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 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.

Bradykinin does not mediate cutaneous active vasodilation during heat stress in humans

2002 ◽  
Vol 93 (4) ◽  
pp. 1215-1221 ◽  
Author(s):  
D. L. Kellogg ◽  
Y. Liu ◽  
K. McAllister ◽  
C. Friel ◽  
P. E. Pérgola
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Receptor Antagonist ◽  
Healthy Subjects ◽  
Ringer Solution ◽  
Vascular Conductance ◽  
Doppler Flowmetry ◽  
Hoe 140 ◽  
Control Body ◽  
Cutaneous Vascular Conductance

To test the hypothesis that bradykinin effects cutaneous active vasodilation during hyperthermia, we examined whether the increase in skin blood flow (SkBF) during heat stress was affected by blockade of bradykinin B2 receptors with the receptor antagonist HOE-140. Two adjacent sites on the forearm were instrumented with intradermal microdialysis probes for local delivery of drugs in eight healthy subjects. HOE-140 was dissolved in Ringer solution (40 μM) and perfused at one site, whereas the second site was perfused with Ringer alone. SkBF was monitored by laser-Doppler flowmetry (LDF) at both sites. Mean arterial pressure (MAP) was monitored from a finger, and cutaneous vascular conductance (CVC) was calculated (CVC = LDF/MAP). Water-perfused suits were used to control body temperature and evoke hyperthermia. After hyperthermia, both microdialysis sites were perfused with 28 mM nitroprusside to effect maximal vasodilation. During hyperthermia, CVC increased at HOE-140 (69 ± 2% maximal CVC, P < 0.01) and untreated sites (65 ± 2% maximal CVC, P < 0.01). These responses did not differ between sites ( P > 0.05). Because the bradykinin B2-receptor antagonist HOE-140 did not alter SkBF responses to heat stress, we conclude that bradykinin does not mediate cutaneous active vasodilation.

The magnitude of heat stress-induced reductions in cerebral perfusion does not predict heat stress-induced reductions in tolerance to a simulated hemorrhage

2013 ◽  
Vol 114 (1) ◽  
pp. 37-44 ◽  
Author(s):  
Joshua F. Lee ◽  
Michelle L. Harrison ◽  
Skyler R. Brown ◽  
R. Matthew Brothers
Keyword(s):  
Heat Stress ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Cerebral Perfusion ◽  
Lower Body Negative Pressure ◽  
Small Difference ◽  
Blood Velocity ◽  
Stress Index ◽  
Cumulative Stress ◽  
Simulated Hemorrhage

The mechanisms responsible for heat stress-induced reductions in tolerance to a simulated hemorrhage are unclear. Although a high degree of variability exists in the level of reduction in tolerance amongst individuals, syncope will always occur when cerebral perfusion is inadequate. This study tested the hypothesis that the magnitude of reduction in cerebral perfusion during heat stress is related to the reduction in tolerance to a lower body negative pressure (LBNP) challenge. On different days (one during normothermia and the other after a 1.5°C rise in internal temperature), 20 individuals were exposed to a LBNP challenge to presyncope. Tolerance was quantified as a cumulative stress index, and the difference in cumulative stress index between thermal conditions was used to categorize individuals most (large difference) and least (small difference) affected by the heat stress. Cerebral perfusion, as indexed by middle cerebral artery blood velocity, was reduced during heat stress compared with normothermia ( P < 0.001); however, the magnitude of reduction did not differ between groups ( P = 0.51). In the initial stage of LBNP during heat stress (LBNP 20 mmHg), middle cerebral artery blood velocity and end-tidal Pco2 were lower; whereas, heart rate was higher in the large difference group compared with small difference group ( P < 0.05 for all). These data indicate that variability in heat stress-induced reductions in tolerance to a simulated hemorrhage is not related to reductions in cerebral perfusion in this thermal condition. However, responses affecting cerebral perfusion during LBNP may explain the interindividual variability in tolerance to a simulated hemorrhage when heat stressed.

scholarly journals Plasma hyperosmolality improves tolerance to combined heat stress and central hypovolemia in humans

2017 ◽  
Vol 312 (3) ◽  
pp. R273-R280 ◽  
Author(s):  
Daniel Gagnon ◽  
Steven A. Romero ◽  
Hai Ngo ◽  
Paula Y. S. Poh ◽  
Craig G. Crandall
Keyword(s):  
Heart Rate ◽  
Heat Stress ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve Activity ◽  
Lower Body Negative Pressure ◽  
Muscle Sympathetic Nerve Activity ◽  
Plasma Osmolality ◽  
Lower Body ◽  
Nerve Activity

Heat stress profoundly impairs tolerance to central hypovolemia in humans via a number of mechanisms including heat-induced hypovolemia. However, heat stress also elevates plasma osmolality; the effects of which on tolerance to central hypovolemia remain unknown. This study examined the effect of plasma hyperosmolality on tolerance to central hypovolemia in heat-stressed humans. With the use of a counterbalanced and crossover design, 12 subjects (1 female) received intravenous infusion of either 0.9% iso-osmotic (ISO) or 3.0% hyperosmotic (HYPER) saline. Subjects were subsequently heated until core temperature increased ~1.4°C, after which all subjects underwent progressive lower-body negative pressure (LBNP) to presyncope. Plasma hyperosmolality improved LBNP tolerance (ISO: 288 ± 193 vs. HYPER: 382 ± 145 mmHg × min, P = 0.04). However, no differences in mean arterial pressure ( P = 0.10), heart rate ( P = 0.09), or muscle sympathetic nerve activity ( P = 0.60, n = 6) were observed between conditions. When individual data were assessed, LBNP tolerance improved ≥25% in eight subjects but remained unchanged in the remaining four subjects. In subjects who exhibited improved LBNP tolerance, plasma hyperosmolality resulted in elevated mean arterial pressure (ISO: 62 ± 10 vs. HYPER: 72 ± 9 mmHg, P < 0.01) and a greater increase in heart rate (ISO: +12 ± 24 vs. HYPER: +23 ± 17 beats/min, P = 0.05) before presyncope. No differences in these variables were observed between conditions in subjects that did not improve LBNP tolerance (all P ≥ 0.55). These results suggest that plasma hyperosmolality improves tolerance to central hypovolemia during heat stress in most, but not all, individuals.

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 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.

Neurohormonal responses to oscillatory lower body negative pressure in healthy subjects

2021 ◽  
Author(s):  
Akanksha Singh ◽  
Shival Srivastav ◽  
Kavita Yadav ◽  
Dinu S. Chandran ◽  
Ashok Kumar Jaryal ◽  
...  
Keyword(s):  
Negative Pressure ◽  
Healthy Subjects ◽  
Lower Body Negative Pressure ◽  
Lower Body

Reflex control of the cutaneous circulation during passive body core heating in humans

2000 ◽  
Vol 88 (5) ◽  
pp. 1756-1764 ◽  
Author(s):  
Jochen K. Peters ◽  
Takeshi Nishiyasu ◽  
Gary W. Mack
Keyword(s):  
Blood Pressure ◽  
Heat Stress ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Laser Doppler ◽  
Vascular Conductance ◽  
Arterial Blood ◽  
Body Core ◽  
Doppler Techniques ◽  
The Impact

The impact of body core heating on the interaction between the cutaneous and central circulation during blood pressure challenges was examined in eight adults. Subjects were exposed to −10 to −90 mmHg lower body negative pressure (LBNP) in thermoneutral conditions and −10 to −60 mmHg LBNP during heat stress. We measured forearm vascular conductance (FVC; ml ⋅ min−1 ⋅ 100 ml−1 ⋅ mmHg−1) by plethysmography; cutaneous vascular conductance (CVC) by laser-Doppler techniques; and central venous pressure, arterial blood pressure, and cardiac output by impedance cardiography. Heat stress increased FVC from 5.7 ± 0.9 to 18.8 ± 1.3 conductance units (CU) and CVC from 0.21 ± 0.07 to 1.02 ± 0.20 CU. The FVC-CVP relationship was linear over the entire range of LBNP and was shifted upward during heat stress with a slope increase from 0.46 ± 0.10 to 1.57 ± 0.3 CU/mmHg CVP ( P < 0.05). Resting CVP was lower during heat stress (6.3 ± 0.6 vs. 7.7 ± 0.6 mmHg; P < 0.05) but fell to similar levels during LBNP as in normothermic conditions. Data analysis indicates an increased capacity, but not sensitivity, of peripheral baroreflex responses during heat stress. Laser-Doppler techniques detected thermoregulatory responses in the skin, but no significant change in CVC occurred during mild-to-moderate LBNP. Interestingly, very high levels of LBNP produced cutaneous vasodilation in some subjects.

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