Changes in electrically evoked skeletal muscle contractions during 17-day spaceflight and bed rest
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short duration↗
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Prevention of hypercalciuria and stone-forming propensity during prolonged bedrest by alendronate
The bone loss and hypercalciuria induced by immobilization or the decreased gravitational forces of space are well described. Using a model of bedrest immobilization, the ability of a potent aminobisphosphonate, alendronate, to avert hypercalciuria and stone-forming propensity was tested. Sixteen male subjects participated in a randomized, placebo-controlled trial in which they received either 20 mg of alendronate or placebo 2 weeks prior to and during 3 weeks of strict bedrest. Parameters of bone and calcium metabolism and urinary crystallization of stone-forming salts were measured before and at the end of bedrest. In the placebo group, bedrest increased urinary calcium (209 +/- 47 to 267 +/- 60 mg/day, p < 0.01) and the saturation of calcium phosphate. Before bedrest, the alendronate group had a significantly lower serum calcium (8.8 +/- 0.4 vs. 9.6 +/- 0.5 mg/dl, p < 0.01) and higher serum PTH (62.4 +/- 33.1 vs. 23.1 +/- 7.5 pg/ml, p < 0.01) compared with the placebo group. Moreover, the alendronate group had a lower urinary calcium (75 +/- 41 mg/day) and saturation of calcium oxalate and calcium phosphate. These effects of alendronate were sustained during bedrest. Following bedrest in the alendronate group, urinary calcium rose to 121 +/- 50 mg/day, a value less than that in the placebo group before or during bedrest. Similarly, urinary saturation of calcium oxalate and calcium phosphate rose with bedrest in the alendronate-treated patients but remained lower than values obtained in placebo-treated patients before or during bedrest. Alendronate inhibits bone mineral loss and averts the hypercalciuria and increased propensity for the crystallization of stone-forming calcium salts which occurs during 3 weeks of strict bedrest.
Non-NASA Center↗
Spaceflight and the skeleton: lessons for the earthbound
Loss of bone during extended space flight has long been a concern that could limit the ability of humans to explore the universe. Surprisingly the available data do not support the concept that weightlessness leads inexorably to a depleted skeleton unable to withstand the stress of a return to a 1g environment. Nevertheless, some bone loss does occur especially in those bones most stressed by gravity prior to flight, providing confirmation of the proposal formulated over a century ago by Julius Wolff that mechanical stress determines the form and function of bone. Although the phenomenon of bone loss with skeletal unloading, whether by space flight or immobilization or just taking a load off your feet (literally) is well established, the mechanisms by which bone senses load and adjusts to it are not so clear. What actually is the stimulus and what are the sensors? What are the target cells? How do the sensors communicate the message into the cells, and by what pathways do the cells respond? What is the role of endocrine factors versus paracrine or autocrine factors in mediating or modulating the response? None of these questions has been answered with certainty, but as will become apparent in this review, we have some clues directing us to the answers. Although the focus of this review concerns space flight, it seems highly likely that the mechanisms mediating the transmission of mechanical load to changes in bone formation and resorption apply equally well to all forms of disuse osteoporosis, and are likely to be the same mechanisms affected by other etiologies of osteoporosis.
NASA Discipline Musculoskeletal↗
Nitric oxide in microgravity-induced orthostatic intolerance: relevance to spinal cord injury
Prolonged exposure to microgravity results in cardiovascular deconditioning which is marked by orthostatic intolerance in the returning astronauts and recovering bed-ridden patients. Recent studies conducted in our laboratories at University of California, Irvine have revealed marked elevation of nitric oxide (NO) production in the kidney, heart, brain, and systemic arteries coupled with significant reduction of NO production in the cerebral arteries of microgravity-adapted animals. We have further demonstrated that the observed alteration of NO metabolism is primarily responsible for the associated cardiovascular deconditioning. Recovery from acute spinal cord injury (SCI) is frequently complicated by orthostatic intolerance that is due to the combined effects of the disruption of efferent sympathetic pathway and cardiovascular deconditioning occasioned by prolonged confinement to bed. In this presentation, I will review the nature of altered NO metabolism and its role in the pathogenesis of microgravity-induced cardiovascular deconditioning. The possible relevance of the new findings to orthostatic intolerance in patients with acute SCI and its potential therapeutic implications will be discussed.
Review↗
An overview of the issues: physiological effects of bed rest and restricted physical activity
Reduction of exercise capacity with confinement to bed rest is well recognized. Underlying physiological mechanisms include dramatic reductions in maximal stroke volume, cardiac output, and oxygen uptake. However, bed rest by itself does not appear to contribute to cardiac dysfunction. Increased muscle fatigue is associated with reduced muscle blood flow, red cell volume, capillarization and oxidative enzymes. Loss of muscle mass and bone density may be reflected by reduced muscle strength and higher risk for injury to bones and joints. The resultant deconditioning caused by bed rest can be independent of the primary disease and physically debilitating in patients who attempt to reambulate to normal active living and working. A challenge to clinicians and health care specialists has been the identification of appropriate and effective methods to restore physical capacity of patients during or after restricted physical activity associated with prolonged bed rest. The examination of physiological responses to bed rest deconditioning and exercise training in healthy subjects has provided significant information to develop effective rehabilitation treatments. The successful application of acute exercise to enhance orthostatic stability, daily endurance exercise to maintain aerobic capacity, or specific resistance exercises to maintain musculoskeletal integrity rather than the use of surgical, pharmacological, and other medical treatments for clinical conditions has been enhanced by investigation and understanding of underlying mechanisms that distinguish physical deconditioning from the disease. This symposium presents an overview of cardiovascular and musculoskeletal deconditioning associated with reduced physical work capacity following prolonged bed rest and exercise training regimens that have proven successful in ameliorating or reversing these adverse effects.
NASA Program Space Physiology and Countermeasures↗
Recent bed rest results and countermeasure development at NASA
Bedrest studies of normal subjects provide opportunities to understand physiologic responses to supine posture and inactivity. Furthermore, head-down tilt has been a valuable procedure to investigate adaptation to microgravity and development of countermeasures to maintain the health and well-being of humans during space-flight. Recent bedrest experiments at NASA have ranged in duration from a few hours to 17 weeks. Acute studies of 6 degrees head-down tilt indicate that elevation of capillary blood pressure from 28 to 34 mm Hg and increased capillary perfusion in tissues of the head cause facial and intracranial edema. Intracranial pressure increases from 2 to 17 mm Hg going from upright posture to 6 degrees head-down tilt. Microvessels of the head have a low capacity to constrict and diminish local perfusion. Elevation of blood and tissue fluid pressures/flow in the head may also explain the higher headward bone density associated with long-term head-down tilt. These mechanistic studies of head-down tilt, along with a better understanding of the relative stresses involved with upright posture and lower body negative pressure, have facilitated development of suitable physiologic countermeasures to maintain astronaut health during microgravity. Presently no exercise hardware is available to provide a blood pressure gradient from head to feet in space. However, recent studies in our laboratory suggest that treadmill exercise using a graded lower-body compression suit and 100 mmHg lower body negative pressure provides equivalent or greater physiologic stress than similar upright exercise on Earth. Therefore, exercise within a lower body negative pressure chamber may provide a cost-effective and simple countermeasure to maintain the cardiovascular and neuro-musculoskeletal systems of astronauts during long-duration flight.
manned↗
Use of lower body negative pressure to counter symptoms of orthostatic intolerance in patients, bed rest subjects, and astronauts
This report briefly discusses some aspects of autonomic cardiovascular dysfunction as related to changes in orthostatic function in patients, bed rest subjects, and astronauts. This relationship is described in normal individuals to provide the basis for discussion of parameters that may be altered in patients, bed rest subjects, and astronauts. The relationships between disease states, age, periods of weightlessness during space flight, and autonomic dysfunction, and their contribution to changes in orthostatic tolerance are presented. The physiologic effects of lower body negative pressure are illustrated by presenting data obtained in bed rest subjects and in astronauts. Finally, the usefulness of lower body negative pressure to counter symptoms of orthostatic intolerance in patients, bed rest subjects, and astronauts is discussed.
Review, Tutorial↗
Orthostatic hypotension in patients, bed rest subjects, and astronauts
Orthostatic hypotension after even short space flights has affected a significant number of astronauts. Given the need for astronauts to function at a high level of efficiency during and after their return from space, the application of pharmacologic and other treatments is strongly indicated. This report addresses the clinical problem of orthostatic hypotension and its treatments to ascertain whether pharmacologic or physiologic treatment may be useful in the prevention of orthostatic hypotension associated with space flight. Treatment of orthostatic hypotension in patients now includes increasing intravascular volume with high sodium intake and mineralocorticoids, or increasing vascular resistance through the use of drugs to stimulate alpha or block beta vascular receptors. Earlier treatment used oral sympathomimetic ephedrine hydrochloride alone or with "head-up" bed rest. Then long-acting adrenocortical steroid desoxycorticosterone preparations with high-salt diets were used to expand volume. Fludrocortisone was shown to prevent the orthostatic drop in blood pressure. The combination of the sympathomimetic amine hydroxyamphetamine and a monoamine oxidase inhibitor tranylcypromine has been used, as has indomethacin alone. Davies et al. used mineralocorticoids at low doses concomitantly with alpha-agonists to increase vasoconstrictor action. Schirger et al used tranylcypromine and methylphenidate with or without a Jobst elastic leotard garment or the alpha-adrenergic agonist midodrine (which stimulates both arterial and venous systems without direct central nervous system or cardiac effects). Vernikos et al established that the combination of fludrocortisone, dextroamphetamine, and atropine exhibited a beneficial effect on orthostatic hypotension induced by 7-day 6 degrees head-down bed rest (a model used to simulate the weightlessness of space flight). Thus, there are numerous drugs that, in combination with mechanical techniques, including lower body negative pressure to elevate transmural pressure, could be studied to treat orthostatic hypotension after space flight.
Review↗
Intensive exercise training suppresses testosterone during bed rest
Spaceflight and prolonged bed rest (BR) alter plasma hormone levels inconsistently. This may be due, in part, to prescription of heavy exercise as a countermeasure for ameliorating the adverse effects of disuse. The initial project was to assess exercise programs to maintain aerobic performance and leg strength during BR. The present study evaluates the effect of BR and the performance of the prescribed exercise countermeasures on plasma steroid levels. In a 30-day BR study of male subjects, the efficacy of isotonic (ITE, n = 7) or isokinetic exercise (IKE, n = 7) training was evaluated in contrast to no exercise (n = 5). These exercise countermeasures protected aerobic performance and leg strength successfully. BR alone (no-exercise group) did not change steroidogenesis, as assessed by the plasma concentrations of cortisol, progesterone, aldosterone, and free (FT) and total testosterone (TT). In the exercise groups, both FT and TT were decreased (P < 0.05): FT during IKE from 24 +/- 1.7 to 18 +/- 2.0 pg/ml and during ITE from 21 +/- 1.5 to 18 +/- 1 pg/ml, and TT during IKE from 748 +/- 68 to 534 +/- 46 ng/dl and during ITE from 565 +/- 36 to 496 +/- 38 ng/dl. The effect of intensive exercise countermeasures on plasma testosterone was not associated with indexes of overtraining. The reduction in plasma testosterone associated with both the IKE and ITE countermeasures during BR supports our hypothesis that intensive exercise countermeasures may, in part, contribute to changes in plasma steroid concentrations during spaceflight.
Clinical Trial↗
Effects of three day bed-rest on circulatory, metabolic and hormonal responses to oral glucose load in endurance trained athletes and untrained subjects
Endurance trained long distance runners and untrained individuals underwent three days of bed rest and oral glucose loading. Before and after bed rest, individuals were given glucose tolerance tests, and their heart rates, blood pressure, blood glucose levels, insulin levels, and catecholamine interactions were measured. Results indicated that glucose tolerance is more affected by bed rest-induced deconditioning in untrained individuals than in trained individuals.
NASA Discipline Regulatory Physiology↗
Effect of three day bed-rest on circulatory and hormonal responses to active orthostatic test in endurance trained athletes and untrained subjects
Circulatory and hormonal parameters were measured in endurance-trained athletes and control subjects during orthostatic tolerance tests conducted prior to and after three days of bed rest. Heart rate and blood pressure changes due to bed rest appeared to be the same in both groups. Hormonal changes, however, were different between the two groups, with the athletes having decreased sympathoadrenal activity and increased plasma renin activity. Untrained subjects had changes in cortisol secretion only.
NASA Center ARC↗
Use of bed rest and head-down tilt to simulate spaceflight-induce immune system changes
Bed rest, both with and without head-down tilt, has been extensively used as an earth-bound analog to study physiologic effects mimicking those occurring in weightlessness during spaceflight. We have been able to show in six subjects that 4 weeks of head-down tilt bed rest induces a significant decrease in interleukin-2 secretion by PHA-stimulated T lymphocytes. Another study, lasting 113 days, with two subjects showed a decreased interleukin-2 receptor expression in PHA-stimulated peripheral blood mononuclear cells but a decreased interleukin-2 production in one subject only. Under the same conditions, interleukin-1 production was largely increased in both subjects. Several other immune parameters were also analyzed. Increased interleukin-1 production could contribute to bone mineral loss encountered during bed rest and decreased interleukin-2 secretion could play a role in the appearance of infectious diseases often observed during bed red.
NASA Discipline Neuroscience↗
Cardiovascular consequences of bed rest: effect on maximal oxygen uptake
Maximal oxygen uptake (VO2max) is reduced in healthy individuals confined to bed rest, suggesting it is independent of any disease state. The magnitude of reduction in VO2max is dependent on duration of bed rest and the initial level of aerobic fitness (VO2max), but it appears to be independent of age or gender. Bed rest induces an elevated maximal heart rate which, in turn, is associated with decreased cardiac vagal tone, increased sympathetic catecholamine secretion, and greater cardiac beta-receptor sensitivity. Despite the elevation in heart rate, VO2max is reduced primarily from decreased maximal stroke volume and cardiac output. An elevated ejection fraction during exercise following bed rest suggests that the lower stroke volume is not caused by ventricular dysfunction but is primarily the result of decreased venous return associated with lower circulating blood volume, reduced central venous pressure, and higher venous compliance in the lower extremities. VO2max, stroke volume, and cardiac output are further compromised by exercise in the upright posture. The contribution of hypovolemia to reduced cardiac output during exercise following bed rest is supported by the close relationship between the relative magnitude (% delta) and time course of change in blood volume and VO2max during bed rest, and also by the fact that retention of plasma volume is associated with maintenance of VO2max after bed rest. Arteriovenous oxygen difference during maximal exercise is not altered by bed rest, suggesting that peripheral mechanisms may not contribute significantly to the decreased VO2max. However reduction in baseline and maximal muscle blood flow, red blood cell volume, and capillarization in working muscles represent peripheral mechanisms that may contribute to limited oxygen delivery and, subsequently, lowered VO2max. Thus, alterations in cardiac and vascular functions induced by prolonged confinement to bed rest contribute to diminution of maximal oxygen uptake and reserve capacity to perform physical work.
Non-NASA Center↗
Effect of leg exercise training on vascular volumes during 30 days of 6 degrees head-down bed rest
Plasma and red cell volumes, body density, and water balance were measured in 19 men (32-42 yr) confined to bed rest (BR). One group (n = 5) had no exercise training (NOE), another near-maximal variable-intensity isotonic exercise for 60 min/day (ITE; n = 7), and the third near-maximal intermittent isokinetic exercise for 60 min/day (IKE; n = 7). Caloric intake was 2,678-2,840 kcal/day; mean body weight (n = 19) decreased by 0.58 +/- 0.35 (SE) kg during BR due to a negative fluid balance (diuresis) on day 1. Mean energy costs for the NOE, and IKE, and ITE regimens were 83 (3.6 +/- 0.2 ml O2.min-1.kg-1), 214 (8.9 +/- 0.5 ml.min-1.kg-1), and 446 kcal/h (18.8 +/- 1.6 ml.min-1.kg-1), respectively. Body densities within groups and mean urine volumes (1,752-1,846 ml/day) between groups were unchanged during BR. Resting changes in plasma volume (ml/kg) after BR were -1.5 +/- 2.3% (NS) in ITE, -14.7 +/- 2.8% (P less than 0.05) in NOE, and -16.8 +/- 2.9% (P less than 0.05) in IKE, and mean water balances during BR were +295, -106, and +169 ml/24 h, respectively. Changes in red cell volume followed changes in plasma volume. The significant chronic decreases in plasma volume in the IKE and NOE groups and its maintenance in the ITE group could not be accounted for by water balance or by responses of the plasma osmotic, protein, vasopressin, or aldosterone concentrations or plasma renin activity. There was close coupling between resting plasma volume and plasma protein and osmotic content.(ABSTRACT TRUNCATED AT 250 WORDS).
NASA Discipline Regulatory Physiology↗
The ratio of animal protein intake to potassium intake is a predictor of bone resorption in space flight analogues and in ambulatory subjects
BACKGROUND: Bone loss is a critical concern for space travelers, and a dietary countermeasure would be of great benefit. Dietary protein and potassium-associated bicarbonate precursors may have opposing effects on the acid-base balance in the body and therefore on bone loss. OBJECTIVE: In 2 studies, we examined the ability of dietary protein and potassium to predict markers of bone metabolism. DESIGN: In the first study, 8 pairs of male identical twins were assigned to 1 of 2 groups: bed rest (sedentary, or SED, group) or bed rest with supine treadmill exercise in a lower-body negative pressure chamber (EX group). In a second study, groups of 4 subjects lived in a closed chamber for 60 or 91 d, and dietary data were collected for two or three 5-d sessions. Urinary calcium, N-telopeptide, and pyridinium cross-links were measured before bed rest; on bed rest days 5-6, 12-13, 19-20, and 26-27; and daily during the chamber studies. Data were analyzed by Pearson's correlation (P < 0.05). RESULTS: The ratio of animal protein intake to potassium intake was significantly correlated with N-telopeptide in the SED group during bed rest weeks 3 and 4 (r = 0.77 and 0.80) and during the 91-d chamber study (r = 0.75). The ratio of animal protein intake to potassium intake was positively correlated with pyridinium cross-links before bed rest in the EX group (r = 0.83), in the EX group during bed rest week 1 (r = 0.84), and in the SED group during bed rest week 2 (r = 0.72) but not during either chamber study. In both studies, these relations were not significant with the ratio of vegetable protein intake to potassium intake. CONCLUSIONS: The ratio of animal protein intake to potassium intake may affect bone in ambulatory and bed-rest subjects. Changing this ratio may help to prevent bone loss on Earth and during space flight.
Clinical Trial↗
Measurement of nutritional status in simulated microgravity by bioelectrical impedance spectroscopy
The potential of bioelectrical impedance spectroscopy (BIS) for assessing nutritional status in spaceflight was tested in two head-down-tilt bed-rest studies. BIS-predicted extracellular water (ECW), intracellular water (ICW), and total body water (TBW) measured using knee-elbow electrode placement were compared with deuterium and bromide dilution (DIL) volumes in healthy, 19- to 45-yr-old subjects. BIS was accurate during 44 h of head-down tilt with mean differences (BIS - DIL) of 0-0.1 kg for ECW, 0.3-0.5 for ICW, and 0.4-0.6 kg for TBW (n = 28). At 44 h, BIS followed the within-individual change in body water compartments with a relative prediction error (standard error of the estimate/baseline volume) of 2.0-3.6% of water space. In the second study, BIS did not detect an acute decrease (-1.41 +/- 0.91 kg) in ICW secondary to 48 h of a protein-free, 800 kcal/day diet (n = 18). BIS's insensitivity to ICW losses may be because they were predominantly (65%) localized to the trunk and/or because there was a general failure of BIS to measure ICW independently of ECW and TBW. BIS may have potential for measuring nutritional status during spaceflight, but its limitations in precision and insensitivity to acute ICW changes warrant further validation studies.
Non-NASA Center↗
Attenuation of the protein wasting associated with bed rest by branched-chain amino acids
Bed rest is generally accepted as being an appropriate ground-based model for human spaceflight. The objectives of this study were to test the hypothesis that increasing the amount of branched-chain amino acids (BCAAs) in the diet could attenuate the protein loss associated with bed rest. Nineteen healthy subjects were randomized into two groups according to diet. During the 6 d of bed rest, the diets were supplemented with either 30 mmol/d each of three non-essential amino acids, glycine, serine, and alanine (control group), or with 30 mmol/d each of the BCAAs, leucine, isoleucine, and valine (BCAA group). Nutrition was supplied as a commercially available defined formula diet at a rate of 1.3 x REE. Nitrogen (N) balance and urinary 3-MeH excretion were determined for the 6 d. In our results, the urine-based estimate of N balance was 22.2 +/- 14.4 (n = 9) mg N.kg-1.d-1 and 60.5 +/- 10.1 mg (n = 8) N.kg-1.d-1 for the control and BCAA-supplemented groups, respectively (P < 0.05). Urinary 3-MeH excretion was unchanged in both groups with bed rest. We conclude that BCAA supplementation attenuates the N loss during short-term bed rest.
Randomized Controlled Trial↗
Bed rest suppresses bioassayable growth hormone release in response to muscle activity
Hormonal responses to muscle activity were studied in eight men before (-13 or -12 and -8 or -7 days), during (2 or 3, 8 or 9, and 13 or 14 days) and after (+2 or +3 and +10 or +11 days) 17 days of bed rest. Muscle activity consisted of a series of unilateral isometric plantar flexions, including 4 maximal voluntary contractions (MVCs), 48 contractions at 30% MVC, and 12 contractions at 80% MVC, all performed at a 4:1-s work-to-rest ratio. Blood was collected before and immediately after muscle activity to measure plasma growth hormone by radioimmunoassay (IGH) and by bioassay (BGH) of tibia epiphyseal cartilage growth in hypophysectomized rats. Plasma IGH was unchanged by muscle activity before, during, or after bed rest. Before bed rest, muscle activity increased (P < 0.05) BGH by 66% at -13 or -12 days (2,146 +/- 192 to 3,565 +/- 197 microg/l) and by 92% at -8 or -7 days (2,162 +/- 159 to 4,161 +/- 204 microg/l). After 2 or 3 days of bed rest, there was no response of BGH to the muscle activity, a pattern that persisted through 8 or 9 days of bed rest. However, after 13 or 14 days of bed rest, plasma concentration of BGH was significantly lower after than before muscle activity (2,594 +/- 211 to 2,085 +/- 109 microg/l). After completion of bed rest, muscle activity increased BGH by 31% at 2 or 3 days (1,807 +/- 117 to 2,379 +/- 473 microg/l; P < 0.05), and by 10 or 11 days the BGH response was similar to that before bed rest (1,881 +/- 75 to 4,160 +/- 315 microg/l; P < 0.05). These data demonstrate that the ambulatory state of an individual can have a major impact on the release of BGH, but not IGH, in response to a single bout of muscle activity.
Non-NASA Center↗