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Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.

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NASA NTRS2001

Cardiac atrophy after bed rest and spaceflight

Cardiac muscle adapts well to changes in loading conditions. For example, left ventricular (LV) hypertrophy may be induced physiologically (via exercise training) or pathologically (via hypertension or valvular heart disease). If hypertension is treated, LV hypertrophy regresses, suggesting a sensitivity to LV work. However, whether physical inactivity in nonathletic populations causes adaptive changes in LV mass or even frank atrophy is not clear. We exposed previously sedentary men to 6 (n = 5) and 12 (n = 3) wk of horizontal bed rest. LV and right ventricular (RV) mass and end-diastolic volume were measured using cine magnetic resonance imaging (MRI) at 2, 6, and 12 wk of bed rest; five healthy men were also studied before and after at least 6 wk of routine daily activities as controls. In addition, four astronauts were exposed to the complete elimination of hydrostatic gradients during a spaceflight of 10 days. During bed rest, LV mass decreased by 8.0 +/- 2.2% (P = 0.005) after 6 wk with an additional atrophy of 7.6 +/- 2.3% in the subjects who remained in bed for 12 wk; there was no change in LV mass for the control subjects (153.0 +/- 12.2 vs. 153.4 +/- 12.1 g, P = 0.81). Mean wall thickness decreased (4 +/- 2.5%, P = 0.01) after 6 wk of bed rest associated with the decrease in LV mass, suggesting a physiological remodeling with respect to altered load. LV end-diastolic volume decreased by 14 +/- 1.7% (P = 0.002) after 2 wk of bed rest and changed minimally thereafter. After 6 wk of bed rest, RV free wall mass decreased by 10 +/- 2.7% (P = 0.06) and RV end-diastolic volume by 16 +/- 7.9% (P = 0.06). After spaceflight, LV mass decreased by 12 +/- 6.9% (P = 0.07). In conclusion, cardiac atrophy occurs during prolonged (6 wk) horizontal bed rest and may also occur after short-term spaceflight. We suggest that cardiac atrophy is due to a physiological adaptation to reduced myocardial load and work in real or simulated microgravity and demonstrates the plasticity of cardiac muscle under different loading conditions.

Flight Experiment↗
NASA NTRS2000

Cardiovascular response to lower body negative pressure stimulation before, during, and after space flight

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.

manned↗