Orthostatic tolerance and hormonal changes in women during 120 days of head-down bed rest

BACKGROUND: Women will be included as mission specialists in the upcoming International Space Station program. This paper describes the changes in volume-regulating hormones and determines the degree of degradation in orthostatic tolerance in a group of women after 120 d of bed rest. The aim of this study was to test a countermeasure program to be used by women during long-duration spaceflights. METHODS: For 120 d of -6 degrees head-down bed rest (HDBR), eight healthy women were assigned either to a no-countermeasure (No-CM, n = 4), or to a countermeasure (CM, n = 4) group. In the countermeasure group, exercise began after 2 wk, pharmacological agents were given during the 1st and 3rd mo, and the "Centaur" suit was worn on the last day of bed rest and during the day time for several days after bed rest. Diet supplements were taken during the 1st and 4th mo of HDBR. Tilt tests were run before and after HDBR. RESULTS: After the HDBR, none of the CM subjects, had pre-syncopal or syncopal symptoms during tilt tests: BP was well maintained in the CM group, while heart rate and BP changed in the No-CM group. In plasma, atrial natriuretic peptide (ANP) increased in both groups and remained high throughout HDBR, while aldosterone increased and remained elevated in the No-CM group. Natriuresis was decreased during HDBR. CONCLUSION: The CM protocols used during this study were efficient and prevented orthostatic intolerance for the four CM subjects. It would be necessary to obtain more data regarding this set of CM protocols on female subjects to lead to statistical and formal conclusions.     

加压套带对抗头低位卧床模拟失重生理影响的作用

为研究四肢加压套带在对抗失重对心血管系统影响中的作用，１２名受试者随机分为对照组和套带组，进行了１０ｄ头低位卧床实验。卧床中套带组四肢使用持续加压套带１２ｈ／ｄ，对照组涂任何对措施，卧床前后检测立位耐力。结果显示：卧床前１人全部通过立位耐力试验；卧床后，套带组６人中通过５人，对照组６人仅通过１人；提示：套带加压能有效阻止头低位卧床模拟失重产生的立位耐力下降。     

Fludrocortisone does not prevent orthostatic hypotension in astronauts after spaceflight

BACKGROUND: During stand/tilt tests after spaceflight, 20% of astronauts experience orthostatic hypotension and presyncope. Spaceflight-induced hypovolemia is a contributing factor. Fludrocortisone, a synthetic mineralocorticoid, has been shown to increase plasma volume and orthostatic tolerance in Earth-bound patients. The efficacy of fludrocortisone as a treatment for postflight hypovolemia and orthostatic hypotension in astronauts has not been studied. Our purpose was to test the hypothesis that astronauts who ingest fludrocortisone prior to landing would have less loss of plasma volume and greater orthostatic tolerance than astronauts who do not ingest fludrocortisone. METHODS: There were 25 male astronauts who were randomized into 2 groups: placebo (n = 18) and fludrocortisone (n = 7), and participated in stand tests 10 d before launch and 2-4 h after landing. Subjects took either 0.3 mg fludrocortisone or placebo orally 7 h prior to landing. Supine plasma and red cell volumes, supine and standing HR, arterial pressure, aortic outflow, and plasma norepinephrine and epinephrine were measured. RESULTS: On landing day, 2 of 18 in the placebo group and 1 of 7 in the fludrocortisone group became presyncopal (chi2 = 0.015, p = 0.90). Plasma volumes were significantly decreased after flight in the placebo group, but not in the fludrocortisone group. During postflight stand tests, standing plasma norepinephrine was significantly less in the fludrocortisone group compared with the placebo group. CONCLUSIONS: Treatment with a single dose of fludrocortisone results in protection of plasma volume but no protection of orthostatic tolerance. Fludrocortisone is not recommended as a countermeasure for spaceflight-induced orthostatic intolerance.     

21d头低位卧床过程中套带对抗心血管脱适应的作用

目的在２１ ｄ 头低位卧床的１ ～１０ ｄ 使用套带,能明显阻止立位耐力下降,在后续卧床中观察套带组不使用套带时的心血管脱适应变化,以进一步验证套带的防护效果。方法 套带组继卧床第１ ～１０ 天使用套带后、卧床第１１ ～１７ 天不使用套带,最后４ ｄ 再使用套带。在卧床第１７ 、２１ 天时进行正立位７５°耐力检查。结果套带组５ 人（ 卧床第１０ 天时都通过２０ ｍｉｎ 立位） 停用套带１ ｗｋ ,５ 人中有２ 人未通过２０ ｍｉｎ 立位,一名１７ ｍｉｎ 出现晕厥前症状,另一名４ ｍｉｎ 出现晕厥。再用套带４ｄ ,套带组５ 人又全部通过２０ ｍｉｎ 立位。结论（１） 停止使用持续加压套带引起了心血管脱适应,（２）卧床后期四肢使用持续加压套带４ ｄ 能有效阻止立位耐力下降。     

Effects of occlusive cuffs "Braslet" on crew hemodynamics in short space flights and orthostatic stability post flight]

Effects of prophylactic device Braslet (occlusive cuffs wrapped around the calf) on hemodynamics were studied at rest and during the LBNP test during and on orthostatic stability post short (one-month) space flights. The ultrasonic procedure was applied to seven cosmonauts who had and six cosmonauts who had not worn the cuffs while in orbit. The device markedly alleviated the subjective feeling of discomfort caused by blood shift toward the cranial end at the beginning of adaptation to microgravity. Reductions in the central and peripheral hemodynamics, cervico-cephalic venous plethora specifically, were sequel to staying in microgravity. Testing of the hemodynamic reactions to LBNP during and after shortflights failed to discover noticeable deltas among the cosmonauts who had and had not worn the cuffs. The first analysis of objective in- and postflight data did not suggest any determent in orthostatic stability of cosmonauts due to application of the Braslet cuffs.     

Decreased venous contamination on 3D gadolinium-enhanced bolus chase peripheral mr angiography using thigh compression

OBJECTIVE: We evaluated the potential for improving bolus chase peripheral MR angiography in patients with fast arterial flow using thigh compression to prevent venous contamination. SUBJECTS AND METHODS: We performed bolus chase peripheral MR angiography in 32 consecutive patients in whom the travel time for a contrast agent to reach the popliteal artery trifurcation was less than 25 sec. Thigh compression was applied by a tourniquet (n = 13) or blood pressure cuff inflated to 60 mm Hg (n = 19). We compared the results with those of 36 consecutive patients who underwent angiography without thigh compression. The effect of thigh compression on arterial flow and tissue enhancement was assessed in patients with symmetric travel time in both legs by applying compression to one leg during the time-resolved 2D-projection MR angiography with 6 mL of gadolinium. On 3D bolus chase MR angiography, thigh compression was applied bilaterally. Venous contamination on the 3D images of the calf was graded as 0, none; 1, trace; 2, mild; 3, moderate; and 4, severe. Signal-to-noise ratio was measured in the popliteal artery. RESULTS: Thigh compression slowed the arterial travel time by a mean +/- SD of 4.7 +/- 2 sec (p < 0.001) with a blood pressure cuff and 3.1 +/- 1 sec (p < 0.001) with a tourniquet. Blood pressure cuffs reduced the score of venous contamination on the calf station from 1.9 to 0.4 (p < 0.05) for intermediate flow (contrast travel time, 20-25 sec) and from 2.5 to 0.9 (p < 0.05) for fast flow (< 20 sec). Thigh compression increased the popliteal artery signal-to-noise ratio (81 vs 52, p < 0.001). CONCLUSION: Thigh compression with blood pressure cuffs inflated to 60 mm Hg slows down arterial flow, increases arterial signal-to-noise ratio, and reduces venous contamination on 3D gadolinium-enhanced bolus chase peripheral MR angiography.     

Hemodynamic reactions to modified orthostatic test in persons with different +Gz tolerance

Hemodynamic responses to the passive and modified orthostatic tests were investigated in 27 low and 13 high +Gz susceptibility individuals. The modified orthostatic test included 5 min head-down tilt (-30 degrees) and head-up tilt (78 degrees) with occlusion cuffs (50 mm Hg and 100 mm Hg) applied to the upper third of the hip. Analysis of typological reactions in low and high +Gz susceptibility individuals revealed no significant differences in their tolerance to the above tests. It was found that during the 1st minute of the modified orthostatic test with 100 mm Hg pressure in the occlusion cuffs heart rate was lower and systolic blood volume was higher (p less than 0.05) than during the passive test. Differences in these parameters disappeared by the 10th minute of exposure. During the modified orthostatic test with 50 mm Hg pressure in the occlusion cuffs these parameters did not show statistically significant differences.     

Effect of lower body negative pressure against orthostatic intolerance induced by 21 days head-down tilt bed rest

BACKGROUND: Exposure to actual or simulated weightlessness is known to induce orthostatic intolerance in humans. Many different methods have been suggested to counteract orthostatic hypotension. The repetitive or prolonged application of lower body negative pressure (LBNP) has shown beneficial effects to counter orthostatic intolerance, but devoting so much time to countermeasures is not compatible with space mission objectives or costs. The purpose of the present study was to assess the effects of brief LBNP sessions against orthostatic intolerance during a 21-d head-down tilt (HDT) bed rest. METHODS: There were 12 healthy male volunteers who were exposed to -6 degrees HDT bed rest for 21 d. Six subjects received -30 mm Hg LBNP sessions for 1 h x d(-1) from day 15 to day 21 of the HDT, and six others served as control. Orthostatic tolerance was assessed by means of standard tilt test. RESULTS: Before HDT, all the subjects in the two groups completed the tilt tests. After 21 d of HDT, five subjects of the control group and one subject of the LBNP group could not complete the tilt test due to presyncopal or syncopal symptoms. The mean upright time in the control group 13.0 +/- 4.0 min) was significantly shorter (p < 0.05) than that in the LBNP group (19.0 +/- 2.2 min). Body weight decreased significantly in the control group during HDT, while increasing significantly on day 21 of HDT in the LBNP group. Urine volume increased on days 15-21 of HDT in the control group, but remained unchanged throughout HDT in the LBNP group. A significant decrease in cardiac output and cardiac index, and a significant increase in total peripheral resistance, pre-ejection period, plasma renin activity, aldosterone, and prostaglandin 12 were observed during HDT in both groups. There were no significant differences in these parameters between the two groups. CONCLUSIONS: Brief daily LBNP sessions were effective in preventing orthostatic intolerance induced by 21 d HDT bed rest. However, it did not improve cardiac pump and systolic functions and did not preserve volume regulating hormones.     

Yohimbine administration prevents over-responsiveness to epinephrine induced by simulated microgravity

BACKGROUND: Simulated microgravity produces sustained inhibition of sympathoneural release, turnover, and synthesis of norepinephrine (NE) and hypersensitization of beta-adrenergic pathways. These changes may explain the orthostatic intolerance experienced by astronauts returning from spaceflights. HYPOTHESIS: Chronic administration of yohimbine would prevent the increase of beta-adrenergic hypersensitivity to epinephrine (Epi) induced by simulated microgravity. METHODS: Eight healthy young subjects received 8 mg of yohimbine (an antagonist of alpha2adrenoceptors) orally twice a day during the simulated microgravity achieved through -6 degrees head-down bed rest (HDBR). The catecholamine-induced lipolysis was studied on isolated fat cells from subcutaneous adipose tissue before HDBR and on the fifth day of HDBR. Epi was infused at three graded rates (0.01, 0.02, and 0.03 microg x kg(-1) x min(-1) for 40 min each) before and at the end of the HDBR period. The effects of Epi on the sympathetic nervous system (SNS) activity-assessed by plasma NE levels and spectral analysis of systolic BP and heart rate variability-and on plasma levels of glycerol, non-esterified fatty acids, glucose, and insulin and on energy expenditure were evaluated. RESULTS: Under yohimbine treatment, HDBR failed to modify urinary NE excretion and spectral variability of systolic BP in the mid-frequency range. The beta- and alpha-adrenergic sensitivity of fat cells were not modified by HDBR nor were plasma NE levels and spectral variability of systolic BP induced by Epi infusion. No alteration of Epi-induced changes in heart rate and systolic and diastolic BPs were observed after HDBR. Epi-induced increases in plasma glucose, insulin, glycerol, and non-esterified fatty acid levels as well as energy expenditure were also unmodified by HDBR. Only the Epi-induced plasma lactate level was increased by HDBR. CONCLUSION: Our data suggest that the increase in the effects of Epi induced during microgravity could be attenuated by chronic administration of yohimbine. An explanation for this effect could be SNS activation brought about by the alpha2-adrenoceptor antagonist properties of yohimbine.     

低氧、气功对抗模拟失重后立位中心脏节律变化的观察

目的探讨新的对抗失重措施。方法１５名、年龄１９～２２岁的健康男性青年为被试者。头低位－６°卧床（－６°ＨＤＢＲ）模拟失重,持续２１ｄ。实验分对照组（单纯卧床）、低氧组（卧床＋低氧）和气功组（卧床＋气功）。低氧组卧床期间每人每天吸两次低氧,每次２０ｍｉｎ。气功组卧床中每天练功三次,每次４５ｍｉｎ。三组卧床前、后进行２０ｍｉｎ＋７５°的立位实验。结果三组被试者在卧床前立位中的心电图未发生明显变化,心律正常。卧床２１ｄ后立位实验中对照组２人出现房性和窦性心律紊乱;气功组２人出现结性心律紊乱。低氧组所有人均未发生心律紊乱。结论低氧对抗卧床后立位耐立降低效果较好。     

Evaluation of cardiovascular risks of spaceflight does not support the NASA bioastronautics critical path roadmap

INTRODUCTION: Occurrence of serious cardiac dysrhythmias and diminished cardiac and vascular function are the primary cardiovascular risks of spaceflight identified in the 2005 NASA Bioastronautics Critical Path Roadmap. METHODS: A review of the literature was conducted on experimental results and observational data obtained from spaceflight and relevant ground simulation studies that addressed occurrence of cardiac dysrhythmias, cardiac contractile and vascular function, manifestation of asymptomatic cardiovascular disease, orthostatic intolerance, and response to exercise stress. RESULTS: Based on data from astronauts who have flown in space, there is no compelling experimental evidence to support significant occurrence of cardiac dysrhythmias, manifestation of asymptomatic cardiovascular disease, or reduction in myocardial contractile function. Although there are post-spaceflight data that demonstrate lower peripheral resistance in astronauts who become presyncopal compared with non-presyncopal astronauts, it is not clear that these differences are the result of decreased vascular function. However, the evidence of postflight orthostatic intolerance and reduced exercise capacity is well substantiated by both spaceflight and ground experiments. Although attenuation of baroreflex function(s) may contribute to postflight orthostatic instability, a primary mechanism of orthostatic intolerance and reduced exercise capacity is reduced end-diastolic and stroke volume associated with lower blood volumes and consequent cardiac remodeling. CONCLUSION: Data from the literature on the current population of astronauts support the notion that the primary cardiovascular risks of spaceflight are compromised hemodynamic responses to central hypovolemia resulting in reduced orthostatic tolerance and exercise capacity rather than occurrence of cardiac dysrhythmias, reduced cardiac contractile and vascular function, or manifestation of asymptomatic cardiovascular disease. These observations warrant a critical review and revision of the 2005 Bioastronautics Critical Path Roadmap.     

Maximal exercise as a countermeasure to orthostatic intolerance after spaceflight

Previous investigators have suggested that maximal exercise performed 24 h before the end of bed rest, a spaceflight analog, restores prebed rest plasma volume, baroreflex responses, and orthostatic tolerance. PURPOSE: In this case report, we examined the effect of a similar exercise protocol 24 h before a Shuttle landing on the orthostatic responses of four crewmembers (EX) after spaceflights of 8-14 d. Four additional crewmembers (CON) served as controls and did not perform exercise during the final day of the flight. METHODS: Each crewmember performed a 10-min stand test approximately 10 d before launch (L-10) and within 1-2 h of landing (R+0). Cardiac stroke volume was measured (Doppler ultrasound) supine and during each min of standing for three EX and three CON subjects. RESULTS: Preflight, all crewmembers completed the stand test and each group had similar heart rate and blood pressure responses. Postflight, all subjects also completed the 10-min stand test. Each group had similarly elevated supine and standing heart rates, elevated diastolic and mean arterial blood pressures, and reduced pulse pressures compared to L-10. However, postflight cardiac output, mean +/- SEM, (EX: 4.5+/-0.6 L x min(-1); CON: 3.1+/-0.3 L x min(-1)) and stroke volume (EX: 43+/-7 mL x beat; CON: 30+/-6 mL x beat) were higher after 10 min standing in the EX subjects compared to CON subjects. CONCLUSIONS: For these four crewmembers, maximal exercise performed 24 h before landing may have helped maintain stroke volume but did not maintain heart rate and blood pressure responses during standing compared to preflight.     

Vasomotor sympathetic nerve activity in men during bed rest and on orthostasis after bed rest

BACKGROUND: Alterations in autonomic function are commonly seen during and after spaceflight, and its ground-based analog, 6 degrees head-down bed rest (HDBR). They may include peripheral vascular regulation, but vasomotor sympathetic efferent nerve discharges to peripheral vasculatures have not been examined. The aim of our study was to examine changes in vasomotor sympathetic nerve activity during HDBR and under orthostasis after HDBR. METHODS: We performed 6 d of HDBR on six male subjects, and measured muscle sympathetic nerve activity (MSNA) together with plasma norepinephrine concentrations in the supine position before HDBR and in 6 degrees head-down position on the sixth day (HDBR6) of HDBR. We also measured MSNA in head-up tilt (HUT) test before and after HDBR. RESULTS: On HDBR6, MSNA burst rate was the same (17+/-4 bursts x min(-1)) as that in supine position before HDBR (15+/-2 bursts min(-1)), but plasma norepinephrine concentrations were decreased to 1.14+/-0.10 pmol x ml(-1) compared with the supine value before HDBR (1.56+/-0.20 pmol x ml(-1), p<0.05). After HDBR, supine MSNA burst rate significantly increased by 58% to 24+/-4 bursts x min(-1). MSNA increment in response to HUT was similar between before (34+/-3 bursts min(-1) x sin HUT(-1)) and after (40+/-6 bursts x min(-1) x sin HUT(-1)) HDBR. CONCLUSIONS: Our findings suggest that: a) the relationship between MSNA and plasma norepinephrine concentrations was altered on the sixth day during HDBR; b) the vasomotor sympathetic nerve activity was enhanced after HDBR; and c) the augmentation of vasomotor sympathetic outflow to muscles under orthostasis was preserved after HDBR.     

血容量减少对立位应激反应影响的仿真研究

目的 研究不同程度的血容量减少对心血管系统立位应激反应的影响,探讨血容量降低在航天失重后心血管失调和立位耐力降低机理中的意义。方法 在仿真下体负压（LBNP）暴露时心血管系统反应模型的血液重新分配子模型中引入血容量减少因素,仿真血容量减少0－25％后LBNP时心率（HR）和血压BP变化,结果 血容量减少低于总血量的5％条件下,心血管系统可以通过压力反射调节作用维持LBNP时政党的HR和BP;血容量减少超过约15％,在安静仰卧位时,HR和BP正常,但LBNP时BP迅速降低,系统可失去稳定性。结论 血容量减少将导致心血管系统对立位应激反应的改变。     

21d头低位卧床对人体左心舒张功能的影响

目的观察模拟失重条件对人体左心舒张功能的影响 ,探讨其在航天后心血管功能失调中的作用。方法采用超声多谱勒技术观察了 6名健康青年男性在 2 1d - 6°头低卧位模拟失重前、实验第 1 0、2 1天及实验后左心舒张功能变化 ,同时检查其卧床前后的立位耐力改变。结果被试者左心舒张功能指标 :经二尖瓣血流E峰最大流速 (PEV)、A峰最大流速 (PAV)、E峰血流速度积分 (VTIE)指标在实验第1 0、2 1天均较实验前有明显的降低 (P <0 .0 5 ) ;而A峰血流速度积分 (VTIA) ,峰值血流速度比值 (A/E)及血流速度积分比值 (VTIA/E)的下降则未达到显著水平 (P >0 .0 5 )。 6名被试者均未能通过立位耐力检查。结论模拟失重可引起人体左心舒张功能的显著下降     

Thigh compartment syndrome in a football athlete: a case report and review of the literature.

Although contusions of the thigh are common in all sports, a compartment syndrome from closed blunt trauma without a femur fracture is rare. Thigh compartment syndrome is unusual due to increased compliance of the thigh to accommodate increased expansion from hematoma or third space fluid. Compartment syndrome of the thigh is characterized by unrelenting pain, swelling, and limited knee range of motion. A single case of a thigh compartment syndrome caused by a direct blow to the anterior aspect of the thigh from a football helmet during kickoff occurred. Immediate thigh fasciotomy was performed. Early diagnosis with appropriate emergency treatment can avoid serious and permanent complications.     

Sodium intake does not influence bioimpedance-derived extracellular volume loss in head-down rest

INTRODUCTION: There is disagreement regarding the impact of dietary sodium on alterations in extracellular volume during head-down bed rest (HDBR). The primary purpose of this study was to assess the effects of salt intake on extracellular volume (ECV) during HDBR. METHODS: We performed whole-body bioimpedance spectroscopy with controlled sodium intake during 4 d of ambulation and 8 d of -6 degrees HDBR in 10 normotensive men. Each subject performed an initial 12-d familiarization run with moderate sodium (246 +/- 12 mmol x L(-1) x d(-1) excreted) during which no measurements were made. They then participated in treatment runs involving low sodium (LS: 143 +/- 10 mmol x L(-1) x d(-1) Na+ excreted) and high sodium (HS: 434 +/- 17 mmol x L(-1) x d(-1) Na+ excreted). The different treatments were separated by > or =1 mo and the order of LS and HS was balanced among the subjects. These treatments were based on controlled food and drink supplies as prepared by a dietitian. We monitored sodium output and measured aldosterone, plasma renin activity (PRA), and vasopressin. Bioimpedance was measured every second day in supine position using tetrapolar electrodes. RESULTS: Based on exponential data fitting, we calculated an ECV decrease of 0.79 +/- 0.32 L (-5.8%; p = 0.018) in LS, and 1.21 +/- 0.31 L (-4.0%; p = 0.002) in HS during HDBR. LS and HS were not different (p > 0.1); 4 d pre-HDBR sodium adjustment produced a fall in ECV in the LS group only (-3.7%, p = 0.023). Hormone levels were not changed by HDBR. Plasma aldosterone was lower in HS (69 +/- 7 pg x ml(-1)) than in LS (180 +/- 24 pg x ml(-1)). DISCUSSION: Our bioimpedance data confirm that low sodium intake decreases ECV in ambulatory conditions and indicate that 8 d of HDBR produce a loss of ECV of about 5% (p < 0.05). The loss did not seem to be influenced by sodium intake between approximately 3 and approximately 10 g x d(-1).     

Acceleration with exercise during head-down bed rest preserves upright exercise responses

INTRODUCTION: This study was designed to elucidate the effect of short-arm centrifuge-induced artificial gravity with exercise training during ground-based simulated spaceflight, i.e., prolonged head-down bed rest (HDBR), on respiratory and cardiovascular responses to upright exercise. METHODS: There were 10 healthy men who underwent 20 d of -6 degrees HDBR, and were assigned to either a countermeasure (CM) group (n = 5) or a no countermeasure (No-CM) group (n = 5). The subjects in the CM group performed two sessions (20 min each session, 40 min total) of short-arm centrifuge-induced artificial gravity with exercise training in a supine position on alternate days (10 d total) during HDBR. The first session was set at 0.8-1.4 G load at heart level with a constant exercise intensity (60 W), and the second session began with a 0.3 G load at heart level with an interval exercise protocol (40-80% peak oxygen uptake; VO2peak). The measurements of respiratory and cardiovascular responses to incremental exercise were performed pre- and post-HDBR. RESULTS: The 20 d of HDBR increased minute expired ventilation, heart rate, and respiratory exchange ratio and decreased stroke volume during submaximal exercise in the No-CM group, whereas these parameters were unchanged in the CM group. In the No-CM group, VO2peak decreased significantly (47.0 +/- 8.6 to 34.8 +/- 6.8 ml x kg(-1) x min(-1), p < 0.05), whereas VO2peak in the CM group did not show a significant decrease following 20 d of HDBR (47.7 +/- 10.0 to 43.9 +/- 8.9 ml x kg(-1) x min(-1)). These results suggest that short-arm centrifuge-induced artificial gravity with exercise training is effective in maintaining respiratory and cardiovascular responses to upright exercise.     

Changes in leg volume during microgravity simulation.

Little published information exists regarding the magnitude and time course of cephalad fluid shift resulting from microgravity simulations. Six subjects were exposed to 150 min each at horizontal bed rest, 6 degrees head-down tilt, and horizontal water immersion. Fluid shift was estimated by calculating leg volumes from eight serial girth measurements from groin to ankle before, during, and after exposure. Results were compared with data from the first 3 h of spaceflight. By the end of exposure, total leg volume for the six subjects decreased by 2.6 +/- 0.8%, 1.7 +/- 1.2%, and 4.0 +/- 1.6% for horizontal, head-down, and immersion, respectively. Changes had plateaued for horizontal and head-down and had slowed for immersion. Relatively more fluid was lost from the lower leg than the thigh for all three conditions, particularly head-down. During the first 3 h of spaceflight, total leg volume decreased by 8.6%, and relatively more fluid was lost from the thigh than the lower leg. The difference in volume changes in microgravity and simulated microgravity may be caused by the small transverse pressures still present in ground-based simulations and the extremely nonlinear compliance of tissue.     

Bed rest affects ventricular and arterial elastances in monkeys: implications for humans

METHODS: Experimental data were obtained from five chronically instrumented rhesus monkeys exposed to 96 h of 10 degrees head-down bed rest (HDBR) and another 96 h of 80 degrees upright control separated by 9 d of ambulatory recovery in a counter-balanced, crossover experiment design to test the hypotheses that: 1) headward and footward fluid shifts would increase systemic arterial (Eart) and left ventricular end-systolic (Ees) elastances; and 2) changes in Eart and Ees would be related in magnitude and direction. Ees and Eart were calculated from measurements taken during five observation periods for initial 2-h and 4-d exposures to HDBR that produced headward volume shifts, and acute exposure to graded levels of lower body negative pressure (LBNP) designed to produce orthostatic volume shifts. RESULTS: There was no effect of HDBR on Ees and Eart for any observation period (initial 2-h, 4-d, or LBNP). Eart increased in a similar pattern during the 4-d exposure to both control and HDBR. Ees increased with increasing LBNP levels for both control and HDBR while Eart remained unchanged. CONCLUSION: Our data are consistent with the notion that elevated Eart may represent an adaptation to physical inactivity that is associated with cardiovascular deconditioning.