Cholinergic nerve contribution to cutaneous active vasodilation in response to exercise heat‐loading is similar to passive whole‐body heat‐loading

Context: Conditions such as osteoarthritis, obesity, and spinal cord injury limit the ability of patients to exercise, preventing them from experiencing many well-documented physiologic stressors. Recent evidence indicates that some of these stressors might derive from exercise-induced body temperature increases. Objective: To determine whether whole-body heat stress without exercise triggers cardiovascular, hormonal, and extra-cellular protein responses of exercise. Design: Randomized controlled trial. Setting: University research laboratory. Patients or Other Participants: Twenty-five young, healthy adults (13 men, 12 women; age = 22.1 ± 2.4 years, height = 175.2 ± 11.6 cm, mass = 69.4 ± 14.8 kg, body mass index = 22.6 ± 4.0) volunteered. Intervention(s): Participants sat in a heat stress chamber with heat (73°C) and without heat (26°C) stress for 30 minutes on separate days. We obtained blood samples from a subset of 13 participants (7 men, 6 women) before and after exposure to heat stress. Main Outcome Measure(s): Extracellular heat shock protein (HSP72) and catecholamine plasma concentration, heart rate, blood pressure, and heat perception. Results: After 30 minutes of heat stress, body temperature measured via rectal sensor increased by 0.8°C. Heart rate increased linearly to 131.4 ± 22.4 beats per minute (F6,24 = 186, P < .001) and systolic and diastolic blood pressure decreased by 16 mm Hg (F6,24 = 10.1, P < .001) and 5 mm Hg (F6,24 = 5.4, P < .001), respectively. Norepinephrine (F1,12 = 12.1, P = .004) and prolactin (F1,12 = 30.2, P < .001) increased in the plasma (58% and 285%, respectively) (P < .05). The HSP72 (F1,12 = 44.7, P < .001) level increased with heat stress by 48.7% ± 53.9%. No cardiovascular or blood variables showed changes during the control trials (quiet sitting in the heat chamber with no heat stress), resulting in differences between heat and control trials. Conclusions: We found that whole-body heat stress triggers some of the physiologic responses observed with exercise. Future studies are necessary to investigate whether carefully prescribed heat stress constitutes a method to augment or supplement exercise.

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Effect of high local temperature on reflex cutaneous vasodilation

Journal of Applied Physiology ◽

10.1152/jappl.1984.57.1.191 ◽

1984 ◽

Vol 57 (1) ◽

pp. 191-196 ◽

Cited By ~ 174

Author(s):

W. F. Taylor ◽

J. M. Johnson ◽

D. O'Leary ◽

M. K. Park

Keyword(s):

Blood Flow ◽

Whole Body ◽

Ambient Conditions ◽

Basal Tone ◽

Forearm Skin ◽

Local Warming ◽

C 30 ◽

Average Rise ◽

Reflex Cutaneous Vasodilation ◽

Body Heat

We examined the effect of high local forearm skin temperature (Tloc) on reflex cutaneous vasodilator responses to elevated whole-body skin (Tsk) and internal temperatures. One forearm was locally warmed to 42 degrees C while the other was left at ambient conditions to determine if a high Tloc could attenuate or abolish reflex vasodilation. Forearm blood flow (FBF) was monitored in both arms, increases being indicative of increases in skin blood flow (SkBF). In one protocol, Tsk was raised to 39–40degrees C 30 min after Tloc in one arm had been raised to 42 degrees C. In a second protocol, Tsk andTloc were elevated simultaneously. In protocol 1, the locally warmed arm showed little or no change in blood flow in response to increasing Tsk and esophageal temperature (average rise = 0.76 +/-1.18 ml X 100 ml-1 X min-1), whereas FBF in the normothermic arm rose by an average of 8.84 +/- 3.85 ml X 100 ml-1 X min-1. In protocol 2, FBF in the normothermic arm converged with that in the warmed arm in three of four cases but did not surpass it. We conclude that local warming to 42 degrees C for 35–55 min prevents reflex forearm cutaneous vasodilator responses to whole-body heat stress. The data strongly suggest that this attenuation is via reduction or abolition of basal tone in the cutaneous arteriolar smooth muscle and that at a Tloc of 42 degrees C a maximum forearm SkBF has been achieved. Implicit in this conclusion is that local warming has been applied for a duration sufficient to achieve a plateau in FBF.

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The independent effect of sex on whole‐body heat loss during exercise in the heat

The FASEB Journal ◽

10.1096/fasebj.25.1_supplement.1053.12 ◽

2011 ◽

Vol 25 (S1) ◽

Author(s):

Daniel Gagnon ◽

Glen P Kenny

Keyword(s):

Heat Loss ◽

Whole Body ◽

Independent Effect ◽

Body Heat

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Carotid baroreflex control of heart rate is enhanced during whole‐body heat stress

The FASEB Journal ◽

10.1096/fasebj.27.1_supplement.1118.33 ◽

2013 ◽

Vol 27 (S1) ◽

Author(s):

Davor Krnjajic ◽

Cory L Butts ◽

W Shane Warren ◽

Mitchel R Samels ◽

David M Keller

Keyword(s):

Heart Rate ◽

Heat Stress ◽

Whole Body ◽

Baroreflex Control ◽

Carotid Baroreflex ◽

Whole Body Heat Stress ◽

Body Heat

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Roles of nitric oxide synthase isoforms in cutaneous vasodilation induced by local warming of the skin and whole body heat stress in humans

Journal of Applied Physiology ◽

10.1152/japplphysiol.00690.2009 ◽

2009 ◽

Vol 107 (5) ◽

pp. 1438-1444 ◽

Cited By ~ 90

Author(s):

Dean L. Kellogg ◽

Joan L. Zhao ◽

Yubo Wu

Keyword(s):

Nitric Oxide ◽

Heat Stress ◽

No Synthase ◽

Whole Body ◽

Doppler Flowmetry ◽

Vasodilator Response ◽

Cutaneous Vasodilation ◽

Forearm Skin ◽

Whole Body Heat Stress ◽

Body Heat

Nitric oxide (NO) participates in the cutaneous vasodilation caused by increased local skin temperature (Tloc) and whole body heat stress in humans. In forearm skin, endothelial NO synthase (eNOS) participates in vasodilation due to elevated Tloc and neuronal NO synthase (nNOS) participates in vasodilation due to heat stress. To explore the relative roles and interactions of these isoforms, we examined the effects of a relatively specific eNOS inhibitor, Nω-amino-l-arginine (LNAA), and a specific nNOS inhibitor, Nω-propyl-l-arginine (NPLA), both separately and in combination, on skin blood flow (SkBF) responses to increased Tloc and heat stress in two protocols. In each protocol, SkBF was monitored by laser-Doppler flowmetry (LDF) and mean arterial pressure (MAP) by Finapres. Cutaneous vascular conductance (CVC) was calculated (CVC = LDF/MAP). Intradermal microdialysis was used to treat one site with 5 mM LNAA, another with 5 mM NPLA, a third with combined 5 mM LNAA and 5 mM NPLA (Mix), and a fourth site with Ringer only. In protocol 1, Tloc was controlled with combined LDF/local heating units. Tloc was increased from 34°C to 41.5°C to cause local vasodilation. In protocol 2, after a period of normothermia, whole body heat stress was induced (water-perfused suits). At the end of each protocol, all sites were perfused with 58 mM nitroprusside to effect maximal vasodilation for data normalization. In protocol 1, at Tloc = 34°C, CVC did not differ between sites ( P > 0.05). LNAA and Mix attenuated CVC increases at Tloc = 41.5°C to similar extents ( P < 0.05, LNAA or Mix vs. untreated or NPLA). In protocol 2, in normothermia, CVC did not differ between sites ( P > 0.05). During heat stress, NPLA and Mix attenuated CVC increases to similar extents, but no significant attenuation occurred with LNAA ( P < 0.05, NPLA or Mix vs. untreated or LNAA). In forearm skin, eNOS mediates the vasodilator response to increased Tloc and nNOS mediates the vasodilator response to heat stress. The two isoforms do not appear to interact during either response.

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Impaired whole-body heat loss in type 1 diabetes during exercise in the heat: a cause for concern?

Diabetologia ◽

10.1007/s00125-019-4858-5 ◽

2019 ◽

Vol 62 (6) ◽

pp. 1087-1089 ◽

Cited By ~ 4

Author(s):

Sean R. Notley ◽

Martin P. Poirier ◽

Jane E. Yardley ◽

Ronald J. Sigal ◽

Glen P. Kenny

Keyword(s):

Type 1 Diabetes ◽

Heat Loss ◽

Whole Body ◽

Body Heat

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Ventilatory control during exercise with peripheral chemoreceptor stimulation: hypoxia vs. domperidone

Journal of Applied Physiology ◽

10.1152/jappl.1989.67.6.2438 ◽

1989 ◽

Vol 67 (6) ◽

pp. 2438-2446 ◽

Cited By ~ 11

Author(s):

S. L. Schaefer ◽

G. S. Mitchell

Keyword(s):

Dopamine D2 Receptor ◽

D2 Receptor ◽

Whole Body ◽

Co2 Production ◽

Peripheral Chemoreceptor ◽

Arterial Pco2 ◽

Ventilatory Responses ◽

Response To Exercise ◽

Dopamine D2 Receptor Antagonist ◽

Made In

Hypoxia potentiates the ventilatory response to exercise, eliciting a greater decrease in arterial PCO2 (PaCO2) from rest to exercise than in normoxia. The mechanism of this hypoxia-exercise interaction requires intact carotid chemoreceptors. To determine whether carotid chemoreceptor stimulation alone is sufficient to elicit the mechanism without whole body hypoxia, ventilatory responses to treadmill exercise were compared in goats during hyperoxic control conditions, moderate hypoxia (PaO2 = 38-44 Torr), and peripheral chemoreceptor stimulation with the peripheral dopamine D2-receptor antagonist, domperidone (Dom; 0.5 mg/kg iv). Measurements with Dom were made in both hyperoxia (Dom) and hypoxia (Dom/hypoxia). Finally, ventilatory responses to inspired CO2 at rest were compared in each experimental condition because enhanced CO2 chemoreception might be expected to blunt the PaCO2 decrease during exercise. At rest, PaCO2 decreased from control with Dom (-5.0 +/- 0.9 Torr), hypoxia (-4.1 +/- 0.5 Torr), and Dom/hypoxia (-11.1 +/- 1.2 Torr). The PaCO2 decrease from rest to exercise was not significantly different between control (-1.7 +/- 0.6 Torr) and Dom (-1.4 +/- 0.8 Torr) but was significantly greater in hypoxia (-4.3 +/- 0.7 Torr) and Dom/hypoxia (-3.5 +/- 0.9 Torr). The slope of the ventilation vs. CO2 production relationship in exercise increased with Dom (16%), hypoxia (18%), and Dom/hypoxia (68%). Ventilatory responses to inspired CO2 at rest increased from control to Dom (236%) and Dom/hypoxia (295%) and increased in four of five goats in hypoxia (mean 317%).(ABSTRACT TRUNCATED AT 250 WORDS)

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Intermittent sequential pneumatic compression does not enhance whole-body heat loss in elderly adults during extreme heat exposure

Applied Physiology Nutrition and Metabolism ◽

10.1139/apnm-2019-0364 ◽

2019 ◽

Vol 44 (12) ◽

pp. 1383-1386

Author(s):

Andrew W. D’Souza ◽

Sean R. Notley ◽

Robert D. Meade ◽

Glen P. Kenny

Keyword(s):

Mean Arterial Pressure ◽

Arterial Pressure ◽

Heat Loss ◽

Lower Limb ◽

Vascular Function ◽

Heat Exposure ◽

Extreme Heat ◽

Whole Body ◽

Elderly Adults ◽

Body Heat

Lower-limb intermittent sequential pneumatic compression (ISPC) improves circulation and vascular function in elderly adults. We evaluated the hypothesis that ISPC would also augment whole-body heat loss (WBHL) in elderly adults (aged 69 ± 4 years) resting in extreme heat (40 °C). While ISPC increased mean arterial pressure (91 ± 9 mm Hg) relative to no-ISPC (83 ± 5 mm Hg; P = 0.013) at the end of the exposure, no influence on WBHL was observed (81 ± 7 and 86 ± 11 W for ISPC and no-ISPC, respectively, P = 0.310). Novelty When assessed in elderly adults during an extreme heat exposure, intermittent sequential pneumatic compression augmented mean arterial pressure but did not enhance whole-body heat loss.

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Light masking of circadian rhythms of heat production, heat loss, and body temperature in squirrel monkeys

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1999.276.2.r298 ◽

1999 ◽

Vol 276 (2) ◽

pp. R298-R307 ◽

Cited By ~ 1

Author(s):

Edward L. Robinson ◽

Charles A. Fuller

Keyword(s):

Body Temperature ◽

Heat Loss ◽

Heat Production ◽

Whole Body ◽

Direct Calorimetry ◽

Set Point ◽

Subjective Night ◽

Timing System ◽

Circadian Timing System ◽

Body Heat

Whole body heat production (HP) and heat loss (HL) were examined to determine their relative contributions to light masking of the circadian rhythm in body temperature (Tb). Squirrel monkey metabolism ( n = 6) was monitored by both indirect and direct calorimetry, with telemetered measurement of body temperature and activity. Feeding was also measured. Responses to an entraining light-dark (LD) cycle (LD 12:12) and a masking LD cycle (LD 2:2) were compared. HP and HL contributed to both the daily rhythm and the masking changes in Tb. All variables showed phase-dependent masking responses. Masking transients at L or D transitions were generally greater during subjective day; however, L masking resulted in sustained elevation of Tb, HP, and HL during subjective night. Parallel, apparently compensatory, changes of HL and HP suggest action by both the circadian timing system and light masking on Tb set point. Furthermore, transient HL increases during subjective night suggest that gain change may supplement set point regulation of Tb.

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