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PubMed1985

Cardiovascular deconditioning produced by 20 hours of bedrest with head-down tilt (-5 degrees) in middle-aged healthy men.

Cardiovascular deconditioning after prolonged bedrest has been attributed to inactivity. To examine the role of the altered distribution of body fluids, 5 healthy men, aged 41 to 48 years, were studied before, during and after a 20-hour period of bedrest with head-down tilt (-5 degrees). This intervention produces a marked central shift of intravascular and interstitial fluid, but the short duration minimizes the effects of inactivity. Central venous pressure, cardiac output and stroke volume all increased significantly (p less than 0.05) from supine baseline mean values; central venous pressure from 8.6 to 12.6 cm H2O, cardiac output from 6.9 to 7.9 liters/min, and stroke volume from 104 to 113 ml after 15 minutes of tilt, but all values returned to baseline within 20 hours. Supine central venous pressure after tilt was 7.4 cm H2O, cardiac output 5.7 liters/min and stroke volume 84 ml. Blood volume decreased 0.51 liters. After tilt, orthostatic stress produced a higher heart rate (90 +/- 18 vs 68 +/- 12 beats/min). Maximal oxygen consumption decreased (2.36 +/- 0.41 vs 2.62 +/- 0.48 liters/min), mainly owing to reduced stroke volume (87 +/- 22 vs 107 +/- 18 ml, p less than 0.05). Thus, tilt produced a transient increase in central venous pressure, stroke volume and cardiac output, but supine mean values were below baseline levels after 20 hours. The post-tilt state was qualitatively and quantitatively similar to that seen after 2 to 3 weeks of bedrest or several days of spaceflight. These results are also similar to those from a previously studied group of ten 20- to 30-year-old normal men.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1985

Beta blockade in the compensation for bed-rest cardiovascular deconditioning: physiologic and pharmacologic observations.

Beta-adrenergic blockade using intravenous propranolol was evaluated as a countermeasure for bedrest-induced cardiovascular deconditioning. After propranolol administration, tolerance to a maximal lower body negative pressure (LBNP) test after bed rest improved to at least the -70 mm Hg level; following this, there was a sharp decrease in tolerance time. Propranolol decreased mean tolerance time by 36% (17.7 +/- 2.4 to 11.5 +/- 2.3 minutes) before bed rest, and by only half as much (16.6%) after bed rest (14.4 +/- 2.2 to 12.0 +/- 2.3 minutes). Systemic vascular resistance was maintained and even slightly increased after propranolol despite a decrease in cardiac output, indicating beta 2-adrenergic blockade. Heart rates at all levels of LBNP were lower during beta blockade, yet increases occurred with successive LBNP steps, both before and after bed rest, indicating withdrawal of parasympathetic nervous system influences. Results support the use of propranolol in small dosages as a countermeasure after bed rest, and the findings may also be extrapolated to space-flight deconditioning.

Adult↗
PubMed2002

[Correlation between empirical and statistical indices of cardiovascular deconditioning in response to orthostatic exposures].

Data of heart rate and blood pressure from 26 astronauts during orthostatic testing before and after space flight and 15 healthy men during orthostatic testing before and after 10-days head-down tilt (HDT) were used to correlate two integral indices of cardiovascular deconditioning. The first, very simple index, was used earlier by Bungo M. W. et al. in order to ascertain the efficiency of peroral body dehydratation as a measure to prevent orthostatic intolerance in astronauts after space flight. This index sums up HR and BP variations from one orthosatic probe to another. The choice of the another index was based on our investigation of HDT effects on the healthy human cardiovascular system. This index was determined as a difference between linear discriminant function values separating distinctly groups of men with normal and lowered orthostatic tolerance. Analysis of regression showed a high correlation between these indices: 0.71 for the group of astronauts and 0.88 for the group of healthy men. The linear regression equations allowed calculate value of one index from value of the other with an admissible standard error.

Astronauts↗
PubMed1989

[Cardiovascular deconditioning syndrome during space flight].

Weightlessness results, in Man, in a redistribution of organic fluids from the lower half of the body to the thoraco-cephalic areas. This fluid transfer is responsible, in the course of the flight, for a series of subjective and objective disorders which the astronauts will experience. These disorders are related to venous stasis in the thoraco-cephalic area. Moreover, upon return of any space mission, regardless of its length, the astronauts will experience a disadaptation of their cardiovascular system indicated by hypotension with the possible occurrence of a presyncopal state, or even a syncope and a lowered stress capability. The haemodynamic consequences of this fluid transfer, from central and peripheral standpoint, and the mechanisms implicated in the cardiovascular deconditioning syndrome, are presented and discussed.

Blood Circulation↗
PubMed1987

Spacelab Life Sciences flight experiments: an integrated approach to the study of cardiovascular deconditioning and orthostatic hypotension.

The microgravity environment of spaceflight produces rapid cardiovascular changes which are adaptive and appropriate in that setting, but are associated with significant deconditioning and orthostatic hypotension on return to Earth's gravity. The rapidity with which these space flight induced changes appear and disappear provides an ideal model for studying the underlying pathophysiological mechanisms of deconditioning and orthostatic hypotension, regardless of etiology. Since significant deconditioning is seen after flights of very short duration, muscle atrophy due to inactivity plays, at most, a small role. These changes in circulatory control associated with cephalad fluid shifts, rather than inactivity per se, are probably more important factors. In order to test this hypothesis in a systematic way, a multidisciplinary approach which defines and integrates inputs and responses from a wide variety of circulatory sub-systems is required. The cardiovascular experiments selected for Spacelab Life Sciences flights 1 and 2 provide such an approach. Both human and animal models will be utilized. Pre- and post-flight characterization of the payload crew includes determination of maximal exercise capacity (bicycle ergometry), orthostatic tolerance (lower body negative pressure), alpha and beta adrenergic sensitivity (isoproterenol and phenylephrine infusions), baroreflex sensitivity (ECG-gated, stepwise changes in carotid artery transmural pressure with a pneumatic neck collar), and responses to a 24 h period of 5 deg head-down tilt. Measurements of cardiac output (CO2 and C2H2 rebreathing), cardiac chamber dimensions (phased-array 2-dimensional echocardiography), direct central venous pressure, leg volume (Thornton sock), limb blood flow and venous compliance (occlusion plethysmography), blood and plasma volumes, renal plasma flow and glomerular filtration rates, and various hormonal levels including catecholamines and atrial natriuretic factor will also be obtained. The central venous catheter will be inserted immediately pre-launch and monitored with heart rate and blood pressure in-flight until cardiac output, respiratory gas exchange and quantitative 2D echocardiography measurements can be performed. In-flight hemodynamic measurements will be repeated at rest and during submaximal exercise daily and also during maximal exercise midway through the flight to document the timecourse and extent of cardiovascular changes in the payload crew. Parallel studies are planned for the animals. In addition to measurements of right atrial and aortic pressures and cardiac output, a dorsal micro-circulatory chamber will allow determinations of changes in capillary and venular architecture and function in six of the rats. The techniques and findings from many of the SLS-1 and 2 supporting studies have already yielded significant information about circulatory regulation in patients with both hypo- and hypertension. The flight experiments themselves will provide new data to test the validity of both animal and human models currently used for simulating the fluid shifts of a micro-gravity environment. The development of effective countermeasures, not only for short and long duration space travellers, but also for Earth-bound medical patients can then be physiologically based on experimental data rather than anecdote.

Animals↗
PubMed1999

Head-out immersion in the non-human primate: a model of cardiovascular deconditioning during microgravity.

BACKGROUND: Orthostatic intolerance is a common complication associated with spaceflight. It has been speculated that this is due to changes in blood volume and alterations in cardiovascular reflexes. The objective of the current study was to develop a model that would allow us to study the cardiovascular system and the regulation of blood volume during short-term microgravity exposure in the primate with the intent of eventually being able to elucidate those factors responsible for the orthostatic intolerance. HYPOTHESIS: Head-out water immersion in the conscious non-human primate simulates the cardiovascular and volume regulatory responses observed in astronauts during exposure to microgravity. METHODS: Four monkeys were chronically instrumented for measuring BP and heart rate and then conditioned to the primate restraint chair. They were then subjected to 72 h of head-out water immersion (two immersions in three monkeys and one immersion in the fourth) in order to simulate the cardiovascular and renal effects of the microgravity environment. RESULTS: During the immersion, there was an increase in arterial BP (ABP) and central venous pressure (CVP) and a reflex decrease in heart rate (HR). Urine flow (UV) increased and water intake decreased, producing a negative water balance. This was not associated with an alteration in food intake. CVP and UV decreased following de-immersion. There was also resetting of the arterial baroreflex control of HR. Significant tachycardia occurred after the immersion that was associated with a decrease in ABP. CONCLUSION: These results are similar to those observed in astronauts during and after spaceflight, suggesting that head-out water immersion of the non-human primate provides a good model for studying cardiovascular and renal adaptations to spaceflight.

Animals↗
PubMed1985

Cardiovascular deconditioning during space flight and the use of saline as a countermeasure to orthostatic intolerance.

Alterations in the physiology of the cardiovascular system have been noted during all exposures to the microgravity experienced in space flight. Of most importance to the operational function of Space Shuttle crewmembers is orthostatic intolerance. Although complex changes occur as a result of adaptation to weightlessness, the redistribution and loss of body fluid apparently plays a substantial role. Utilizing ground-based bed rest data as an analog to the absence of gravitational force encountered in orbital flight, a saline loading countermeasure was developed. In this study, 17 crewmembers consumed various amounts of salt and fluid prior to the reentry phase of Space Shuttle flights; 9 other astronauts served as control subjects. The countermeasure reduced the heart rate response to orthostatic stress 29% and reversed the fall in mean blood pressure. A Cardiovascular Index of Deconditioning (defined as CID = delta HR - delta SBP + delta DBP) equalled 21 in those who utilized the countermeasure, a significant improvement toward baseline (p less than 0.003) when compared to the control group CID = 49. The encouraging results of these investigations have led to the adoption of the countermeasure as an operational procedure by Shuttle crewmembers.

Blood Pressure↗
PubMed1998

Further study on the carotid baroreflex system in the cardiovascular deconditioning induced by head-down tilt.

HYPOTHESIS: The responses of the carotid baroreflex and of the peripheral sympathetic system to stimulations induced by either lower body negative pressure (LBNP -40 mmHg) or cold pressor test were investigated in eight volunteers before and after 48 h in the -6 degrees head-down tilt (HDT). METHODS: Geometry (diastolic diameter and pulsatile distention) and dynamics (cross-sectional compliance and tangential tension) of the bulb and the common carotid artery were investigated using ultrasonic devices, echotracking and aplanation tonometry. The activity of the sympathetic system was evaluated through measurements of plasma concentrations of catecholamines (CAs) and 3,4-dihydroxyphenyl glycol (DHPG). RESULTS: During LBNP -40 mmHg, the pulsed tangential tension was decreased and the pressure amplification, induced by the reflexion of the pressure wave, was increased with no difference between before and after HDT. Since cross-sectional compliance and distensibility coefficient remained unchanged and the carotid contour of the waveform unaltered, it is concluded that the carotid reflexogenic area reads the same message during LBNP whether the cardiovascular system was deconditioned or not. Nonetheless, during LBNP after 48 h HDT, the heart rate accelerated faster and CAs and DHPG concentrations increased out of proportion, suggesting that the peripheral sympathetic activity was more reactive after HDT than before. Finally, forearm vascular resistances were measured in response to cold pressor test; they increased in the same proportion after HDT when compared with before. CONCLUSION: Results indicate that the carotid baroreflex and the peripheral sympathetic system were not deficient after 48 h HDT.

Adolescent↗
PubMed1964

Cardiovascular deconditioning: role of blood volume and sympathetic neurohormones.

Studies of prolonged bed rest and water immersion have amply demonstrated that serious deconditioning of certain gravity-oriented biologic systems occurs with extended exposures to environments in which the necessity for gravity compensation has been reduced. The precise physiologic mechanisms responsible for the loss of orthostatic tolerance following such studies are unknown, but may be related to diminished blood volume, decreased muscle or tissue pressure in the extremities or to functional alterations in the sympathetic nervous system. In view of the fact that noradrenaline is the principal agent for maintaining vascular tone the author has focused his attention on the sympathetic nervous system as being the system most likely responsible for the loss of orthostatic tolerance following such experiments. The contributory effects of diminished circulating blood volume resulting from such environments are also discussed.

Adult↗
PubMed1998

Chronic fatigue syndrome: physical and cardiovascular deconditioning.

We investigated whether chronic fatigue syndrome (CFS) patients have physical and/or cardiovascular de-conditioning, in 273 CFS patients and 72 healthy controls. We used laboratory tests to assess haematological, biochemical, endocrinological and immunological systems. The cardiovascular system was assessed by echocardiography and carotid echography. Body composition was determined by dual energy X-ray absorptiometry (DEXA). CFS patients had smaller left ventricular end systolic (p < 0.001) and diastolic (p = 0.008) dimensions but thinner posterior walls (p = 0.02) than corresponding values in healthy controls. Left ventricular mass was also reduced in CFS patients (p = 0.006). Both maximum (p < 0.001) and minimum (p < 0.008) diameter of the carotid artery were smaller in CFS patients. The laboratory screening tests showed significant differences in serum albumin (p = 0.05), phosphate (p = 0.02), HDL-cholesterol (p = 0.03), HDL:total cholesterol ratio (p = 0.01), triglycerides (p = 0.02), neutrophils (p = 0.01) and thyroid-stimulating hormone (p = 0.04) between CFS patients and controls. Male CFS patients had an increased percentage of fat mass compared with healthy male subjects (p = 0.02). This large group of CFS patients had evidence of physical and cardiovascular de-conditioning, suggesting that in these patients a graded exercise programme could lead to physical reconditioning and could increase their ability to perform physical activities.

Adult↗