Mechanisms of orthostatic intolerance during heat stress

Schlader, Zachary J.; Wilson, Thad E.; Crandall, Craig G.

doi:10.1016/j.autneu.2015.12.005

Cited by 61 publications

(43 citation statements)

References 170 publications

(272 reference statements)

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“…These data directly support previous observations that the increase in blood pressure during a sympathoexcitatory manoeuvre (i.e. the cold pressor test) is attenuated during heat stress (Cui et al, 2010) and also support the findings that heat stress challenges the maintenance of blood pressure during an orthostatic challenge (Schlader et al, 2016b).…”

Section: Heat Stress Attenuates Increases In Vascular Resistance and supporting

confidence: 90%

“…Thus, we speculate that the lack of increase in vascular resistance was not attributable to altered sympathetic activation during heat stress. Rather, our observations are probably related to differential vascular responsiveness to sympathetic activation (Schlader, Wilson, & Crandall, 2016b). For instance, a given dose of phenylephrine (a noradrenaline analogue) results in a diminished increase in vascular resistance during heat stress (Cui, Wilson, & Crandall, 2002).…”

Section: Heat Stress Attenuates Increases In Vascular Resistance and mentioning

confidence: 76%

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Face cooling reveals a relative inability to increase cardiac parasympathetic activation during passive heat stress

Schlader

O'Leary

Sackett

et al. 2018

Experimental Physiology

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We tested the hypothesis that passive heat stress attenuates the increase in cardiac parasympathetic stimulation, vascular resistance and blood pressure evoked by face cooling. During normothermia and when intestinal temperature was elevated by 1.0 ± 0.2°C, 10 healthy young adults underwent 3 min of face cooling. Face cooling was accomplished by placing a 2.5 litre bag of ice water (0 ± 0°C) over the cheeks, eyes and forehead. Primary variables included forehead skin temperature, mean arterial pressure and systemic, forearm and cutaneous vascular resistances. Indices of heart rate variability in the time domain provided an index of cardiac parasympathetic activity. The magnitude of reduction in forehead skin temperature during face cooling was slightly greater during normothermia (-17.6 ± 1.9 versus -16.3 ± 3.0°C, P = 0.03). Increases in heart rate variability evoked by face cooling were attenuated during heat stress. Changes in systemic, forearm and cutaneous vascular resistances during face cooling were virtually abolished during heat stress (P < 0.01). However, when forearm and vascular data were reported as conductance, differences between normothermia and heat stress were not apparent (P ≥ 0.62). Nevertheless, the increase in mean arterial pressure was attenuated during heat stress with face cooling (at 3 min: 2 ± 7 mmHg) compared with normothermia (at 3 min: 19 ± 7 mmHg, P < 0.01). These data indicate that passive heat stress attenuates face cooling-evoked increases in cardiac parasympathetic activation, vascular resistance and blood pressure. However, they also indicate that changes in indices of vascular resistance do not always reflect equivalent changes in conductance.

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Section: Heat Stress Attenuates Increases In Vascular Resistance and supporting

confidence: 90%

Section: Heat Stress Attenuates Increases In Vascular Resistance and mentioning

confidence: 76%

Face cooling reveals a relative inability to increase cardiac parasympathetic activation during passive heat stress

Schlader

O'Leary

Sackett

et al. 2018

Experimental Physiology

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“…The mechanisms by which heat stress, with or without dehydration, reduces tolerance to simulated hemorrhage are multifactorial (33). The reduction in compensatory reserve with passive heating and exercise-induced dehydration demonstrates the ability of the compensatory reserve index to capture physiological changes that occur with these conditions.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Passive Heat Stress and Exercise-Induced Dehydration on the Compensatory Reserve During Simulated Hemorrhage

Gagnon

Schlader

Adams

et al. 2016

Shock

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Compensatory reserve represents the proportion of physiological responses engaged to compensate for reductions in central blood volume before the onset of decompensation. We hypothesized that compensatory reserve would be reduced by hyperthermia and exercise-induced dehydration, conditions often encountered on the battlefield. Twenty healthy males volunteered for two separate protocols during which they underwent lower-body negative pressure (LBNP) to hemodynamic decompensation (systolic blood pressure <80 mm Hg). During protocol #1, LBNP was performed following a passive increase in core temperature of ~1.2°C (HT) or a normothermic time-control period (NT). During protocol #2, LBNP was performed following exercise during which: fluid losses were replaced (hydrated), fluid intake was restricted and exercise ended at the same increase in core temperature as hydrated (isothermic dehydrated), or fluid intake was restricted and exercise duration was the same as hydrated (time-match dehydrated). Compensatory reserve was estimated with the compensatory reserve index (CRI), a machine-learning algorithm that extracts features from continuous photoplethysmograph signals. Prior to LBNP, CRI was reduced by passive heating [NT: 0.87 (SD 0.09) vs. HT: 0.42 (SD 0.19) units, P <0.01] and exercise-induced dehydration [hydrated: 0.67 (SD 0.19) vs. isothermic dehydrated: 0.52 (SD 0.21) vs. time-match dehydrated: 0.47 (SD 0.25) units; P <0.01 vs. hydrated]. During subsequent LBNP, CRI decreased further and its rate of change was similar between conditions. CRI values at decompensation did not differ between conditions. These results suggest that passive heating and exercise-induced dehydration limit the body’s physiological reserve to compensate for further reductions in central blood volume.

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“…To compensate, the body reacts by raising heart rate in order to maintain blood pressure (Schlader and Wilson, 2016).…”

Section: Discussionmentioning

confidence: 99%

Students’ blood pressure and heart rate in learning environments with thermal changes

Carvalho¹,

Barroso²,

Silva³

et al. 2018

IJOOES

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The increase in global temperature in recent years (which is likely to continue) has the power to affect the temperatures of indoor workplaces. This increase may in turn, be reflected in human performance. The present article analyzes the relationship between air temperature, blood pressure and heart rate variation in students in a learning environment through Video Display Terminals (VDT), located in northeastern Brazil. The thermal conditions were analyzed during three consecutive days, according to ISO 7726: 1998; in the group of students who underwent changes in indoor air temperature, their blood pressure and heart rate were also measured. When the air temperature was of 20ºC, 24% of the subjects' heart rate exceeded 100bpm, while for 30 °C this number reached 51%. The results revealed changes in diastolic blood pressure and heart rate when air temperature increases.

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Mechanisms of orthostatic intolerance during heat stress

Cited by 61 publications

References 170 publications

Face cooling reveals a relative inability to increase cardiac parasympathetic activation during passive heat stress

Face cooling reveals a relative inability to increase cardiac parasympathetic activation during passive heat stress

The Effect of Passive Heat Stress and Exercise-Induced Dehydration on the Compensatory Reserve During Simulated Hemorrhage

Students’ blood pressure and heart rate in learning environments with thermal changes

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