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.

scholarly journals Skin surface cooling improves orthostatic tolerance following prolonged head-down bed rest

2011 ◽  
Vol 110 (6) ◽  
pp. 1592-1597 ◽  
Author(s):  
David M. Keller ◽  
David A. Low ◽  
Scott L. Davis ◽  
Jeff Hastings ◽  
Craig G. Crandall
Keyword(s):  
Negative Pressure ◽  
Prolonged Exposure ◽  
Lower Body Negative Pressure ◽  
Thermal Conditions ◽  
Bed Rest ◽  
Skin Surface ◽  
Stress Index ◽  
Orthostatic Tolerance ◽  
Thermal Stimulus ◽  
Surface Cooling

Prolonged exposure to microgravity, as well as its ground-based analog, head-down bed rest (HDBR), reduces orthostatic tolerance in humans. While skin surface cooling improves orthostatic tolerance, it remains unknown whether this could be an effective countermeasure to preserve orthostatic tolerance following HDBR. We therefore tested the hypothesis that skin surface cooling improves orthostatic tolerance after prolonged HDBR. Eight subjects (six men and two women) participated in the investigation. Orthostatic tolerance was determined using a progressive lower-body negative pressure (LBNP) tolerance test before HDBR during normothermic conditions and on day 16 or day 18 of 6° HDBR during normothermic and skin surface cooling conditions (randomized order post-HDBR). The thermal conditions were achieved by perfusing water (normothermia ∼34°C and skin surface cooling ∼12–15°C) through a tube-lined suit worn by each subject. Tolerance tests were performed after ∼30 min of the respective thermal stimulus. A cumulative stress index (CSI; mmHg LBNP·min) was determined for each LBNP protocol by summing the product of the applied negative pressure and the duration of LBNP at each stage. HDBR reduced normothermic orthostatic tolerance as indexed by a reduction in the CSI from 1,037 ± 96 mmHg·min to 574 ± 63 mmHg·min ( P < 0.05). After HDBR, skin surface cooling increased orthostatic tolerance (797 ± 77 mmHg·min) compared with normothermia ( P < 0.05). While the reduction in orthostatic tolerance following prolonged HDBR was not completely reversed by acute skin surface cooling, the identified improvements may serve as an important and effective countermeasure for individuals exposed to microgravity, as well as immobilized and bed-stricken individuals.

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.

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.

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 Active and passive heat stress similarly compromise tolerance to a simulated hemorrhagic challenge

2014 ◽  
Vol 307 (7) ◽  
pp. R822-R827 ◽  
Author(s):  
J. Pearson ◽  
R. A. I. Lucas ◽  
Z. J. Schlader ◽  
J. Zhao ◽  
D. Gagnon ◽  
...  
Keyword(s):  
Heat Stress ◽  
Skin Temperature ◽  
Lower Body Negative Pressure ◽  
Stress Index ◽  
Lower Body ◽  
Cumulative Stress ◽  
Hot Environment ◽  
Simulated Hemorrhage ◽  
Exercise Induced ◽  
Skin Temperatures

Passive heat stress increases core and skin temperatures and reduces tolerance to simulated hemorrhage (lower body negative pressure; LBNP). We tested whether exercise-induced heat stress reduces LBNP tolerance to a greater extent relative to passive heat stress, when skin and core temperatures are similar. Eight participants (6 males, 32 ± 7 yr, 176 ± 8 cm, 77.0 ± 9.8 kg) underwent LBNP to presyncope on three separate and randomized occasions: 1) passive heat stress, 2) exercise in a hot environment (40°C) where skin temperature was moderate (36°C, active 36), and 3) exercise in a hot environment (40°C) where skin temperature was matched relative to that achieved during passive heat stress (∼38°C, active 38). LBNP tolerance was quantified using the cumulative stress index (CSI). Before LBNP, increases in core temperature from baseline were not different between trials (1.18 ± 0.20°C; P > 0.05). Also before LBNP, mean skin temperature was similar between passive heat stress (38.2 ± 0.5°C) and active 38 (38.2 ± 0.8°C; P = 0.90) trials, whereas it was reduced in the active 36 trial (36.6 ± 0.5°C; P ≤ 0.05 compared with passive heat stress and active 38). LBNP tolerance was not different between passive heat stress and active 38 trials (383 ± 223 and 322 ± 178 CSI, respectively; P = 0.12), but both were similarly reduced relative to active 36 (516 ± 147 CSI, both P ≤ 0.05). LBNP tolerance is not different between heat stresses induced either passively or by exercise in a hot environment when skin temperatures are similarly elevated. However, LBNP tolerance is influenced by the magnitude of the elevation in skin temperature following exercise induced heat stress.

Skin cooling maintains cerebral blood flow velocity and orthostatic tolerance during tilting in heated humans

2002 ◽  
Vol 93 (1) ◽  
pp. 85-91 ◽  
Author(s):  
Thad E. Wilson ◽  
Jian Cui ◽  
Rong Zhang ◽  
Sarah Witkowski ◽  
Craig G. Crandall
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Heat Stress ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Cerebral Blood Flow Velocity ◽  
Skin Surface ◽  
Orthostatic Tolerance ◽  
Surface Cooling ◽  
Arterial Blood

Orthostatic tolerance is reduced in the heat-stressed human. The purpose of this project was to identify whether skin-surface cooling improves orthostatic tolerance. Nine subjects were exposed to 10 min of 60° head-up tilting in each of four conditions: normothermia (NT-tilt), heat stress (HT-tilt), normothermia plus skin-surface cooling 1 min before and throughout tilting (NT-tiltcool), and heat stress plus skin-surface cooling 1 min before and throughout tilting (HT-tiltcool). Heating and cooling were accomplished by perfusing 46 and 15°C water, respectively, though a tube-lined suit worn by each subject. During HT-tilt, four of nine subjects developed presyncopal symptoms resulting in the termination of the tilt test. In contrast, no subject experienced presyncopal symptoms during NT-tilt, NT-tiltcool, or HT-tiltcool. During the HT-tilt procedure, mean arterial blood pressure (MAP) and cerebral blood flow velocity (CBFV) decreased. However, during HT-tiltcool, MAP, total peripheral resistance, and CBFV were significantly greater relative to HT-tilt (all P< 0.01). No differences were observed in calculated cerebral vascular resistance between the four conditions. These data suggest that skin-surface cooling prevents the fall in CBFV during upright tilting and improves orthostatic tolerance, presumably via maintenance of MAP. Hence, skin-surface cooling may be a potent countermeasure to protect against orthostatic intolerance observed in heat-stressed humans.

Arterial pulse pressure and vasopressin release in humans during lower body negative pressure

1993 ◽  
Vol 264 (5) ◽  
pp. R1024-R1030 ◽  
Author(s):  
P. Norsk ◽  
P. Ellegaard ◽  
R. Videbaek ◽  
C. Stadeager ◽  
F. Jessen ◽  
...  
Keyword(s):  
Pulse Pressure ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Plasma Norepinephrine ◽  
Lower Body ◽  
Arterial Pulse ◽  
Vasopressin Release ◽  
Arterial Pulse Pressure ◽  
Arterial Plasma

The hypothesis was tested that narrowing of arterial pulse pressure (PP) is a determinant of arginine vasopressin (AVP) release in humans. Six normal males completed a two-step lower body negative pressure (LBNP) protocol of -20 and -50 mmHg, respectively, for 10 min each. None of these subjects experienced presyncopal symptoms. Arterial plasma AVP and plasma renin activity (PRA) (at 2-min intervals) only increased subsequent to a decrease in PP (invasive brachial arterial measurements) and stroke volume (ultrasound Doppler technique, n = 4). Simultaneously, mean arterial pressure did not change. A selective decrease in central venous pressure and left atrial diameter (echocardiography, n = 4) at LBNP of -20 mmHg did not affect AVP or PRA, whereas arterial plasma norepinephrine increased (n = 4). During LBNP, significant (P < 0.05) intraindividual linear correlations were observed between log(AVP) and PP in four of the subjects with r values from -0.75 to -0.99 and between log(PRA) and PP in all six subjects with r values from -0.89 to -0.98. In conclusion, these results are in compliance with the hypothesis that narrowing of PP in humans during central hypovolemia is a determinant of AVP and renin release.

scholarly journals Effect of acute hypoxemia on cerebral blood flow velocity control during lower body negative pressure

2018 ◽  
Vol 6 (4) ◽  
pp. e13594 ◽  
Author(s):  
Noud van Helmond ◽  
Blair D. Johnson ◽  
Walter W. Holbein ◽  
Humphrey G. Petersen-Jones ◽  
Ronée E. Harvey ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Flow Velocity ◽  
Negative Pressure ◽  
Blood Flow Velocity ◽  
Cerebral Blood Flow Velocity ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Velocity Control

Effects of 18 days of bed rest on leg and arm venous properties

2004 ◽  
Vol 96 (3) ◽  
pp. 840-847 ◽  
Author(s):  
M. W. P. Bleeker ◽  
P. C. E. De Groot ◽  
J. A. Pawelczyk ◽  
M. T. E. Hopman ◽  
B. D. Levine
Keyword(s):  
Orthostatic Intolerance ◽  
Lower Body Negative Pressure ◽  
Bed Rest ◽  
Venous Occlusion ◽  
Stress Index ◽  
Orthostatic Tolerance ◽  
Venous Compliance ◽  
Venous Flow ◽  
Gravitational Gradients ◽  
Small Change

Venous function may be altered by bed rest deconditioning. Yet the contribution of altered venous compliance to the orthostatic intolerance observed after bed rest is uncertain. The purpose of this study was to assess the effect of 18 days of bed rest on leg and arm (respectively large and small change in gravitational gradients and use patterns) venous properties. We hypothesized that the magnitude of these venous changes would be related to orthostatic intolerance. Eleven healthy subjects (10 men, 1 woman) participated in the study. Before (pre) and after (post) 18 days of 6° head-down tilt bed rest, strain gauge venous occlusion plethysmography was used to assess limb venous vascular characteristics. Leg venous compliance was significantly decreased after bed rest (pre: 0.048 ± 0.007 ml·100 ml-1·mmHg-1, post: 0.033 ± 0.007 ml·100 ml-1·mmHg-1; P < 0.01), whereas arm compliance did not change. Leg venous flow resistance increased significantly after bed rest (pre: 1.73 ± 1.08 mmHg·ml-1·100 ml·min, post: 3.10 ± 1.00 mmHg·ml-1·100 ml·min; P < 0.05). Maximal lower body negative pressure tolerance, which was expressed as cumulative stress index (pressure·time), decreased in all subjects after bed rest (pre: 932 mmHg·min, post: 747 mmHg·min). The decrease in orthostatic tolerance was not related to changes in leg venous compliance. In conclusion, this study demonstrates that after bed rest, leg venous compliance is reduced and leg venous outflow resistance is enhanced. However, these changes are not related to measures of orthostatic tolerance; therefore, alterations in venous compliance do not to play a major role in orthostatic intolerance after 18 days of head-down tilt bed rest.

Hemodynamic Strategies in Blood Pressure Regulation During Orthostatic Challenge in Women

1997 ◽  
Vol 22 (4) ◽  
pp. 351-367
Author(s):  
Tania L. Culham ◽  
Gabrielle K. Savard
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Peripheral Resistance ◽  
Orthostatic Tolerance ◽  
Lower Body ◽  
Orthostatic Challenge ◽  
Carotid Baroreflex

Several studies indicate that carotid baroreflex responsiveness is a good predictor of orthostatic tolerance. Two groups of healthy women with high (HI) and low (LO) carotid baroreflex responsiveness were studied (a) to determine any differences in the level of orthostatic tolerance of the two groups, and (b) to study the hemodynamic strategies used by HI and LO responders to regulate arterial pressure during the orthostatic challenge of lower body negative pressure (LBNP). Orthostatic tolerance was similar between the two groups, whereas the hemodynamic strategies recruited to maintain blood pressure at −40 mmHg LBNP differed: HI responders exhibited greater LBNP-induced decreases in stroke volume and cardiac output, as well as a greater increase in peripheral resistance compared to LO responders (p < .05). In addition, a significant increase in plasma renin activity during LBNP was found in the HI responders only. No significant between-group differences were found in arterial and cardiopulmonary control of vascular resistance or arterial haroreflex control of heart rate during LBNP. Key words: arterial pressure, carotid baroreceptor, lower body negative pressure, orthostatic tolerance, stroke volume

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