Background Exposure to actual and simulated microgravity induces cardiovascular deconditioning through a variety of factors. Although the mechanisms involved remain uncertain, one involves alterations in volume-regulating systems—the hypothesis being tested in this study. To maximize our ability to detect subtle changes in the volume-regulating systems, subjects were studied on a high-average salt intake to maximally suppress these systems basally.
Methods Fourteen healthy male subjects underwent 14-day head-down tilt bed rest (HDTB) during which a constant 200 mEq sodium, 100 mEq potassium diet was maintained. Daily 24-hour urine collection was performed; plasma renin activity, serum aldosterone, plethysmography, and cardiovascular system identification were performed during a control period (pre-HDTB) and at the end of HDTB (end HDTB).
Results Sodium excretion increased initially (pre-HDTB = 182.8 ± 10.4 mEq/total volume; early HDTB = 236.4 ± 13.0; p = .002) and then returned to baseline values. Potassium excretion increased 4 days after the initiation of HDTB and remained elevated thereafter (pre-HDTB = 82.2 ± 2.4/total volume; mid- to late HDTB = 89.4 ± 2.1; p = .02). Plasma renin activity increased significantly with HDTB (pre-HDTB = 1.28 ± 0.21 ng/mL/h; end HDTB = 1.69 ± 0.18; p = .01), but serum aldosterone did not change. A significant decrease in autonomic responsiveness and an increase in leg compliance were observed.
Conclusions We conclude that even in the presence of a high-average salt intake diet, simulated microgravity leads to renal, cardioendocrine, and cardiovascular system alterations that likely contribute to cardiovascular deconditioning.
- renin-angiotensin-aldosterone system
- autonomic function
- simulated microgravity
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