Endocrine responses to 7 days of head-down bed rest and orthostatic tests in men and women.

The objective of this study was to investigate plasma volume (PV), total body water, hormones and hydroelectrolyte responses in eight males (25-40 years) and eight females (25-31 years) during 7 days of exposure to simulated microgravity (-6 degrees head-down bed rest, HDBR). Bed rest is a model that has commonly been used to simulate spaceflight. Heart rate (HR), blood pressure (BP) and vasoactive hormone responses were studied before and after HDBR during a 10-min stand test. No change in total body water and body mass was noted in either sex. The decrease in PV was similar in both men (9.1 +/- 1.4%) and women (9.4 +/- 0.8%). Urinary normetanephrine (NMN) was decreased during HDBR in both sexes. Urinary metanephrine (MN) and plasma catecholamines were unchanged. Daily urinary excretion of urea, an indirect index of protein breakdown, was increased only in the female subjects during HDBR. Plasma active renin (AR) and aldosterone were increased in both sexes, but urinary atrial natriuretic peptide (ANP) and arginine vasopressin (AVP) were unchanged throughout the study. Also, the hormonal responses to 7 days of HDBR were comparable between men and women. Moreover, the results show similar cardiovascular and endocrine responses to standing after HDBR. However, the orthostatic intolerance following HDBR was associated with a blunted increase in noradrenaline (NA) only in the women during the stand test. It is concluded that: (i) 7 days of physical inactivity achieved during HDBR resulted in a reduced sympathetic activity in both sexes and alterations in protein metabolism in women and (ii) standing after HDBR resulted in an attenuated release of noradrenaline in women.     

Femoral to cerebral arterial blood flow redistribution and femoral vein distension during orthostatic tests after 4 days in the head-down tilt position or confinement

The first objective of this study was to confirm that 4 days of head-down tilt (HDT) were sufficient to induce orthostatic intolerance, and to check if 4 days of physical confinement may also induce orthostatic intolerance. Evidence of orthostatic intolerance during tilt-up tests was obtained from blood pressure and clinical criteria. The second objective was to quantify the arterial and venous changes associated with orthostatic intolerance and to check whether abnormal responses to the tilt test and lower body negative pressure (LBNP) may occur in the absence of blood pressure or clinical signs of orthostatic intolerance. The cerebral and lower limb arterial blood flow and vascular resistance, the flow redistribution between these two areas, and the femoral vein distension were assessed during tilt-up and LBNP by ultrasound. Eight subjects were given 4 days of HDT and, 1 month later, 4 days of physical confinement. Tilt and LBNP test were performed pre- and post-HDT and confinement. Orthostatic intolerance was significantly more frequent after HDT (63%) than after confinement (25%, P<0.001). Cerebral haemodynamic responses to tilt-up and LBNP tests were similar pre- and post-HDT or confinement. Conversely, during both tilt and LBNP tests the femoral vascular resistances increased less (P<0.002), and the femoral blood flow reduced less (P<0.001) after HDT than before HDT or after confinement. The cerebral to femoral blood flow ratio increased less after HDT than before (P<0.002) but remained unchanged before and after confinement. This ratio was significantly more disturbed in the subjects who did not complete the tilt test. The femoral superficial vein was more distended during post-HDT LBNP than pre-HDT or after confinement (P<0.01). In conclusion, 4 days of HDT were enough to alter the lower limb arterial vasoconstriction and venous distensibility during tilt-up and LBNP, which reduced the flow redistribution in favour of the brain in all HDT subjects. Confinement did not alter significantly the haemodynamic responses to orthostatic tests. The cerebral to femoral blood flow ratio measured during LBNP was the best predictor of orthostatic intolerance.     

Resistance exercise training and the orthostatic response

Resistance exercise has been suggested to increase blood volume, increase the sensitivity of the carotid baroreceptor cardiac reflex response (BARO), and decrease leg compliance, all factors that are expected to improve orthostatic tolerance. To further test these hypotheses, cardiovascular responses to standing and to pre-syncopal limited lower body negative pressure (LBNP) were measured in two groups of sedentary men before and after a 12-week period of either exercise (n = 10) or no exercise (control, n = 9). Resistance exercise training consisted of nine isotonic exercises, four sets of each, 3 days per week, stressing all major muscle groups. After exercise training, leg muscle volumes increased (P?P = 0.00) by 2.0 (0.5)?kg, leg compliance and BARO were not significantly altered, and the maximal LBNP tolerated without pre-syncope was not significantly different. Supine resting heart rate was reduced (P = 0.03) without attenuating the heart rate or blood pressure responses during the stand test or LBNP. Also, blood volume (¹²⁵I and ⁵¹Cr) and red cell mass were increased (P?相似文献   

Aortic,cerebral and lower limb arterial and venous response to orthostatic stress after a 60-day bedrest

The objective of this study is to assess by echography and Doppler the Cerebral (Vmca), Aortic (Vao) and Femoral (Vfem) arterial flow velocity and calf vein (Tibial, Gastrocnemius) section (Tib, Gast) during orthostatic intolerance (OI) test after a 60-day, head down tilt bed rest (HDBR). Twenty-four women (25–40 years) underwent a 60-day HDBR at −6°: eight as control (Con), eight with exercise against lower body negative pressure (Ex-Lb) and eight with nutrition supplement (Nut). Before and after (R0) HDBR, all subjects underwent a 10-min, 80° tilt followed by progressive LBNP until presyncope. After the post-HDBR Tilt + LBNP test, two groups were identified: finishers (F, n = 11) who completed the Tilt and non-finishers (NF, n = 13). A higher percentage decrease in Vao flow, higher percentage distension of Tib vein and a lack of increase in Vmca/Vfem ratio during the post-HDBR Tilt + LBNP compared to pre-HDBR were correlated to OI, but not all of these abnormal responses were present in each of the NF subjects. Abnormal responses were more frequent in Con and Nut than in Ex-Lb subjects. (1) HDBR did not affect the cardiac, arterial and venous responses to the orthostatic test to the same extent in each subject. (2) Exercise within LBNP partially preserved the cardiovascular response to Tilt, while Nutrition supplementation had no efficacy. (3) Cerebral/femoral flow ratio and aortic flow were the parameters most closely related to OI. (4) Reduction in aortic flow was not the major hemodynamic change preceding syncope.     

Heart rate variability after prolonged spaceflights

Astronauts returning from spaceflight often experience post-flight orthostatic intolerance. This study was designed to determine whether cosmonauts with post-flight syncope could be distinguished from those with no post-flight syncope. The autonomic function was determined in a group of ten subjects, with no previous history of syncope, during a stand test before and after a long-term spaceflight (90 to 198 days). Heart rate (HR) and systolic blood pressure (SBP) were measured beat-by-beat, pre- and post-flight and the spontaneous baroreflex sensitivity and HR variability were studied. Individuals were categorized according to their ability to remain standing for 5 min the day after landing. Three of the ten cosmonauts failed to finish the standing test performed the day after landing (non-finishers). The spontaneous baroreflex slope was reduced in both groups after the spaceflight. The non-finisher group had a lower SBP (P<0.05) at rest in pre-flight tests than the group that completed the test (finisher group). The non-finisher group also had higher indicators of parasympathetic activity when supine, both pre- and post-flight, but this difference disappeared with standing. At the end of the stand test, SBP and HR were lower in non-finisher cosmonauts than the finishers, while HR did not increase compared to early measurements in the stand test of the finisher group. These results suggest an impairment in autonomic control of HR, which might contribute to the fainting response. Electronic Publication     

Cardiovascular responses to an orthostatic challenge and electrical-stimulation-induced leg muscle contractions in individuals with paraplegia

The purpose of this study was to investigate the cardiovascular and haemodynamic responses that occur during moderate orthostatic challenge in people with paraplegia, and the effect of electrical stimulation (ES)-induced leg muscle contractions on their responses to orthostatic challenge. Eight males with complete spinal lesions between the 5th and 12th thoracic vertebrae (PARA) and eight able-bodied individuals (AB) volunteered for this study. Changes in heart rate (f _c), stroke volume (SV), cardiac output (Q˙ _c), mean arterial pressure (MAP), total peripheral resistance (TPR), limb volumes and indices of neural modulation of f _c, [parasympathetic (PNS) and sympathetic (SNS) nervous system indicators] were assessed during: (1) supine rest (REST), (2) REST with lower-body negative pressure at ?30 torr (LBNP ?30, where 1 torr?=?133.32?N/m²), and (3) for PARA only, LBNP ?30 with ES-induced leg muscle contractions (LBNP?+?ES). LBNP ?30 elicited a decrease in SV (by 23% and 22%), Q˙ _c (by 15% and 18%) and the PNS indicator, but an increase in f _c (by 10% and 9%), TPR (by 23% and 17%) and calf volume (by 1.51% and 4.04%) in both PARA and AB subjects, respectively. The SNS indicator was increased in the AB group only. Compared to LBNP ?30, LBNP?+?ES increased SV (by 20%) and Q˙ _c (by 16%), and decreased TPR (by 12%) in the PARA group. MAP was unchanged from REST during all trials, for both groups. The orthostatic challenge induced by LBNP ?30 elicited similar cardiovascular adaptations in PARA and AB subjects. ES-induced muscle contractions during LBNP ?30 augmented the cardiovascular responses exhibited by the PARA group, probably via reactivation of the skeletal muscle pump and improved venous return.     

Contributory factors to orthostatic intolerance after simulated weightlessness.

Various factors may contribute to orthostatic intolerance (OI) observed after space flights or simulated weightlessness such as bed rest experiments: individual physical and physiological factors (arterial blood pressure (BP), height), physiological changes induced by real or simulated weightlessness (hypovolaemia, increase in venous distensibility), and space flight or simulation conditions (duration and counter-measure application). Our purpose was to test which of these factors were dominant in contributing to the OI. This was assessed in 47 healthy men participating in bed rest experiments of 4, 14, 28, 30 and 42 days, with or without counter-measures (medical stockings, lower-body negative pressure (LBNP), LBNP + muscular exercise). Nineteen subjects did not finish the orthostatic test (60 degrees head-up tilt or stand test) after bed rest. The occurrence of OI was associated with greater height, low resting BP, greater changes in resting lower-limb venous distensibility throughout the bed rest, and absence of counter-measures.     

Numerical Simulation of the Influence of Gravity and Posture on Cardiac Performance

A numerical model of the cardiovascular system was used to quantify the influences on cardiac function of intrathoracic pressure and intravascular and intraventricular hydrostatic pressure, which are fundamental biomechanical stimuli for orthostatic response. The model included a detailed arterial circulation with lumped parameter models of the atria, ventricles, pulmonary circulation, and venous circulation. The venous circulation was divided into cranial, central, and caudal regions with nonlinear compliance. Changes in intrathoracic pressure and the effects of hydrostatic pressure were simulated in supine, launch, sitting, and standing postures for 0, 1, and 1.8 G. Increasing intrathoracic pressure experienced with increasing gravity caused 12% and 14% decreases in cardiac output for 1 and 1.8 G supine, respectively, compared to 0 G. Similar results were obtained for launch posture, in which the effects of changing intrathoracic pressure dominated those of hydrostatic pressure. Compared to 0 G, cardiac output decreased 0.9% for 1 G launch and 15% for 1.8 G launch. In sitting and standing, the position of the heart above the hydrostatic indifference level caused the effects of changing hydrostatic pressure to dominate those of intrathoracic pressure. Compared to 0 G, cardiac output decreased 13% for 1 G sitting and 23% for 1.8 G sitting, and decreased 17% for 1 G standing and 31% for 1.8 G standing. For a posture change from supine to standing in 1 G, cardiac output decreased, consistent with the trend necessary to explain orthostatic intolerance in some astronauts during postflight stand tests. Simulated lower body negative pressure (LBNP) in 0 G reduced cardiac output and mean aortic pressure similar to 1 G standing, suggesting that LBNP provides at least some cardiovascular stimuli that may be useful in preventing postflight orthostatic intolerance. A unifying concept, consistent with the Frank–Starling mechanism of the heart, was that cardiac output was proportional to cardiac diastolic transmural pressure for all postures and gravitational accelerations. © 2002 Biomedical Engineering Society. PAC2002: 8765+y, 8719Bb, 8719Uv, 8719Hh     

Delaying orthostatic syncope with mental challenge: a pilot study

At orthostatic vasovagal syncope there appears to be a sudden decline of sympathetic activity. As mental challenge activates the sympathetic system, we hypothesized that doing mental arithmetic in volunteers driven to the end point of their cardiovascular stability may delay the onset of orthostatic syncope. We investigated this in healthy male subjects. Each subject underwent a head up tilt (HUT)+ graded lower body negative pressure (LBNP) up to presyncope session (control) to determine the orthostatic tolerance time, OTT (Time from HUT commencement to development of presyncopal symptoms/signs). Once the tolerance time was known, a randomized crossover protocol was used: either 1) Repeat HUT+LBNP to ensure reproducibility of repeated run or 2) HUT+LBNP run but with added mental challenge (2 min before the expected presyncope time). Test protocols were separated by 2 weeks. Our studies on five male test subjects indicate that mental challenge improves orthostatic tolerance significantly. Additional mental loading could be a useful countermeasure to alleviate the orthostatic responses of persons, particularly in those with histories of dizziness on standing up, or to alleviate hypotension that frequently occurs during hemodialysis or on return to earth from the spaceflight environment of microgravity.     

The effects of isometric exercise training on resting blood pressure and orthostatic tolerance in humans

Isometric exercise training has been shown to reduce resting blood pressure, but the effect that this might have on orthostatic tolerance is poorly understood. Changes in orthostatic tolerance may also be dependent on whether the upper or lower limbs of the body are trained using isometric exercise. Twenty-seven subjects were allocated to either a training or control group. A training group first undertook 5 weeks of isometric exercise training of the legs, and after an 8 week intervening period, a second training group containing six subjects from the initial training group, undertook 5 weeks of isometric arm-training. The control group were asked to continue their normal daily activities throughout the 18 weeks of the study. In all subjects orthostatic tolerance, assessed using lower body negative pressure (LBNP), and resting blood pressure were measured before and after each of the 5 week training or control periods. Estimated lean leg volume was determined before and after leg-training. During all LBNP tests, heart rate and blood pressure were recorded each minute, and the time taken to reach the highest heart rate was derived (time to peak HR). Resting systolic blood pressure (mean +/- S.D.), when measured during the last week of training, was significantly reduced after both leg (-10 +/- 8.7 mmHg) and arm (-12.4 +/- 9.3 mmHg; P < 0.05) isometric exercise training, compared to controls. This reduction disappeared when blood pressure was measured immediately before the LBNP tests, which followed training. Orthostatic tolerance only increased after leg-training (20.8 +/- 16.4 LTI; P < 0.05) and was accompanied by an increased time to peak HR (119.8 +/- 106.3 beats min(-1); P < 0.05) in this group. Blood pressure responses to LBNP did not change after arm-training, leg-training or in controls (P > 0.05). There was a small but significant increase in estimated lean leg volume after leg-training (0.1 +/- 0.1 1; P < 0.05). These results suggest that lower resting blood pressure is probably not responsible for the increased orthostatic tolerance after isometric exercise training of the legs. Rather, it is possible that the training altered some other aspect of cardiovascular control during orthostatic stress that was apparent in the changes in heart rate. Leg-training was accompanied by increases in estimated lean leg volume. The effects of isometric training on orthostatic tolerance appear to be specific to limbs that are directly involved in LBNP testing.     

失重后血量减少致立位应激时心血管反应改变的仿真研究

我们将计算机仿真的实验方法引入重力重力生理学研究领域。以Melchior（1994)工作为基础，建立一个仿真立位应激（下体负压）时心血管反应的数学模型，模型包括血液重新分配、左室充盈、左室工作、外周循环、心率调节调节、外周阻力调节、静脉紧张程度调节等七个模型。然后仿真人体在下体负压时血压和心率变化，结果与同步进行的人体下体负压实验结果吻合。基于此模型，仿真研究了血量减少对立位应激时血压、心率和休克指数的影响。结果表明，超过总血量15%的血量减少将导致立位应激时心血管反应的明显改变；但是当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时正常的HR和BP。本结果证明血量减少是失重后人体立位耐力不良的主要因素之一。     

Hypergravity exercise against bed rest induced changes in cardiac autonomic control

An intermittent exposure to artificial hypergravity with physical exercise by a human centrifuge may provide a countermeasure against various physiological problems after space flight. To test the effects of hypergravity with ergometric exercise on dynamic regulation of heart rate during weightlessness, we quantified autonomic cardiovascular control before and after head-down-tilt bed rest (HDBR) with and without the countermeasure. Twelve male subjects underwent a 14-day period of HDBR. Six of them were exposed to a hypergravity (+1.2 Gz acceleration at heart level) for 30 min with ergometric exercise (60 W, n=4; 40 W, n=2) as a countermeasure on day 1, 2, 3, 5, 7, 9, 11, 12, 13 and 14, during HDBR (CM group). The remaining six were not exposed to a hypergravity exercise during HDBR (control group). Blood pressure and ECG were recorded at a supine position before and after HDBR. The high frequency power of R–R interval (HFRR; 1,008±238 to 353±56 ms² P<0.05) as an index of cardiac parasympathetic activity, and transfer function gain between BP and R–R interval in the high frequency range (GainHF; 21.9±5.4 to 14.5±4.2 ms/mmHg, P<0.01) as an index of vagally mediated arterial-cardiac baroreflex, decreased significantly after HDBR in the control group. However, these changes were not statistically significant in the CM group (HFRR, 1,150±344 to 768±385 ms²; GainHF, 21.5±3.3 to 18.6±3.4 ms/mmHg). Moreover, baroreflex gain by sequence analysis showed similar results. This observation suggests that the intermittent exposure to hypergravity with ergometric exercise may attenuate the decreases in the parasympathetic activity and the spontaneous arterial-cardiac baroreflex function after weightlessness.     

Effects of coffee on cardiovascular responses to stress: a 14-week controlled trial.

We studied the cardiovascular responses to orthostatic and mental stress of 43 healthy subjects who daily received six cups of boiled or filtered coffee and of 21 healthy subjects who abstained from caffeine-containing beverages. All 64 subjects first received six cups of filtered coffee/day for 2 weeks. Then blood pressure (BP) and heart rate (HR) were recorded before, during, and after a "stand upright" test and a mental arithmetic test. Subjects were then randomized to either complete abstinence from caffeine-containing beverages (n = 21), or consumption of six cups of filtered coffee (n = 21), or consumption of six cups of boiled coffee/day (n = 22). The stress tests were repeated after subjects had been on these regimens for 8 weeks. Abstinence from coffee did not affect the responses of BP or HR to orthostatic stress, or the response of BP to mental stress. The increase in HR caused by mental stress was five beats/min less (p = 0.02) in the no-coffee group than in the filtered- (95% confidence interval -8.8 to -1.2) or boiled- (95% confidence interval -8.4 to -0.8) coffee group. It is concluded that elimination of caffeine decreases the HR response to mental stress.     

Lower Body Negative Pressure and Effects of Autonomic Heart Blockade on Cardiovascular Responses

Heart rate, arterial pressure and cardiac output were recorded in eight healthy male volunteers during exposure to 80 mmHg of lower body negative pressure (LBNP) in the supine position before and after beta-adrenergic and combined beta-adrenergic and parasympathetic blockade of the heart as induced by the i.v. administration of propranolol 0.25 mg/kg b.wt. and atropine 0.04 mg/kg b.wt. After propranolol, heart rate response to LBNP averaged 48 % of that observed without blockade indicating that LBNP-induced cardioacceleration is of both sympathetic and parasympathetic origin. Tolerance to LBNP was reduced by beta-adrenergic blockade, since the decrease in mean arterial pressure during LBNP was exaggerated by such blockade. Although the addition of atropine markedly elevated mean arterial pressure and cardiac output in the control situation, tolerance to LBNP was not enhanced by this drug as judged from the arterial pressure response. Post-LBNP overshoot in mean arterial pressure was strikingly augmented by combined cardiac effector blockade and was in part due to a lingering elevation of total peripheral resistance, cardiac output remaining decreased for more than 110 s after release of LBNP.     

Lower body negative pressure and effects of autonomic heart blockade on cardiovascular responses.

Heart rate, arterial pressure and cardiac output were recorded in eight healthy male volunteers during exposure to 80 mmHg of lower body negative pressure (LBNP) in the supine position before and after beta-adrenergic and combined beta-adrenergic and parasympathetic blockade of the heart as induced by the i.v. administration of propranolol 0.25 mg/kg b.wt. and atropine 0.04 mg/kg b.wt. After propranolol, heart rate response to LBNP averaged 48% of that observed without blockade indicating that LBNP-induced cardioacceleration is of both sympathetic and parasympathetic origin. Tolerance to LBNP was reduced by beta-adrenergic blockade, since the decrease in mean arterial pressure during LBNP was exaggerated by such blockade. Although the addition of atropine markedly elevated mean arterial pressure and cardiac output in the control situation, tolerance to LBNP was not enhanced by this drug as judged from the arterial pressure response. Post-LBNP overshoot in mean arterial pressure was strikingly augmented by combined cardiac effector blockade and was in part due to a lingering elevation of total peripheral resistance, cardiac output remaining decreased for more than 110 s after release of LBNP.     

Hypotension induced by central hypovolaemia and hypoxaemia

Our question was whether the reduced orthostatic tolerance that accompanies hypoxaemia in some (not all) subjects might be associated with an abnormally large release of adrenaline. Eight normal young men were exposed to lower body negative pressure (LBNP) at -30 to -40 mmHg while breathing air or 10% O2 in N2. Four subjects developed hypotension and bradycardia whenever LBNP was applied during hypoxaemia; four showed a rise in heart rate and stable blood pressure. During normoxia plasma adrenaline concentration did not rise during LBNP in any subject, nor during hypoxaemia plus LBNP in the subjects who remained normotensive. In the four men whose heart rates and blood pressures fell during LBNP with hypoxaemia, adrenaline rose markedly, reaching 200-1600 pg ml-1. All subjects showed similar elevations in noradrenaline concentration during LBNP in both normoxia and hypoxaemia. The results suggest that reduced tolerance to central hypovolaemia during hypoxaemia could stem from known vasomotor and cardiac effects attending high plasma concentrations of adrenaline.     

Vasomotor responses to decreased venous return: effects of cardiac deafferentation in humans

We compared haemodynamic and peripheral vasomotor responses to lower body negative pressure (LBNP) in cardiac transplant recipients who had undergone bicaval anastomoses, involving right atrial deafferentation (−RA), and the conventional procedure in which some atrial baroreceptor afferents remain intact (+RA). We measured mean forearm blood flow (FBF) responses using Doppler/ultrasound during three randomised trials involving 0 (baseline), −20 and −40 mmHg LBNP in 15 transplant recipients (9 −RA, 6 +RA) and in eight healthy matched controls. A significant effect of LBNP on FBF existed between control and transplant groups ( P < 0.05; two-way ANOVA). Mild LBNP (−20 mmHg), significantly decreased FBF by 29.7 ± 10.0% relative to baseline in +RA subjects ( P < 0.05), whereas the 17.7 ± 10.3% decrease in −RA subjects was not significant. In response to −40 mmHg LBNP, FBF significantly decreased in control (42.4 ± 4.6%, P < 0.05) and +RA subjects (33.3 ± 11.4%, P < 0.05) with no significant change in the −RA group. The response of systolic blood pressure (SBP) to −40 mmHg significantly differed between groups ( P < 0.05): −RA subjects decreased significantly ( P < 0.05) whilst the decrease in SBP in +RA subjects did not achieve significance and control subjects exhibited an increase. The heart rate increase from baseline to −40 mmHg was significantly attenuated in −RA relative to controls and the +RA group ( P < 0.05). The present study demonstrates that atrial deafferentation impairs reflex vasomotor control of the circulation in response to low- and high-level LBNP, indicating that atrial deafferentation may contribute to abnormal arterial pressure regulation.     

Hemodynamic and neurohumoral responses to the restriction of femoral blood flow by KAATSU in healthy subjects

The application of an orthostatic stress such as lower body negative pressure (LBNP) has been proposed to minimize the effects of weightlessness on the cardiovascular system and subsequently to reduce the cardiovascular deconditioning. The KAATSU training is a novel method to induce muscle strength and hypertrophy with blood pooling in capacitance vessels by restricting venous return. Here, we studied the hemodynamic, autonomic nervous and hormonal responses to the restriction of femoral blood flow by KAATSU in healthy male subjects, using the ultrasonography and impedance cardiography. The pressurization on both thighs induced pooling of blood into the legs with pressure-dependent reduction of femoral arterial blood flow. The application of 200 mmHg KAATSU significantly decreased left ventricular diastolic dimension (LVDd), cardiac output (CO) and diameter of inferior vena cava (IVC). Similarly, 200 mmHg KAATSU also decreased stroke volume (SV), which was almost equal to the value in standing. Heart rate (HR) and total peripheral resistance (TPR) increased in a similar manner to standing with slight change of mean blood pressure (mBP). High-frequency power (HF_RR) decreased during both 200 mmHg KAATSU and standing, while low-frequency/high-frequency power (LF_RR/HF_RR) increased significantly. During KAATSU and standing, the concentration of noradrenaline (NA) and vasopressin (ADH) and plasma renin activity (PRA) increased. These results indicate that KAATSU in supine subjects reproduces the effects of standing on HR, SV, TPR, etc., thus stimulating an orthostatic stimulus. And, KAATSU training appears to be a useful method for potential countermeasure like LBNP against orthostatic intolerance after spaceflight.     

Sympathetic responses to Valsalva's manoeuvre following bed rest.

The purpose of this study was to examine whether 14 days of head-down tilt bed rest (HDBR) alters autonomic regulation during Valsalva's manoeuvre (VM) and if this would predict blood pressure control during a 60 degrees head-up tilt (HUT) test. To examine autonomic control of blood pressure, we measured the changes in systolic (delta SBP) and diastolic (delta DBP) blood pressure between baseline and the early straining (Phase IIE) period of VM (20 sec straining to 40 mmHg; N = 7) in conjunction with changes in muscle sympathetic nerve activity (MSNA; microneurography) burst frequency (B/min) and total activity (% delta) from baseline over the 20-sec straining period. MSNA data were successfully recorded from 6 of the 7 individuals. The averaged responses from three repeated VMs performed in the supine position were compared between the pre- and post-HDBR tests. Compared with the pre-HDBR test, a greater reduction in SBP, DBP, and MAP was observed during Phase IIE following HDBR, p < 0.05. The increase in MSNA burst frequency during straining was augmented in the post- compared with the pre-HDBR test, p < 0.0001, as was the Phase IV blood pressure overshoot, p < 0.05. Although all subjects completed the 20-min pre-HDBR tilt test without evidence of hypotension or orthostatic intolerance, the post-HDBR test was stopped early in 5 of the 7 subjects due to systolic hypotension. The responses during the VM suggest that acute autonomic adjustments to rapid blood pressure changes are preserved after bed rest. Furthermore, MSNA and blood pressure responses during VM did not predict blood pressure control during orthostasis following HDBR.