Women have lower tolerance to lower body negative pressure than men

1996 ◽  
Vol 80 (4) ◽  
pp. 1138-1143 ◽  
Author(s):  
D. D. White ◽  
R. W. Gotshall ◽  
A. Tucker
Keyword(s):  
Negative Pressure ◽  
Heart Rate Response ◽  
Lower Body Negative Pressure ◽  
Cardiovascular Response ◽  
Stress Index ◽  
Lower Body ◽  
Men And Women ◽  
Cumulative Stress ◽  
Cardiovascular Variables ◽  
Lower Tolerance

Studies of the cardiovascular response to lower body negative pressure (LBNP) in men and women have suggested that women may have less tolerance to LBNP than men, although tolerance per se was not determined. To investigate the effect of gender on tolerance to LBNP, 10 men 10 women were subjected to increasing levels of LBNP until presyncopal symptoms developed. The cumulative stress index (CSI) score was determined, as were cardiovascular variables. Women had 62% less tolerance to LBNP with a CSI of 412 +/- 43 mmHg/min compared with a CSI of 1,070 +/- 149 mmHg/min for men. Cardiovascular changes associated with LBNP were similar for men and women when expressed relative to the occurrence of presyncope, but women had a higher heart rate response when the data were expressed at absolute levels of LBNP (-30 and -50 mmHg LBNP). Thus men and women had similar cardiovascular adjustments to the LBNP, with the changes in women occurring lower levels of LBNP. These data are important in a consideration of the development of antigravitational countermeasures for women. These data raise questions as to the manner in which blood pools within the lower body in men and women under LBNP.

scholarly journals Differentiating compensatory mechanisms associated with low tolerance to central hypovolemia in women

2019 ◽  
Vol 316 (3) ◽  
pp. H609-H616 ◽  
Author(s):  
Taylor Elyse Schlotman ◽  
Kevin S. Akers ◽  
Shawn C. Nessen ◽  
Victor A. Convertino
Keyword(s):  
Blood Volume ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Reduction Rate ◽  
Lower Body ◽  
Men And Women ◽  
Compensatory Responses ◽  
Arterial Blood ◽  
Compensatory Reserve ◽  
Lower Tolerance

Women generally display lower tolerance to acute central hypovolemia than men. The measurement of compensatory reserve (CRM) is a novel metric that provides information about the sum total of all mechanisms that together work to compensate for the relative blood volume deficit. Hemodynamic decompensation occurs with depletion of the CRM (i.e., 0% CRM). In the present study, we hypothesized that the lower tolerance to progressive central hypovolemia reported in women can be explained by a faster reduction rate in CRM compared with men rather than sex differences in absolute integrated compensatory responses. Continuous, noninvasive measures of CRM were collected from 208 healthy volunteers (107 men and 85 women) who underwent progressive stepwise central hypovolemia induced by lower body negative pressure to the point of presyncope. Comparisons revealed shorter ( P < 0.01) times in female participants compared with male participants to reach 30% and 0% CRM. Similarly, the lower body negative pressure level, represented by the cumulative stress index, was less at 30% and 0% CRM in women compared with men ( P < 0.01). Changes in hemodynamic responses and frequency-domain data (oscillations in cerebral blood flow velocity and mean arterial blood pressure) were similar between men and women at 0% CRM ( P > 0.05). We conclude that compensatory responses to central hypovolemia in women were similar to men but were depleted at a faster rate compared with men. The earlier depletion of the compensatory reserve in women appears to be influenced by failure to maintain adequate cerebral oxygen delivery. NEW & NOTEWORTHY We compared hemodynamic and metabolic responses in men and women to experimentally controlled reductions in central blood volume at physiologically equivalent levels of compensatory reserve. We corroborated previous findings that females have lower tolerance to central hypovolemia than males but demonstrated for the first time that compensatory responses are similar. Our findings suggest lower tolerance to central hypovolemia in women results from reaching critical cerebral delivery of oxygen faster than men.

scholarly journals Hypercapnia-induced increases in cerebral blood flow do not improve lower body negative pressure tolerance during hyperthermia

2013 ◽  
Vol 305 (6) ◽  
pp. R604-R609 ◽  
Author(s):  
Rebekah A. I. Lucas ◽  
James Pearson ◽  
Zachary J. Schlader ◽  
Craig G. Crandall
Keyword(s):  
Negative Pressure ◽  
Cerebral Perfusion ◽  
Lower Body Negative Pressure ◽  
Blood Velocity ◽  
Stress Index ◽  
Gas Mixture ◽  
Lower Body ◽  
Cumulative Stress ◽  
Pressure Tolerance ◽  
End Tidal

Heat-related decreases in cerebral perfusion are partly the result of ventilatory-related reductions in arterial CO2 tension. Cerebral perfusion likely contributes to an individual's tolerance to a challenge like lower body negative pressure (LBNP). Thus increasing cerebral perfusion may prolong LBNP tolerance. This study tested the hypothesis that a hypercapnia-induced increase in cerebral perfusion improves LBNP tolerance in hyperthermic individuals. Eleven individuals (31 ± 7 yr; 75 ± 12 kg) underwent passive heat stress (increased intestinal temperature ∼1.3°C) followed by a progressive LBNP challenge to tolerance on two separate days (randomized). From 30 mmHg LBNP, subjects inhaled either (blinded) a hypercapnic gas mixture (5% CO2, 21% oxygen, balanced nitrogen) or room air (SHAM). LBNP tolerance was quantified via the cumulative stress index (CSI). Mean middle cerebral artery blood velocity (MCAvmean,) and end-tidal CO2 (PetCO2) were also measured. CO2 inhalation of 5% increased PetCO2 at ∼40 mmHg LBNP (by 16 ± 4 mmHg) and at LBNP tolerance (by 18 ± 5 mmHg) compared with SHAM ( P < 0.01). Subsequently, MCAvmean was higher in the 5% CO2 trial during ∼40 mmHg LBNP (by 21 ± 12 cm/s, ∼31%) and at LBNP tolerance (by 18 ± 10 cm/s, ∼25%) relative to the SHAM ( P < 0.01). However, hypercapnia-induced increases in MCAvmean did not alter LBNP tolerance (5% CO2 CSI: 339 ± 155 mmHg × min; SHAM CSI: 273 ± 158 mmHg × min; P = 0.26). These data indicate that inhaling a hypercapnic gas mixture increases cerebral perfusion during LBNP but does not improve LBNP tolerance when hyperthermic.

scholarly journals Small reductions in skin temperature after onset of a simulated hemorrhagic challenge improve tolerance in exercise heat-stressed individuals

2018 ◽  
Vol 315 (3) ◽  
pp. R539-R546
Author(s):  
Claire E. Trotter ◽  
Faith K. Pizzey ◽  
Philip M. Batterson ◽  
Robert A. Jacobs ◽  
James Pearson
Keyword(s):  
Heat Stress ◽  
Mean Arterial Pressure ◽  
Skin Temperature ◽  
Healthy Subjects ◽  
Lower Body Negative Pressure ◽  
Stress Index ◽  
Lower Body ◽  
Vascular Conductance ◽  
Cumulative Stress ◽  
Cutaneous Vascular Conductance

We investigated whether small reductions in skin temperature 60 s after the onset of a simulated hemorrhagic challenge would improve tolerance to lower body negative pressure (LBNP) after exercise heat stress. Eleven healthy subjects completed two trials (High and Reduced). Subjects cycled at ~55% maximal oxygen uptake wearing a warm water-perfused suit until core temperatures increased by ~1.2°C before lying supine and undergoing LBNP to presyncope. LBNP tolerance was quantified as cumulative stress index (CSI; product of each LBNP level multiplied by time; mmHg·min). Skin temperature was similarly elevated from baseline before LBNP and remained elevated 60 s after the onset of LBNP in both High (37.72 ± 0.52°C) and Reduced (37.95 ± 0.54°C) trials (both P < 0.0001). At 60%CSI skin temperature remained elevated in the High trial (37.51 ± 0.56°C) but was reduced to 34.97 ± 0.72°C by the water-perfused suit in the Reduced trial ( P < 0.0001 between trials). Cutaneous vascular conductance was not different between trials [High: 1.57 ± 0.43 vs. Reduced: 1.39 ± 0.38 arbitrary units (AU)/mmHg; P = 0.367] before LBNP but decreased to 0.67 ± 0.19 AU/mmHg at 60%CSI in the Reduced trial while remaining unchanged in the High trial ( P = 0.002 between trials). CSI was higher in the Reduced (695 ± 386 mmHg·min) relative to the High (441 ± 290 mmHg·min; P = 0.023) trial. Mean arterial pressure was not different between trials at presyncope (High: 62 ± 10 vs. Reduced: 62 ± 9 mmHg; P = 0.958). Small reductions in skin temperature after the onset of a simulated hemorrhagic challenge improve LBNP tolerance after exercise heat stress. This may have important implications regarding treatment of an exercise heat-stressed individual (e.g., soldier) who has experienced a hemorrhagic injury.

Use of Lower Body Negative Pressure to Assess Changes in Heart Rate Response to Orthostatic-like Stress During 17 Weeks of Bed Rest

1994 ◽  
Vol 34 (6) ◽  
pp. 563-570 ◽  
Author(s):  
Claire M. Lathers ◽  
John B. Charles ◽  
Victor S. Schneider ◽  
Mary Anne B. Frey ◽  
Suzanne Fortney
Keyword(s):  
Heart Rate ◽  
Negative Pressure ◽  
Heart Rate Response ◽  
Lower Body Negative Pressure ◽  
Bed Rest ◽  
Lower Body

Simulation of cardiovascular response to lower body negative pressure from 0 to -40 mmHg

1994 ◽  
Vol 77 (2) ◽  
pp. 630-640 ◽  
Author(s):  
F. M. Melchior ◽  
R. S. Srinivasan ◽  
P. H. Thullier ◽  
J. M. Clere
Keyword(s):  
Heart Rate ◽  
Negative Pressure ◽  
Baroreflex Sensitivity ◽  
Lower Body Negative Pressure ◽  
Cardiovascular Response ◽  
Left Ventricular ◽  
Diastolic Filling ◽  
Lower Body ◽  
Arterial Baroreflex ◽  
Arterial Baroreflex Sensitivity

This paper presents a mathematical model for simulation of the human cardiovascular response to lower body negative pressure (LBNP) up to -40 mmHg both under normal conditions and when arterial baroreflex sensitivity or leg blood capacity (LBC) is altered. Development of the model assumes that the LBNP response could be explained solely on the bases of 1) blood volume redistribution, 2) left ventricular end-diastolic filling, 3) interaction between left ventricle and peripheral circulation, and 4) modulations of peripheral resistances and heart rate by arterial and cardiopulmonary baroreflexes. The model reproduced well experimental data obtained both under normal conditions and during complete autonomic blockade; thus it is validated for simulation of the cardiovascular response from 0 to -40 mmHg LBNP. We tested the ability of the model to simulate the changes in LBNP response due to a reduction in LBC. To assess these changes experimentally, six healthy men were subjected to LBNP of -15, -30, and -38 mmHg with and without wearing elastic compression stockings. Stockings significantly reduced LBC (from 3.9 +/- 0.3 to 1.8 +/- 0.4 ml/100 ml tissue at -38 mmHg LBNP; P < 0.01) and attenuated the change in heart rate (from 23 +/- 4 to 8 +/- 3% at -38 mmHg LBNP; P < 0.05). The model accurately reproduced this result. The model is useful for assessing the influence of LBC or other parameters such as arterial baroreflex sensitivity in diminishing the orthostatic tolerance of humans after spaceflight, bed rest, or endurance training.

scholarly journals The influence of combined lower body negative pressure and mental stress on cerebral blood flow in men and women

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Angelea H. Young ◽  
Chelsea R. Strong ◽  
William H. Cooke ◽  
Jason R. Carter ◽  
John J. Durocher
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Negative Pressure ◽  
Mental Stress ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Men And Women

Physical fitness and cardiovascular response to lower body negative pressure

1984 ◽  
Vol 56 (1) ◽  
pp. 138-144 ◽  
Author(s):  
P. B. Raven ◽  
D. Rohm-Young ◽  
C. G. Blomqvist
Keyword(s):  
Negative Pressure ◽  
Maximal Exercise ◽  
Lower Body Negative Pressure ◽  
Cardiovascular Response ◽  
Performance Testing ◽  
Young Male ◽  
Reflex Response ◽  
Lower Body ◽  
Maximal Aerobic Capacity ◽  
Endurance Exercise Training

Fourteen young male volunteers (mean age 28.1 yr) underwent maximal exercise performance testing and lower body negative pressure (LBNP) challenge to -50 Torr. Two distinct groups, fit (F, n = 8), mean maximal aerobic capacity (VO2max) = 70.2 +/- 2.6 (SE) ml O2 kg-1 X min-1, and average fit (AF, n = 6), mean VO2 max V 41.3 +/- 2.9 ml O2 kg-1 X min-1, P less than 0.001, were evaluated. Rebreathing CO2 cardiac outputs, heart rate (HR), blood pressure (BP), and leg circumference changes were monitored at each stage of progressive increases in LBNP to -50 Torr. The overall hemodynamic responses of both groups of subjects to LBNP were qualitatively similar to previous findings. There were no differences between F and AF in peripheral venous pooling as shown by a leg compliance (delta leg volume/delta LBNP) for the F of 12.6 +/- 1.1 and for the AF 11.6 +/- 2.0, P greater than 0.05. The F subjects had significantly less tachycardic response [delta HR/delta systolic BP of F = 0.7 beats/Torr] to LBNP to -50 Torr than the AF subjects [delta HR/delta systolic BP of unfit (UF) = 1.36 beats/Torr], P less than 0.05. In addition, overall calculated peripheral vascular resistance was significantly higher in the AF subjects (P less than 0.001), and there was a more marked decrease in systolic BP of the F subjects between the LBN pressures of -32 to -50 Torr. We concluded that the reflex response to central hypovolemia was altered by endurance exercise training.

Skin surface cooling improves orthostatic tolerance in normothermic individuals

2004 ◽  
Vol 286 (1) ◽  
pp. R199-R205 ◽  
Author(s):  
S. Durand ◽  
J. Cui ◽  
K. D. Williams ◽  
C. G. Crandall
Keyword(s):  
Cerebral Blood Flow Velocity ◽  
Lower Body Negative Pressure ◽  
Skin Surface ◽  
Tolerance Test ◽  
Stress Index ◽  
Plasma Norepinephrine ◽  
Orthostatic Tolerance ◽  
Lower Body ◽  
Surface Cooling ◽  
Cumulative Stress

Previous studies suggest that skin surface cooling (SSC) preserves orthostatic tolerance; however, this hypothesis has not been experimentally tested. Thus the purpose of this project was to identify whether SSC improves orthostatic tolerance in otherwise normothermic individuals. Eight subjects underwent two presyncope limited graded lower-body negative pressure (LBNP) tolerance tests. On different days, and randomly assigned, LBNP tolerance was assessed under control conditions and during SSC (perfused 16°C water through tube-lined suit worn by each subject). Orthostatic tolerance was significantly elevated in each individual due to SSC, as evidenced by a significant increase in a standardized cumulative stress index (normothermia 564 ± 58 mmHg·min; SSC 752 ± 58 mmHg·min; P < 0.05). At most levels of LBNP, blood pressure during the SSC tolerance test was significantly greater than during the control test. Furthermore, the reduction in cerebral blood flow velocity was attenuated during some of the early stages of LBNP for the SSC trial. Plasma norepinephrine concentrations were significantly higher during LBNP with SSC, suggesting that SSC may improve orthostatic tolerance through increased sympathetic activity. These data demonstrate that SSC is effective in improving orthostatic tolerance in otherwise normothermic individuals.

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