n=6). Space flight and Lower body negative pressure (LBNP) vs. Pre-flight baseline was evaluated on Cardiovascular response (heart rate, blood pressure, total peripheral resistance, stroke volume, fluid distribution). Cardiovascular changes observed during lower body negative pressure testing in space flight are a consequence of a fluid deficit rather than changes in autonomic signal processing.
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