Efficacy of the Combined Use of Negative Pressure on the Lower Part of the Body and Negative-Pressure Respiration under Simulated Microgravity

The efficacies of the standard procedure for application of negative pressure on the lower part of the body (NPLB) and a combination of NPLB and negative-pressure respiration (NPR) during a simulated last stage of a spaceflight under conditions of antiorthostatic hypokinesia (ANOH, –6°) and isolation for 7 days have been compared in the course of three series of tests involving six volunteers in an EU-100 pressurized chamber. After the end of the 7-day ANOH and isolation, episodes of orthostatic disorders were observed in all six subjects in the first series of tests (the control series) and in four subjects in the second series (NPLB). In the third series (NPLB + NPR), orthostatic disorders, if any, were slight. Two main conclusions have been made. First, ANOH combined with isolation in a small chamber may be used to simulate the effects of the combined factors of spaceflight on humans in order to obtain model gravitational circulatory disorders. Second, the combined use of NPLB + NPR under these conditions may be effective for the prevention of orthostatic circulatory disorders in humans.     

Application of multivariate statistical analysis to estimate +Gz tolerance based on the changes of hemodynamic parameters during lower body negative pressure (LBNP)

The application of lower body negative pressure (LBNP) is very useful method for simulation of +Gz stress and for evaluation of orthostatic reaction. The different physiological changes that occur during LBNP test and +Gz acceleration test are similar. Lategola and Trent found that supine LBNP exposure at the level of -50 mmHg may be equivalent to +2Gz in producing the changes of heart rate (HR). Polese and coworkers compared hemodynamic changes occurring during upright and supine LBNP at the levels to -70 mmHg with identical measurements made during accelerations to +2Gz, +3Gz, and +4Gz in the same subjects. They noted for example that HR changes during upright LBNP exceeded HR supine levels. Peak values of HR during +3Gz and +4Gz significantly exceeded HR levels during both kinds of LBNP, but HR values at +2Gz were equivalent to those at -40 mmHg of upright and -70 mmHg of supine LBNP. So, the present study was undertaken to evaluate adaptating responses to LBNP stimulus at the level of -60 mmHg, regulatory mechanisms of the circulatory system (central and peripheral) and to look for the possibility of +Gz tolerance prediction based on the changes of some hemodynamic parameters during LBNP.     

Cardiac responses to lower body negative pressure and dynamic leg exercise

Cardiac responses to dynamic leg exercise at 0, 50, and 100 W in the supine position were investigated with and without the lower portion of the body exposed to a pressure of -6.6 kPa (Lower Body Negative Pressure, LBNP). Resting values for heart rate (HR) and stroke volume (SV) were considerably higher and lower, respectively, during LBNP than in the control condition. At the transition from rest to the mildest exercise during LBNP SV showed a prompt increase by about 40%, but no significant change in the control condition. HR, which increased by 17 beats X min-1 in the control condition, showed during LBNP no change initially and subsequently a small but significant drop below its resting value. Steady-state values for HR at the various levels of exercise were not significantly affected by LBNP, whereas corresponding values for SV were considerably lowered, so that exercise values for cardiac output were about 3 l X min-1 less during LBNP than in the control condition. The reductions in SV and cardiac output indicate residual pooling of blood in intra- and extramuscular capacitance vessels of the legs. With a change from rest to exercise at 100 W during LBNP mean systolic ejection rate (MSER) increased by 67%, the relations between SV and MSER suggesting that ventricular performance was maintained by a combination of the Frank-Starling mechanism and enhanced contractile strength.     

Cardiovascular response to lower body negative pressure before and after 20 days horizontal bed rest

To evaluate the effects of 20 days bed rest (BR) on cardiovascular system in normal subjects, left ventricular (LV) echocardiography and vascular ultrasound of the common carotid artery and abdominal aorta were performed during rest and a supine lower body negative pressure (LBNP) test in 14 healthy volunteers (mean age: 22 years) before and after BR. After BR, heart rates (HR) at rest and during LBNP (-40 mmHg) increased. In contrast, LV dimensions, stroke volume, and blood pressures decreased both at rest and during LBNP. Also LBNP tolerance time decreased after BR. Although resting cardiac output (CO) and abdominal aortic flow decreased after bed rest, CO and abdominal aortic flow were unchanged during LBNP comparing before and after BR. Common carotid artery flows both at rest and during LBNP showed no change after BR. LBNP did not increase HR before BR, but increased HR prominently after BR. In conclusion, LBNP tolerance time and LV size during LBNP decreased after BR, suggesting orthostatic intolerance due to a decreased blood volume. However, CO and flow in the abdominal aorta and common carotid artery during LBNP were similar before and after BR due to a compensatory increase after BR.     

Lower body negative pressure as a tool for research in aerospace physiology and military medicine

Lower body negative pressure (LBNP) has been extensively used for decades in aerospace physiological research as a tool to investigate cardiovascular mechanisms that are associated with or underlie performance in aerospace and military environments. In comparison with clinical stand and tilt tests, LBNP represents a relatively safe methodology for inducing highly reproducible hemodynamic responses during exposure to footward fluid shifts similar to those experienced under orthostatic challenge. By maintaining an orthostatic challenge in a supine posture, removal of leg support (muscle pump) and head motion (vestibular stimuli) during LBNP provides the capability to isolate cardiovascular mechanisms that regulate blood pressure. LBNP can be used for physiological measurements, clinical diagnoses and investigational research comparisons of subject populations and alterations in physiological status. The applications of LBNP to the study of blood pressure regulation in spaceflight, groundbased simulations of low gravity, and hemorrhage have provided unique insights and understanding for development of countermeasures based on physiological mechanisms underlying the operational problems.     

Effects of angiotensin blockade on the splanchnic circulation in normotensive humans

The effects of angiotensin-converting enzyme inhibition (ACE-I) by enalapril on splanchnic (n = 10) and central hemodynamics (n = 9) were examined in moderately salt-depleted healthy volunteers, at rest and during 15-20 min of lower body negative pressure (LBNP), reducing mean arterial pressure by 10 mmHg. During LBNP before ACE-I, both splanchnic and total peripheral vascular resistances increased. During ACE-I, splanchnic and total peripheral vascular resistances decreased. After enalapril administration, splanchnic vascular resistance did not increase during LBNP. Total peripheral vascular resistance still increased but not to the same extent as during LBNP before ACE-I. The increases in heart rate and plasma norepinephrine during LBNP were attenuated after ACE-I compared with LBNP before ACE-I. The effectiveness of the ACE-I was clearly demonstrated by unchanged and low plasma angiotensin II levels during ACE-I. We conclude that, in normal sodium-depleted humans, acute ACE-I decreases splanchnic vascular resistance at rest and abolishes splanchnic vasoconstriction during LBNP. Furthermore, it may interfere with autonomic nervous system control of the circulation.     

Construction of a lower body negative pressure chamber

Lower body negative pressure (LBNP) is an established and important technique used to physiologically stress the human body, particularly the cardiovascular system. LBNP is most often used to simulate gravitational stress, but it has also been used to simulate hemorrhage, alter preload, and manipulate baroreceptors. During experimentation, the consequences of LBNP and the reflex increases in heart rate and blood pressure can be manipulated and observed in a well-controlled manner, thus making LBNP an important research tool. Numerous laboratories have developed LBNP devices for use in research settings, and a few devices are commercially available. However, it is often difficult for new users to find adequately described design plans. Furthermore, many available plans require sophisticated and expensive materials and/or technical support. Therefore, we have created an affordable design plan for a LBNP chamber. The purpose of this article was to share our design template with others. In particular, we hope that this information will be of use in academic and research settings. Our pressure chamber has been stress tested to 100 mmHg below atmospheric pressure and has been used successfully to test orthostatic tolerance and physiological responses to -50 mmHg.     

Long-term antiorthostatic hypokinesia stimulates storage of osmotically inactive sodium in the human body

Changes in the water and sodium balances and in the states of the fluid compartments of the human body observed in experiments performed with healthy subjects exposed to long-term (120 days) antiorthostatic hypokinesia (ANOH) were analyzed. A hypothesis was suggested that the normal dietary consumption of sodium could be associated with the accumulation of osmotically inactive sodium in the body of a healthy person (independently of changes in the total water content). The results agree with the assumption that considerable amounts of osmotically inactive sodium may be stored in the human body. This hypothesis was confirmed by the inversion of the correlation between the cumulative sodium balance and the total water content of the body found both in the group-averaged data and in individual data. This nonsmotic sodium accumulation may take place not only during deviations from its normal consumption, but also during its regular dietary supply. Accumulation of sodium in these stores and its depletion are not associated with any significant changes in the volumes of body fluids. Infradian rhythmic changes in the sodium balance observed in some subjects exposed to the long-term ANOH, which were not caused by any periodic external influences, indicated the existence of a specific mechanism regulating the sodium content of the body. This mechanism must be significantly more inert and less precise than the fast regulation of the volume, osmolality, and ionic composition of extracellular fluids.     

Low LBNP tolerance in men is associated with attenuated activation of the renin-angiotensin system

Plasma vasoactive hormone concentrations [epinephrine (p(Epi)), norepinephrine (p(NE)), ANG II (p(ANG II)), vasopressin (p(VP)), endothelin-1 (p(ET-1))] and plasma renin activity (p(RA)) were measured periodically and compared during lower body negative pressure (LBNP) to test the hypothesis that responsiveness of the renin-angiotensin system, the latter being one of the most powerful vasoconstrictors in the body, is of major importance for LBNP tolerance. Healthy men on a controlled diet (2,822 cal/day, 2 mmol. kg(-1). day(-1) Na(+)) were exposed to 30 min of LBNP from -15 to -50 mmHg. LBNP was uneventful for seven men [25 +/- 2 yr, high-tolerance (HiTol) group], but eight men (26 +/- 3 yr) reached presyncope after 11 +/- 1 min [P < 0.001, low-tolerance (LoTol) group]. Mean arterial pressure (MAP) did not change measurably, but central venous pressure and left atrial diameter decreased similarly in both groups (5-6 mmHg, by approximately 30%, P < 0.05). Control (0 mmHg LBNP) hormone concentrations were similar between groups, however, p(RA) differed between them (LoTol 0.6 +/- 0.1, HiTol 1.2 +/- 0.1 ng ANG I. ml(-1). h(-1), P < 0.05). LBNP increased (P < 0. 05) p(RA) and p(ANG II), respectively, more in the HiTol group (9.9 +/- 2.2 ng ANG I. ml(-1). h(-1) and 58 +/- 12 pg/ml) than in LoTol subjects (4.3 +/- 0.9 ng ANG I. ml(-1). h(-1) and 28 +/- 6 pg/ml). In contrast, the increase in p(VP) was higher (P < 0.05) in the LoTol than in the HiTol group. The increases (P < 0.05) for p(NE) were nonsignificant between groups, and p(ET-1) remained unchanged. Thus there may be a causal relationship between attenuated activation of p(RA) and p(ANG II) and presyncope, with p(VP) being a possible cofactor. Measurement of resting p(RA) may be of predictive value for those with lower hypotensive tolerance.     

Effect of lower body negative pressure on orthostatic tolerance and cardiac function during 21 days head-down tilt bed rest

The purpose of the present study was to investigate the changes of orthostatic tolerance and cardiac function during 21 d head-down tilt (HDT) bed rest and effect of lower body negative pressure in the first and the last week in humans. Twelve healthy male volunteers were exposed to -6 degrees HDT bed rest for 21 d. Six subjects received -30 mmHg LBNP sessions for 1 h per day from the 1st to the 7th day and from the 15th to the 21st day of the HDT, and six others served as control. Orthostatic tolerance was assessed by means of standard tilt test. Stroke volume (SV), cardiac output (CO), preejection period (PEP) and left ventricular ejection time (LVET) were measured before and during HDT. Before HDT, all the subjects in the two groups completed the tilt tests. After 10 d and 21 d of HDT, all the subjects of the control group and one subject of the LBNP group could not complete the tilt test due to presyncopal or syncopal symptoms. The mean upright time in the control group (15.0 +/- 3.2 min) was significantly shorter than those in the LBNP group (19.7 +/- 0.9 min). SV and CO decreased significantly in the control group on days 3 and 10 of HDT, but remained unchanged throughout HDT in the LBNP group. A significant increase in PEP/LVET was observed on days 3 and 14 of HDT in both groups. The PEP/LVET in the LBNP group was significantly lower on day 3 of HDT, while LVET in the LBNP group was significantly higher on days 3, 7 and 14 of HDT than those in the control group. The results of this study suggest that brief daily LBNP sessions used in the first and the last weeks of 21 d HDT bed rest were effective in diminished the effect of head-down tilt on orthostatic tolerance, and LBNP might partially improve cardiac pumping function and cardiac systole function.     

Internal synchronization of the main 0.1-Hz rhythms in the autonomic control of the cardiovascular system

Synchronization parameters of 0.1-Hz rhythms isolated from the heart rate and the oscillations of the blood volume in microcirculatory vessels were studied in 12 healthy subjects and 32 patients with acute myocardial infarction. Recordings of the electrocardiogram and the pulsogram from the distal phalanx of the index finger, as well as mechanical recording of respiration with the body in a horizontal position, were performed. In patients with myocardial infarction, the recordings were performed during the first three to five days and the third week after the infarction. Synchronization was tested by plotting phase differences and calculating the total percentage of phase synchronization. Synchronization parameters of 0.1-Hz rhythms were high in healthy subjects. In patients with acute myocardial infarction, synchronization of 0.1-Hz rhythms was considerably poorer. The data obtained suggest that the studied 0.1-Hz rhythms are two independent oscillatory processes that are synchronized in healthy subjects. However, this interaction may be disturbed in cardiovascular pathologies, e.g., myocardial infarction.     

间断下体负压暴露方式对下体负压耐力的影响

目的：探讨不同方式反复下体负压锻炼对下体负压耐力的影响,以期筛选最佳的负压锻炼方式。方法：27名男性健康受试者随机分成3组,分别进行－5.33kPa8min(A组）、6.67kPa4min（B组）、6.67kPa8min（C组）的下体负压锻炼后累积应激指数（CSI）、总耐受时间（DNP）较锻炼前显著提高,A、B组上述指标无显著变化,下体负压暴露时的心率较平静状态显著升高,收缩压显著降低,舒张压无显著变化。结论：经过－6.67kPa/d8min连续8d的间断下体负压可以显著提高下体负压耐力。     

Comparison of muscle sympathetic responses to hemorrhage and lower body negative pressure in humans

We compared changes in muscle sympathetic nerve activity (SNA) during graded lower body negative pressure (LBNP) and 450 ml of hemorrhage in nine healthy volunteers. During LBNP, central venous pressure (CVP) decreased from 6.1 +/- 0.4 to 4.5 +/- 0.5 (LBNP -5 mmHg), 3.4 +/- 0.6 (LBNP -10 mmHg), and 2.3 +/- 0.6 mmHg (LBNP -15 mmHg), and there were progressive increases in SNA at each level of LBNP. The slope relating percent change in SNA to change in CVP during LBNP (mean +/- SE) was 27 +/- 11%/mmHg. Hemorrhage of 450 ml at a mean rate of 71 +/- 5 ml/min decreased CVP from 6.1 +/- 0.5 to 3.7 +/- 0.5 mmHg and increased SNA by 47 +/- 11%. The increase in SNA during hemorrhage was not significantly different from the increase in SNA predicted by the slope relating percent change in SNA to change in CVP during LBNP. These data show that nonhypotensive hemorrhage causes sympathoexcitation and that sympathetic responses to LBNP and nonhypotensive hemorrhage are similar in humans.     

Human cardiovascular reactions to simulated hypovolaemia, modified by the opiate antagonist naloxone

Six healthy males were exposed to 20 mm Hg lower body negative pressure (LBNP) for 8 min followed by 40 mm Hg LBNP for 8 min. Naloxone (0.1 mg.kg-1) was injected intravenously during a 1 h resting period after which the LBNP protocol was repeated. Systolic, mean, and diastolic arterial blood pressures (SAP, MAP, DAP), and central venous pressure (CVP) were obtained using indwelling catheters. Cardiac output (CO), forearm blood flow (FBF), heart rate (HR), left ventricular ejection time (LVET), and electromechanical systole (EMS) were measured non-invasively. Pulse pressure (PP), stroke volume (SV), total peripheral resistance (TPR), forearm vascular resistance (FVR), systolic ejection rate (SER), pre-ejection period (PEP), PEP/LVET and indices for the systolic time intervals (LVETI, EMSI, PEPI) were calculated. During the second LBNP exposure, only two parameters differed from the pre-injection values: DAP at LBNP = 40 mm Hg increased from 60.0 +/- 4.8 mm Hg to 64.8 +/- 4.1 mm Hg (N = 4, p less than 0.02) and LVETI at LBNP = 20 mm Hg increased from 384.4 +/- 5.2 ms to 396.8 +/- 6.2 ms (N = 6, p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)     

Aspects of control of the cardiovascular-respiratory system during orthostatic stress induced by lower body negative pressure

This paper considers a model developed to study the cardiovascular control system response to orthostatic stress as induced by two variations of lower body negative pressure (LBNP) experiments. This modeling approach has been previously applied to study control responses to transition from rest to aerobic exercise, to transition to non-REM sleep and to orthostatic stress as produced by the head up tilt (HUT) experiment. LBNP induces a blood volume shift because negative pressure changes the volume loading characteristics of the compartment which is subject to the negative pressure. This volume shift induces a fall in blood pressure which must be counteracted by a complicated control response involving a variety of mechanisms of the cardiovascular control system. There are a number of medical issues connected to these questions such as orthostatic intolerance in the elderly resulting in dizziness or fainting during the transition from sitting to standing. The model presented here is used to study the interaction of changes in systemic resistance, unstressed venous volume, venous compliance, heart rate, and contractility in the control of orthostatic stress. The overall short term response depends on a combination of these physiological reactions which may vary from individual to individual. There remain open questions about which factors have greater importance. The model simulations are compared to experimental data collected for LBNP exerted from the hips to feet and from ribs to feet.     

Interaction of the vestibular system and baroreflexes on sympathetic nerve activity in humans

Muscle sympathetic nerve activity (MSNA) is altered by vestibular otolith stimulation. This study examined interactive effects of the vestibular system and baroreflexes on MSNA in humans. In study 1, MSNA was measured during 4 min of lower body negative pressure (LBNP) at either -10 or -30 mmHg with subjects in prone posture. During the 3rd min of LBNP, subjects lowered their head over the end of a table (head-down rotation, HDR) to engage the otolith organs. The head was returned to baseline upright position during the 4th min. LBNP increased MSNA above baseline during both trials with greater increases during the -30-mmHg trial. HDR increased MSNA further during the 3rd min of LBNP at -10 and -30 mmHg (Delta32% and Delta34%, respectively; P < 0.01). MSNA returned to pre-HDR levels during the 4th min of LBNP when the head was returned upright. In study 2, MSNA was measured during HDR, LBNP, and simultaneously performed HDR and LBNP. The sum of MSNA responses during individual HDR and LBNP trials was not significantly different from that observed during HDR and LBNP performed together (Delta131 +/- 28 vs. Delta118 +/- 47 units and Delta340 +/- 77 vs. Delta380 +/- 90 units for the -10 and -30 trials, respectively). These results demonstrate that vestibular otolith stimulation can increase MSNA during unloading of the cardiopulmonary and arterial baroreflexes. Also, the interaction between the vestibulosympathetic reflex and baroreflexes is additive in humans. These studies indicate that the vestibulosympathetic reflex may help defend against orthostatic challenges in humans by increasing sympathetic outflow.     

Characterization of the active site and a unique uncompetitive inhibitor of the PPM1-type protein phosphatase PPM1D

Protein phosphatase magnesium-dependent 1, delta (PPM1D) is a member of the PPM1 (formerly PP2C) protein phosphatase family, and is induced in response to DNA damage. The overexpression of PPM1D is thought to exert oncogenic effects through the inhibition of tumor suppressor proteins. PPM1D shows high selectivity for the primary sequence in its substrates when compared with other phosphatases, but the mechanisms underlying substrate recognition by this enzyme is not clearly known. In our present study we wished to identify the active center and further elucidate the substrate preference of PPM1D, and to this end performed sequence alignments among the human PPM1 type phosphatases. The results of this analysis clearly showed that the putative active site residues of PPM1D are highly conserved among the PPM1 family members. Phosphatase analyses using PPM1D mutants further identified the metal-chelating residues and a phosphate binding residue. In kinetic analyses using a series of phosphorylated p53 peptide analogs, the introduction of acidic residues into the region flanking the sites of dephosphorylation enhanced their affinity with PPM1D. Homology modeling of PPM1D also revealed that PPM1D contains two characteristic loops, a Pro-residue rich loop on the opposite side of the active site and a basic-residue rich loop in the vicinity of the active site in the catalytic domain. Interestingly, nonhydrolyzable AP4-3E peptides derived from the acidic p53 peptide analogs very effectively blocked PPM1D activity in an uncompetitive manner, suggesting that AP4-3E peptides may be useful lead compounds in the development of novel inhibitors of PPM1D.     

Laser-Doppler flowmetry reveals rapid perfusion changes in adipose tissue of lean and obese females

The present study aimed to evaluate adipose tissue blood flow (ATBF) by means of laser-Doppler flowmetry (LDF) in humans. Lower body negative pressure (LBNP) and straining known to affect epidermal blood flow through the autonomic nervous system were performed in 11 lean and 11 obese female volunteers. ATBF changes were compared between both groups and also discriminated from skin blood flow (SBF) responses of the immediate vicinity. Additionally, LDF measurements were compared with flow measurements using (133)xenon washout in 10 lean subjects during whole body cooling. LDF estimations of SBF and ATBF showed a positive correlation to (133)Xe during cooling. SBF and ATBF were reduced to the same extent in both lean and obese subjects during LBNP. Straining induced divergent changes in SBF and ATBF: initially SBF decreased while ATBF increased, but toward the end of straining SBF increased above baseline and ATBF returned down to baseline level. Those changes were similar in both weight groups. Interestingly, only in obese subjects, both LBNP and straining were followed by ATBF augmentation, while SBF levels remained stable. In conclusion, LDF compares with (133)Xe washout in monitoring ATBF during tonic perfusion changes. Its strength, however, lies in the detection of rapid flow alterations within the subcutaneous tissue, allowing the evaluation of reflex responses of the subcutaneous microcirculation. Interestingly, those rapid changes in SBF and ATBF can be both concordant and discordant. With regard to ATBF, vasoconstrictor components of the reflex responses were similar in lean and obese subjects, whereas vasodilatory responses were more pronounced in obese volunteers.     

Effect of lymphatic outflow pressure on lymphatic albumin transport in humans.

The effects of posture on the lymphatic outflow pressure and lymphatic return of albumin were examined in 10 volunteers. Lymph flow was stimulated with a bolus infusion of isotonic saline (0.9%, 12.6 ml/kg body wt) under four separate conditions: upright rest (Up), upright rest with lower body positive pressure (LBPP), supine rest (Sup), and supine rest with lower body negative pressure (LBNP). The increase in plasma albumin content (Delta Alb) during the 2 h after bolus saline infusion was greater in Up than in LBPP: 82.9 +/- 18.5 vs. -28.4 mg/kg body wt. Delta Alb was greater in LBNP than in Sup: 92.6 vs. -22.5 +/- 18.9 mg/kg body wt (P < 0.05). The greater Delta Alb in Up and Sup with LBNP were associated with a lower estimated lymphatic outflow pressure on the basis of the difference in central venous pressure (Delta CVP). During LBPP, CVP was increased compared with Up: 3.8 +/- 1.4 vs. -1.2 +/- 1.2 mmHg. During LBNP, CVP was reduced compared with Sup: -3.0 +/- 2.2 vs. 1.7 +/- 1.0 mmHg. The translocation of protein into the vascular space after bolus saline infusion reflects lymph return of protein and is higher in Up than in Sup. Modulation of CVP with LBPP or LBNP in Up and Sup, respectively, reversed the impact of posture on lymphatic outflow pressure. Thus posture-dependent changes in lymphatic protein transport are modulated by changes in CVP through its mechanical impact on lymphatic outflow pressure.     

Haemodynamic responses to nonhypotensive central hypovolaemia induced by lower body negative pressure in men and women.

Haemodynamic responses to low levels of lower body negative pressure (LBNP) were investigated in two groups of healthy, normotensive volunteers (8 men and 8 women) during two repeated experimental runs on two occasions, the latter determined by the different phases of the menstrual cycle in the women. The data consisted of systolic blood pressure (SBP), diastolic blood pressure (DBP) and mean blood pressure (MBP), pulse rate (fc), forearm blood flow (FBF) and forearm vascular conductance (FC). The resting cardiovascular status was similar in men and women, except that women had a significantly higher fc than men. LBNP (1.3, 2.7 and 4 kPa) had no significant effect on any BP variable or on fc. However, FBF and FC were reduced at all levels of LBNP. Significant overshoots in FBF and FC were seen in all subjects following the release of LBNP of 2.7 and 4 kPa and, in most cases, after release of LBNP of 1.3 kPa. There were no significant gender differences in any of the responses to LBNP. Furthermore, none of the cardiovascular variables measured showed significant differences between the follicular and luteal phases of the menstrual cycle in women, either at rest or during exposure to LBNP, and the responses in the men on the two occasions were not different. These findings indicate that gender differences in responses to LBNP hypothesized previously are not apparent during and after exposure to low levels of LBNP.