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At least 199 records · Page 11

Early Fluid and Protein Shifts in Men During Water Immersion

High precision blood and plasma densitometry was used to measure transvascular fluid shifts during water immersion to the neck. Six men (28-49 years) undertook 30 min of standing immersion in water at 35.0 +/- 0.2 C; immersion was preceded by 30 min control standing in air at 28 +/- 1 C. Blood was sampled from an antecubital catheter for determination of Blood Density (BD), Plasma Density (PD), Haematocrit (Ht), total Plasma Protein Concentration (PPC), and Plasma Albumin Concentration (PAC). Compared to control, significant decreases (p less than 0.01) in all these measures were observed after 20 min immersion. At 30 min, plasma volume had increased by 11.0 +/- 2.8%; the average density of the fluid shifted from extravascular fluid into the vascular compartment was 1006.3 g/l; albumin moved with the fluid and its albumin concentration was about one-third of the plasma protein concentration during early immersion. These calculations are based on the assumption that the F-cell ratio remained unchanged. No changes in erythrocyte water content during immersion were found. Thus, immersion-induced haemodilution is probably accompanied by protein (mainly albumin) augmentation which accompanies the intra-vascular fluid shift.

Hinghofer-Szalkay, H.↗

Marked Exacerbation of Orthostatic Intolerance After Long vs. Short-Duration Spaceflight in Veteran Astronauts

The incidence of postflight orthostatic intolerance following short-duration spaceflight is about 20%. However, the incidence following long-duration spaceflight is unknown. We performed tilt tests on six astronauts before and after their long-duration (129 - 190 days) spaceflights and compared these data to those obtained during stand tests before and after their previous short-duration missions and also to tilt test data from 20 different short-duration (8 - 16 days) flight astronauts. Five of these six became presyncopal during tilt testing after long-duration flights: only one had become presyncopal during stand testing after short-duration flights. Five of the twenty astronauts who flew on other short-duration flights, became presyncopal during upright tilt on landing day. Long-duration presyncopal subjects had lower stroke volumes, lower cardiac outputs and higher peripheral vascular resistance than short-duration presyncopal subjects, but their heart rate responses were not different. One subject had subnormal norepinephrine release with upright posture after a long but not short flight. Plasma volume losses were not greater after long flights. Long-duration spaceflight markedly increases orthostatic intolerance, probably related to altered autonomic function.

Fritsch-Yelle, Janice M.↗

Exercise Versus +Gz Acceleration Training

Decreased working capacity and "orthostatic" intolerance are two major problems for astronauts during and after landing from spaceflight in a return vehicle. The purpose was to test the hypotheses that (1) supine-passive-acceleration training, supine-interval-exercise plus acceleration training, and supine exercise plus acceleration training will improve orthostatic tolerance (OT) in ambulatory men; and that (2) addition of aerobic exercise conditioning will not influence this enhanced OT from that of passive-acceleration training. Seven untrained men (24-38 yr) underwent 3 training regimens (30 min/d x 5d/wk x 3wk on the human-powered centrifuge - HPC): (a) Passive acceleration (alternating +1.0 Gz to 50% Gzmax); (b) Exercise acceleration (alternating 40% - 90% V02max leg cycle exercise plus 50% of HPCmax acceleration); and (c) Combined intermittent exercise-acceleration at 40% to 90% HPCmax. Maximal supine exercise workloads increased (P < 0.05) by 8.3% with Passive, by 12.6% with Exercise, and by 15.4% with Combined; but maximal V02 and HR were unchanged in all groups. Maximal endurance (time to cessation) was unchanged with Passive, but increased (P < 0.05) with Exercise and Combined. Resting pre-tilt HR was elevated by 12.9% (P < 0.05) only after Passive training, suggesting that exercise training attenuated this HR response. All resting pre-tilt blood pressures (SBP, DBP, MAP) were not different pre- vs. post-training. Post-training tilt-tolerance time and HR were increased (P < 0.05) only with Passive training by 37.8% and by 29.1%, respectively. Thus, addition of exercise training attenuated the increased Passive tilt tolerance. Resting (pre-tilt) and post-tilt cardiac R-R interval, stroke volume, end-diastolic volume, and cardiac output were all uniformly reduced (P < 0.05) while peripheral resistance was uniformly increased (P < 0.05) pre-and post-training for the three regimens indicating no effect of any training regimen on those cardiovascular variables. Plasma volume (% delta) was uniformly decreased by 8% to 14% (P < 0.05) at tilt-tolerance pre- vs. post-training for all regimens indicating no effect of these training regimens on the level of vascular fluid shifts.

Greenleaf, John E.↗

Hypovolemia Induced Orthostatic Hypotension in Presyncopal Astronauts and Normal Subjects Relates to Hypo-Sympathetic Responsiveness

Circulating blood volume is reduced during spaceflight, leaving astronauts hemodynamically compromised after landing. Because of this hypovolemia, crew members are able to withstand a postflight 10 minute upright tilt test only if they are able to mount a hyper-sympathetic response. Previous work from this laboratory has shown that about 30% of astronauts, primarily female, have postflight sympathetic responses to tilt that are equal to or less than their preflight responses and thus, they become presyncopal. Part of the mission of the cardiovascular lab at the Johnson Space Center is to identify susceptible crewmembers before flight so that individualized countermeasures can be prescribed. The goal of this study was to develop a ground based model of hypovolemia that could be used for this purpose We tested the hypothesis that hypovolemia alone, in the absence of spaceflight, would reproduce the landing day rate of presyncope during upright tilt in normal volunteers. Further, we hypothesized that, during hypovolemia, subjects who had sympathetic responses that were equal to or less than their normovolemic responses would become presyncopal during upright tilt tests. We studied 20 subjects, 13 male and 7 female, on two separate occasions: during normovolemia and hypovolemia. We induced hypovolemia with intravenous furosemide 40 hours prior to the experiment day, followed by a 10MEq Na diet. On the normovolemia and hypovolemia test days, plasma volume, tilt tolerance and supine and standing arterial pressure, heart rate and plasma norepinephrine levels were measured. A two factor, repeated measures analysis of variance was performed to examine the differences between group (presyncopal vs. non-presyncopal) and day (normovolemia vs. hypovolemia) effects. There were no differences in baseline arterial pressure between normovolemia and hypovolemia or between presyncopal and non-presyncopal groups, but heart rates were higher with hypovolemia in both groups (presyncopal: 70 5 bpm vs. 63 3 bpm, P = 0.003, non-presyncopal: 59 2 bpm vs. 52 2 bpm, P = 0.003). Similar to patterns reported after flight, non-presyncopal subjects had greater norepinephrine responses to tilt during hypovolemia compared to normovolemia (580 79 vs. 298 37 pg/ml, P < 0.05), but presyncopal subjects did not (180 44 vs. 145 32 pg/ml, P = NS). This new model has the potential to accelerate the development of countermeasures and save flight resources. It can be used to identify astronauts who will become presyncopal on landing day, so that prospective, individualized countermeasures can be developed. In addition, it can also be used to screen candidate countermeasures prior to requests for bed rest or inflight resources.

Meck, Janice V.↗

Computer simulation of the effect of dDAVP with saline loading on fluid balance after 24-hour head-down tilt

Fluid loading (FL) before Shuttle reentry is a countermeasure currently in use by NASA to improve the orthostatic tolerance of astronauts during reentry and postflight. The fluid load consists of water and salt tablets equivalent to 32 oz (946 ml) of isotonic saline. However, the effectiveness of this countermeasure has been observed to decrease with the duration of spaceflight. The countermeasure's effectiveness may be improved by enhancing fluid retention using analogs of vasopressin such as lypressin (LVP) and desmopressin (dDAVP). In a computer simulation study reported previously, we attempted to assess the improvement in fluid retention obtained by the use of LVP administered before FL. The present study is concerned with the use of dDAVP. In a recent 24-hour, 6 degree head-down tilt (HDT) study involving seven men, dDAVP was found to improve orthostatic tolerance as assessed by both lower body negative pressure (LBNP) and stand tests. The treatment restored Luft's cumulative stress index (cumulative product of magnitude and duration of LBNP) to nearly pre-bedrest level. The heart rate was lower and stroke volume was marginally higher at the same LBNP levels with administration of dDAVP compared to placebo. Lower heart rates were also observed with dDAVP during stand test, despite the lower level of cardiovascular stress. These improvements were seen with only a small but significant increase in plasma volume of approximately 3 percent. This paper presents a computer simulation analysis of some of the results of this HDT study.

NASA Discipline Cardiopulmonary↗

Deterioration of left ventricular chamber performance after bed rest : "cardiovascular deconditioning" or hypovolemia?

BACKGROUND: Orthostatic intolerance after bed rest is characterized by hypovolemia and an excessive reduction in stroke volume (SV) in the upright position. We studied whether the reduction in SV is due to a specific adaptation of the heart to head-down tilt bed rest (HDTBR) or acute hypovolemia alone. METHODS AND RESULTS: We constructed left ventricular (LV) pressure-volume curves from pulmonary capillary wedge pressure and LV end-diastolic volume and Starling curves from pulmonary capillary wedge pressure and SV during lower body negative pressure and saline loading in 7 men (25+/-2 years) before and after 2 weeks of -6 degrees HDTBR and after the acute administration of intravenous furosemide. Both HDTBR and hypovolemia led to a similar reduction in plasma volume. However, baseline LV end-diastolic volume decreased by 20+/-4% after HDTBR and by 7+/-2% after hypovolemia (interaction P<0.001). Moreover, SV was reduced more and the Starling curve was steeper during orthostatic stress after HDTBR than after hypovolemia. The pressure-volume curve showed a leftward shift and the equilibrium volume of the left ventricle was decreased after HDTBR; however, after hypovolemia alone, the curve was identical, with no change in equilibrium volume. Lower body negative pressure tolerance was reduced after both conditions; it decreased by 27+/-7% (P<0.05) after HDTBR and by 18+/-8% (P<0.05) after hypovolemia. CONCLUSIONS: Chronic HDTBR leads to ventricular remodeling, which is not seen with equivalent degrees of acute hypovolemia. This remodeling leads to a greater decrease in SV during orthostatic stress after bed rest than hypovolemia alone, potentially contributing to orthostatic intolerance.

NASA Discipline Cardiopulmonary↗

Deconditioning and Reconditioning: Humans in Stressful Environments

Deconditioning is an integrated physiological response of the body to a reduction in metabolic rate; that is, to a reduction in energy use or in exercise level. While it may involve assumption of a horizontal body position, it certainly perturbs bodily homeostasis - at least temporarily. The reduction in physical activity that causes deconditioning is often associated with an increase in the time spent, for whatever reason, in a sitting or horizontal position. As a result, orthostatic factors may also contribute to the deconditioning mechanism. The word decondition may be defined as "1: to cause extinction of (a conditioned response) 2: to cause to lose physical fitness". This definition implies that psychological/emotional factors may accompany physical deconditioning, and it is this interpretation of the word that is used throughout this volume. It is apparent that deconditioning plays a major role in the mechanism of the general adaptive (homeostatic) response that is initiated by exposure to prolonged bed rest (BR). And the total homeostatic response to BR involves more than deconditioning per se. For example, it has been shown that the restoration of plasma volume and maximal work capacity after 4 weeks of BR deconditioning left other bodily functions (submaximal exercise oxygen uptake and cardiac output, leg proprioception and posterior leg muscle thickness and volume, head-up tilt tolerance, and sleep quality) functioning at decreased levels. The precise effect of deconditioning on BR homeostasis is difficult to determine, because the fundamental interactive neuro-endocrine-immune control networks that facilitate conditioning and deconditioning also act to maintain basic wholebody homeostasis. For example, is the mechanism of BR-induced deconditioning independent of the mechanism that provokes concomitant orthostatic intolerance; that is, fainting? Assumption of the recumbent body position for prolonged periods of time, results in a new adaptive-homeostatic state. This state occurs in response to the mutually interactive effects of the change in bodily position (hydrostatic pressure), to the virtual elimination of longitudinal pressure on the bones, to the increased confinement with possible reduction in total daily energy (exercise) expenditure, to the reorientation of stimuli within the vestibular organs, and (often) to altered socio-psychological conditions. The exercise-training (reconditioning) syndrome affects total body homeostasis by facilitating increases in work capacity and endurance, whereas deconditioning decreases physical performance. There are many interrelated factors that influence the control parameters that seek to maintain the adaptive conditioning-deconditioning syndrome. These control parameters can be better elucidated by subjecting otherwise healthy ambulatory people to various stresses, such as exercise training and prolonged spaceflight, bed rest, water immersion, hyperbaria, and isolation and confinement. Changes in control parameters will be manifested in muscle function, orthostatic tolerance, cardiorespiratory responses, musculo-skeletal systems, free-radical processes, and body thermoregulation with overarching effects on the subjects' psycho-sociological states. A discussion of these factors and the control parameters constitutes the substance of this volume. Special emphasis is placed on delineating practical applications of the findings that will be of special interest to physicians, nurses, and other health-care workers.

Greenleaf, John E.↗

Influence of Gravity on Blood Volume and Flow Distribution

In our previous experiments during NASA Shuttle flights SLS 1 and 2 (9-15 days) and EUROMIR flights (30-90 days) we observed that pulmonary blood flow (cardiac output) was elevated initially, and surprisingly remained elevated for the duration of the flights. Stroke volume increased initially and then decreased, but was still above 1 Gz values. As venous return was constant, the changes in SV were secondary to modulation of heart rate. Mean blood pressure was at or slightly below 1 Gz levels in space, indicating a decrease in total peripheral resistance. It has been suggested that plasma volume is reduced in space, however cardiac output/venous return do not return to 1 Gz levels over the duration of flight. In spite of the increased cardiac output, central venous pressure was not elevated in space. These data suggest that there is a change in the basic relationship between cardiac output and central venous pressure, a persistent "hyperperfusion" and a re-distribution of blood flow and volume during space flight. Increased pulmonary blood flow has been reported to increase diffusing capacity in space, presumably due to the improved homogeneity of ventilation and perfusion. Other studies have suggested that ventilation may be independent of gravity, and perfusion may not be gravity- dependent. No data for the distribution of pulmonary blood volume were available for flight or simulated microgravity. Recent studies have suggested that the pulmonary vascular tree is influenced by sympathetic tone in a manner similar to that of the systemic system. This implies that the pulmonary circulation is dilated during microgravity and that the distribution of blood flow and volume may be influenced more by vascular control than by gravity. The cerebral circulation is influenced by sympathetic tone similarly to that of the systemic and pulmonary circulations; however its effects are modulated by cerebral autoregulation. Thus it is difficult to predict if cerebral perfusion is increased and if there is edema in space. Anecdotal evidence suggests there may be cerebral edema early in flight. Cerebral artery velocity has been shown to be elevated in simulated microgravity. The elevated cerebral artery velocity during simulated microgravity may reflect vasoconstriction of the arteries and not increased cerebral blood flow. The purpose of our investigations was to evaluate the effects of alterations in simulated gravity (+/-), resulting in changes in cardiac output (+/-), and on the blood flow and volume distribution in the lung and brain of human subjects. The first hypothesis of these studies was that blood flow and volume would be affected by gravity, but their distribution in the lung would be independent of gravity and due to vasoactivity changing vascular resistance in lung vessels. The vasodilitation of the lung vasculature (lower resistance) along with increased "compliance" of the heart could account for the absence of increased central venous pressure in microgravity. Secondly, we postulate that cerebral blood velocity is increased in microgravity due to large artery vasoconstriction, but that cerebral blood flow would be reduced due to autoregulation.

Pendergast, D.↗

Performance characteristics of a microwave plasma disk ion source

The development, design, and preliminary performance characteristics of a microwave plasma disk ion source are presented. Several important design concepts indigenous to microwave plasmas have been utilized in the development of this ion source: generation of a resonantly sustained microwave discharge inside a microwave/plasma coupler, probe and length tuning of the microwave/plasma coupler, and minimization of plasma volume. The experimental results for a 2.45 GHz, eight cm ion source excited in the TE(211) and TM(011) modes are described. Results are presented for electromagnetic mode excitation, electron density, coupling efficiency and loaded cavity Q, and I-V characteristics and efficiencies. It is preliminarily shown that a microwave disk-like plasma can be sustained adjacent to the grids with either TE or TM cavity modes at pressures below 2 x 10 to the -4th torr. Over 80% of the power absorbed in the cavity is coupled into the plasma.

Asmussen, J.↗

Carotid-cardiac baroreflex: Relation with orthostatic hypotension following simulated microgravity and implications for development of countermeasures

In a series of studies, we have examined the effects of exposure to simulated microgravity, varying states of vascular volume, and acute exercise on the function of the carotid-cardiac baroreflex in man. In the first study, exposure to simulated microgravity (6 degree headdown bedrest) reduced the sensitivity and buffer capacity of the vagal baroreceptor-cardiac reflex mechanisms and this impaired baroreflex function was associated with orthostatic hypotension. Since the reduction in plasma volume during BR was not correlated with impaired baroreflex function, a second study was conducted which demonstrated that the carotid-cardiac baroreflex response was not affected by either acute hypovolemia or hypervolemia. These results suggest that acute fluid replacement prior to reentry may not reverse impaired baroreflex function associated with postflight hypotension. In a third study, we demonstrated that one bout of maximal exercise increased baroreflex sensitivity and buffer capacity through 24 h post-exercise. These baroreflex changes were opposite to those observed following BR. Taken together, these data suggest that the contributions of reduced blood volume and impaired carotid-cardiac baroreflex function to orthostatic hypotension following exposure to microgravity are probably separate and additive; maximal exercise in addition to fluid replacement may provide an acute effective countermeasure against postflight hypotension.

Convertino, Victor A.↗

Evidence for central venous pressure resetting during initial exposure to microgravity

We measured central venous pressure (CVP); plasma volume (PV); urine volume rate (UVR); renal excretion of sodium (UNa); and renal clearances of creatinine, sodium, and osmolality before and after acute volume infusion to test the hypothesis that exposure to microgravity causes resetting of the CVP operating point. Six rhesus monkeys underwent two experimental conditions in a crossover counterbalance design: 1) continuous exposure to 10 degrees head-down tilt (HDT) and 2) a control, defined as 16 h/day of 80 degrees head-up tilt and 8 h prone. After 48 h of exposure to either test condition, a 120-min course of continuous infusion of isotonic saline (0.4 ml. kg(-1). min(-1) iv) was administered. Baseline CVP was lower (P = 0.011) in HDT (2.3 +/- 0.3 mmHg) compared with the control (4.5 +/- 1.4 mmHg) condition. After 2 h of saline infusion, CVP was elevated (P = 0.002) to a similar magnitude (P = 0.485) in HDT (DeltaCVP = 2.7 +/- 0.8 mmHg) and control (DeltaCVP = 2.3 +/- 0.8 mmHg) conditions and returned to preinfusion levels 18 h postinfusion in both treatments. PV followed the same pattern as CVP. The response relationships between CVP and UVR and between CVP and UNa shifted to the left with HDT. The restoration of CVP and PV to lower preinfusion levels after volume loading in HDT compared with control supports the notion that lower CVP during HDT may reflect a new operating point about which vascular volume is regulated. These results may explain the ineffective fluid intake procedures currently employed to treat patients and astronauts.

NASA Discipline Cardiopulmonary↗

Effect of simulated weightlessness on exercise-induced anaerobic threshold

The effect of simulated weightlessness, induced by ten days of continuous bedrest (BR) in the -6 deg head-down position, on the exercise-induced anaerobic threshold (AT) was determined by comparing specific ventilatory and gas-exchange measurements during an incremental ergometer test performed before and after BR. The primary index for determining the exercise-induced AT values of each subject was visual identification of the workrate or oxygen uptake (VO2) at which the ratio of the expired minute ventilation volume (VE) to VO2 exhibited a systematic increase without a concomitant increase in the VE/VCO2 value. Following BR, the mean VO2max of the subjects decreased by 7.0 percent, and the AT decreased from a mean of 1.26 L/min VO2 before BR to 0.95 L/min VO2 after BR. The decrease in AT was manifested by a decrease in both absolute and relative workrates. The change in AT correlated significantly with the change in plasma volume but not with the change in VO2max. The results suggest that the reduction in AT cannot be completely explained by the reduction in VO2, and that the AT decrease is associated with the reduction in intravascular fluid volume.

Convertino, V. A.↗

Role of thermal and exercise factors in the mechanism of hypervolemia

The present study was undertaken to determine whether the chronic increase in plasma volume, resulting from heat exposure and exercise training, was due only to elevated rectal temperature or whether there were additional nonthermal factors related to the exercise. The study was conducted on eight volunteer, healthy, moderately trained male college subjects (18-26 yr). Exercise-induced hypervolemia was associated with thermal factor(s) that contributed 40% and nonthermal factors that accounted for the remaining 60%. In addition, some nonthermal, exercise-induced factors were twofold increases in plasma osmotic and vasopressin levels during exercise, and a fivefold increase in resting plasma protein content.

Convertino, V. A.↗

Adaptation of Baroreflexes and Orthostatic Hypotension

The footward shift of blood volume and compensatory autonomic reflex responses initiated during the assumption of the upright posture in terrestrial gravity is a common feature in humans. When regular exposure to upright posture is removed, the headward redistribution of blood induces numerous physiological adaptations which compromise this normal response and the development of low blood pressure upon standing (orthostatic hypotension) can ensue. Such microgravity conditions can be produced by prolonged exposure to spaceflight or prolonged bed rest. Since the reduction of blood and plasma volume during exposure to microgravity has been associated with orthostatic instability following spaceflight and bed rest, it has been a reasonable assumption that hypovolemia may be a primary contributing factor to the development of orthostatic hypotension. This view was supported by the observation that the attempt to restore vascular volume in astronauts by drinking saline solutions just prior to re-entry had proven effective in reducing orthostatic instability after spaceflights of short duration. However, as the duration of spaceflight lengthens, orthostatic instability persists despite fluid loading procedures, suggesting that mechanisms other than hypovolemia may contribute to orthostatic hypotension following prolonged exposure to microgravity conditions. Recent evidence has been generated from spaceflight and groundbase experiments that supports the notion that changes in autonomic baroreflexes that control cardiac and vascular responses during orthostatic challenges may be affected by longer periods of microgravity exposure and can contribute to postflight orthostatic instability.

Convertino, Victor A.↗

Hemodynamic and ADH responses to central blood volume shifts in cardiac-denervated humans

Hemodynamic responses and antidiuretic hormone (ADH) were measured during body position changes designed to induce blood volume shifts in ten cardiac transplant recipients to assess the contribution of cardiac and vascular volume receptors in the control of ADH secretion. Each subject underwent 15 min of a control period in the seated posture, then assumed a lying posture for 30 min at 6 deg head down tilt (HDT) followed by 20 min of seated recovery. Venous blood samples and cardiac dimensions (echocardiography) were taken at 0 and 15 min before HDT, 5, 15, and 30 min of HDT, and 5, 15, and 30 min of seated recovery. Blood samples were analyzed for hematocrit, plasma osmolality, plasma renin activity (PRA), and ADH. Resting plasma volume (PV) was measured by Evans blue dye and percent changes in PV during posture changes were calculated from changes in hematocrit. Heart rate (HR) and blood pressure (BP) were recorded every 2 min. Results indicate that cardiac volume receptors are not the only mechanism for the control of ADH release during acute blood volume shifts in man.

Convertino, V. A.↗

Blood and urine responses to ingesting fluids of various salt and glucose concentrations

To compensate for the reduced blood and fluid volumes that develop during weightlessness, the Space Shuttle crewmembers consume salt tablets and water equivalent to 1 l of normal saline, about 2 hrs before landing. This paper compares the effects on blood, urine, and cardiovascular variables of the ingestion of 1 l of normal (0.9 percent) saline with the effects of distilled water, 1 percent glucose, 0.74 percent saline with 1 percent glucose, 0.9 percent saline with 1 percent glucose, and 1.07 percent saline. It was found that the expansion of plasma volume and the concentration of urine were greater 4 hrs after ingestion of 1.07 percent saline solution than after ingestion of normal saline and that the solutions containig glucose did not enhance any variables as compared with normal saline.

Frey, Mary A.↗

Effect of hypovolemia, infusion, and oral rehydration on plasma electrolytes, ADH, renin activity, and +G/z/ tolerance

Effects on plasma volume, electrolyte shifts, and +G(z) tolerance induced by: (1) blood withdrawal; (2) blood infusion; and (3) oral fluid intake, were determined at 0.5 G/min in centrifugation tests of six ambulatory male patients, aged 21 to 27 yrs. Hypovolemia induced by withdrawal of 400 ml blood, blood infusion followed by repeated centrifugation, effects of consuming an isotonic drink (0.9% NaCl) to achieve oral rehydration, and donning of red adaptation goggles were studied for effects on acceleration tolerance, pre-acceleration and post-acceleration plasma renin activity (PRA) and plasma vasopressin levels. No significant changes in post-acceleration PRA compared to pre-acceleration PRA were found, and administration of oral rehydration is found as effective as blood replacement in counteracting hypovolemic effects.

Greenleaf, J. E.↗

Cardiovascular function following reduced aerobic activity

PURPOSE: The aim of this study was to test the hypothesis that a sustained reduction of physical activity (deconditioning) would alter the cardiovascular regulatory function. METHODS: Nineteen young, healthy volunteers participated in physical deconditioning for a period of 8 wk. Before (pre) and following (post) physical deconditioning, the responses of heart rate (HR), mean arterial pressure (MAP, measured by Finapres), central venous pressure (CVP), stroke volume (SV, Doppler), and forearm blood flow (FBF, plethysmography) were determined during lower body negative pressure (LBNP). The carotid baroreflex (CBR) function was assessed using a train of pulsatile neck pressure (NP) and suction, and the aortic baroreflex control of HR was assessed during steady-state phenylephrine (PE) infusion superimposed by LBNP and NP to counteract the PE increased CVP and carotid sinus pressure, respectively. RESULTS: Active physical deconditioning significantly decreased maximal oxygen uptake (-7%) and LBNP tolerance (-13%) without a change in baseline hemodynamics. Plasma volume (-3% at P = 0.135), determined by Evans Blue dilution, and blood volume (-4% at P = 0.107) were not significantly altered. During LBNP -20 to -50 torr, there was a significantly greater drop of SV per unit decrease in CVP in the post- (14.7 +/- 1.6%/mm Hg) than predeconditioning (11.2 +/- 0.7%/mm Hg) test accompanied by a greater tachycardia. Deconditioning increased the aortic baroreflex sensitivity (pre vs post: -0.61 +/- 0.12 vs -0.84 +/- 0.14 bpm.mm-1 Hg, P = 0.009) and the slope of forearm vascular resistance (calculated from [MAP-CVP]/FBF) to CVP (-2.75 +/- 0.26 vs -4.94 +/- 0.97 PRU/mm Hg, P = 0.086). However, neither the CBR-HR (-0.28 +/- 0.03 VS -0.39 +/- 0.10 bpm.mm-1 Hg) nor the CBR-MAP (-0.37 +/- 0.16 vs -0.25 +/- 0.07 mm Hg/mm Hg) gains were statistically different between pre- and postdeconditioning. CONCLUSIONS: We concluded that the functional modification of the cardiac pressure-volume relationship resulted in the reduced LBNP tolerance, despite the accentuated aortic and cardiopulmonary baroreflex function following deconditioning.

Non-NASA Center↗