Artificial gravity training reduces bed rest-induced cardiovascular deconditioning.

We studied 15 men (8 treatment, 7 control) before and after 21 days of 6º head-down tilt to determine whether daily, 1-h exposures to 1.0 G(z) (at the heart) artificial gravity (AG) would prevent bed rest-induced cardiovascular deconditioning. Testing included echocardiographic analysis of cardiac function, plasma volume (PV), aerobic power (VO(2)pk) and cardiovascular and neuroendocrine responses to 80º head-up tilt (HUT). Data collected during HUT were ECG, stroke volume (SV), blood pressure (BP) and blood for catecholamines and vasoactive hormones. Heart rate (HR), cardiac output (CO), total peripheral resistance, and spectral power of BP and HR were calculated. Bed rest decreased PV, supine and HUT SV, and indices of cardiac function in both groups. Although PV was decreased in control and AG after bed rest, AG attenuated the decrease in orthostatic tolerance [pre- to post-bed rest change; control: -11.8 ± 2.0, AG: -6.0 ± 2.8 min (p = 0.012)] and VO(2)pk [pre- to post-bed rest change; control: -0.39 ± 0.11, AG: -0.17 ± 0.06 L/min (p = 0.041)]. AG prevented increases in pre-tilt levels of plasma renin activity [pre- to post-bed rest change; control: 1.53 ± 0.23, AG: -0.07 ± 0.34 ng/mL/h (p = 0.001)] and angiotensin II [pre- to post-bed rest change; control: 3.00 ± 1.04, AG: -0.63 ± 0.81 pg/mL (p = 0.009)] and increased HUT aldosterone [post-bed rest; control: 107 ± 30 pg/mL, AG: 229 ± 68 pg/mL (p = 0.045)] and norepinephrine [post-bed rest; control: 453 ± 107, AG: 732 ± 131 pg/mL (p = 0.003)]. We conclude that AG can mitigate some aspects of bed rest-induced cardiovascular deconditioning, including orthostatic intolerance and aerobic power. Mechanisms of improvement were not cardiac-mediated, but likely through improved sympathetic responsiveness to orthostatic stress.

Cardiovascular adaptations to long-duration head-down bed rest.

INTRODUCTION: Orthostatic hypotension is a serious risk for crewmembers returning from spaceflight. Numerous cardiovascular mechanisms have been proposed to account for this problem, including vascular and cardiac dysfunction, which we studied during bed rest. METHODS: Thirteen subjects were studied before and during bed rest. Statistical analysis was limited to the first 49-60 d of bed rest and compared to pre-bed rest data. Ultrasound data were collected on vascular and cardiac structure and function. Tilt testing was conducted for 30 min or until presyncopal symptoms intervened. RESULTS: Plasma volume was significantly reduced (15%) by day 7 of bed rest. Flow-mediated dilation in the leg was significantly increased at bed rest day 49 (6% from pre-bed rest). Arterial responses to nitroglycerin differed in the arm and leg, but did not change as a result of bed rest. Anterior tibial artery intimal-medial thickness markedly decreased at bed rest days 21 (21%), 35 (22%), and 49 (19%). Several cardiac functional parameters, including isovolumic relaxation time (73 ms to 85 ms at day 7) and myocardial performance index, were significantly increased (0.41 to 0.49 by day 7 of bed rest; indicating a decrease in cardiac function) during bed rest. There was a trend for decreased orthostatic tolerance following 60 d of bed rest (P = 0.1). DISCUSSION: Our data suggest that bed rest altered cardiovascular structure and function in a pattern similar to short-duration spaceflight. Additionally, the vascular alterations were primarily seen in the lower body, while vessels of the upper body were unaffected.

Cardiovascular effects of anti-G suit and cooling garment during space shuttle re-entry and landing.

BACKGROUND: Many cardiovascular changes associated with spaceflight reduce the ability of the cardiovascular system to oppose gravity on return to Earth, leaving astronauts susceptible to orthostatic hypotension during re-entry and landing. Consequently, an anti-G suit was developed to protect arterial pressure during re-entry. A liquid cooling garment (LCG) was then needed to alleviate the thermal stress resulting from use of the launch and entry suit. METHODS: We studied 34 astronauts on 22 flights (4-16 d). Subjects were studied 10 d before launch and on landing day. Preflight, crewmembers were suited with their anti-G suits set to the intended inflation for re-entry. Three consecutive measurements of heart rate and arterial pressure were obtained while seated and then again while standing. Three subjects who inflated the anti-G suits also donned the LCG for landing. Arterial pressure and heart rate were measured every 5 min during the de-orbit maneuver, through maximum G-loading (max-G) and touch down (TD). After TD, crew-members again initiated three seated measurements followed by three standing measurements. RESULTS: Astronauts with inflated anti-G suits had higher arterial pressure than those who did not have inflated anti-G suits during re-entry and landing (133.1 +/- 2.5/76.1 +/- 2.1 vs. 128.3 +/- 4.2/79.3 +/- 2.9, de-orbit; 157.3 +/- 4.5/102.1 +/- 3.6 vs. 145.2 +/- 10.5/95.7 + 5.5, max-G; 159.6 +/- 3.9/103.7 +/- 3.3 vs. 134.1 +/- 5.1/85.7 +/- 3.1, TD). In the group with inflated anti-G suits, those who also wore the LCG exhibited significantly lower heart rates than those who did not (75.7 +/- 11.5 vs. 86.5 +/- 6.2, de-orbit; 79.5 +/- 24.8 vs. 112.1 +/- 8.7, max-G; 84.7 +/- 8.0 vs. 110.5 +/- 7.9, TD). CONCLUSIONS: The anti-G suit is effective in supporting arterial pressure. The addition of the LCG lowers heart rate during re-entry.