Aspirin ingestion does not alter the onset or slope of local sweat rate during whole‐body passive heat stress (1104.12)

The purpose of this study was to compare smokers and nonsmokers' sudomotor and cutaneous vascular responses to whole body passive heat stress. Nine regularly smoking (SMK: 29 ± 9 yr; 10 ± 6 cigarettes/day) and 13 nonsmoking (N-SMK: 27 ± 8 yr) males were passively heated until core temperature (TC) increased 1.5°C from baseline. Forearm local sweat rate (LSR) via ventilated capsule, sweat gland activation (SGA), sweat gland output (SGO), and cutaneous vasomotor activity via laser-Doppler flowmetry (CVC) were measured as mean body temperature increased (ΔTb) during passive heating using a water-perfused suit. Compared with N-SMK, SMK had a smaller ΔTb at the onset of sweating (0.52 ± 0.19 vs. 0.35 ± 0.14°C, respectively; P = 0.03) and cutaneous vasodilation (0.61 ± 0.21 vs. 0.31 ± 0.12°C, respectively; P < 0.01). Increases in LSR and CVC per °C ΔTb (i.e., sensitivity) were similar in N-SMK and SMK (LSR: 0.63 ± 0.21 vs. 0.60 ± 0.40 Δmg/cm2/min/°C ΔTb, respectively, P = 0.81; CVC: 82.5 ± 46.2 vs. 58.9 ± 23.3 Δ%max/°C ΔTb, respectively; P = 0.19). However, the plateau in LSR during whole body heating was higher in N-SMK vs. SMK (1.00 ± 0.13 vs. 0.79 ± 0.26 mg·cm−2·min−1; P = 0.03), which was likely a result of higher SGO (8.94 ± 3.99 vs. 5.94 ± 3.49 μg·gland−1·min−1, respectively; P = 0.08) and not number of SGA (104 ± 7 vs. 121 ± 9 glands/cm2, respectively; P = 0.58). During whole body passive heat stress, smokers had an earlier onset for forearm sweating and cutaneous vasodilation, but a lower local sweat rate that was likely due to lower sweat output per gland. These data provide insight into local (i.e., forearm) thermoregulatory responses of young smokers during uncompensatory whole body passive heat stress.

Download Full-text

Active cutaneous vasodilation in resting humans during mild heat stress

Journal of Applied Physiology ◽

10.1152/japplphysiol.00235.2004 ◽

2005 ◽

Vol 98 (3) ◽

pp. 829-837 ◽

Cited By ~ 37

Author(s):

Yoshi-Ichiro Kamijo ◽

Kichang Lee ◽

Gary W. Mack

Keyword(s):

Blood Flow ◽

Heat Stress ◽

Skin Temperature ◽

Skin Blood Flow ◽

Sweat Rate ◽

Mean Skin Temperature ◽

Local Skin ◽

Mild Heat ◽

Normal Core ◽

Local Sweat Rate

The role of skin temperature in reflex control of the active cutaneous vasodilator system was examined in six subjects during mild graded heat stress imposed by perfusing water at 34, 36, 38, and 40°C through a tube-lined garment. Skin sympathetic nerve activity (SSNA) was recorded from the peroneal nerve with microneurography. While monitoring esophageal, mean skin, and local skin temperatures, we recorded skin blood flow at bretylium-treated and untreated skin sites by using laser-Doppler velocimetry and local sweat rate by using capacitance hygrometry on the dorsal foot. Cutaneous vascular conductance (CVC) was calculated by dividing skin blood flow by mean arterial pressure. Mild heat stress increased mean skin temperature by 0.2 or 0.3°C every stage, but esophageal and local skin temperature did not change during the first three stages. CVC at the bretylium tosylate-treated site (CVCBT) and sweat expulsion number increased at 38 and 40°C compared with 34°C ( P < 0.05); however, CVC at the untreated site did not change. SSNA increased at 40°C ( P < 0.05, different from 34°C). However, SSNA burst amplitude increased ( P < 0.05), whereas SSNA burst duration decreased ( P < 0.05), at the same time as we observed the increase in CVCBT and sweat expulsion number. These data support the hypothesis that the active vasodilator system is activated by changes in mean skin temperature, even at normal core temperature, and illustrate the intricate competition between active vasodilator and the vasoconstrictor system for control of skin blood flow during mild heat stress.

Download Full-text

Sweating sensitivity and capacity of women in relation to age

Journal of Applied Physiology ◽

10.1152/jappl.1982.53.3.671 ◽

1982 ◽

Vol 53 (3) ◽

pp. 671-676 ◽

Cited By ~ 38

Author(s):

B. L. Drinkwater ◽

J. F. Bedi ◽

A. B. Loucks ◽

S. Roche ◽

S. M. Horvath

Keyword(s):

Heat Stress ◽

Older Women ◽

Forearm Blood Flow ◽

Thermal Environment ◽

Sweat Rate ◽

Age Groups ◽

Whole Body ◽

Volume Changes ◽

Younger Women ◽

Significant Difference

Ten postmenopausal and ten younger women rested for 2 h in a 40 degrees C, 22.2-Torr vapor pressure environment. Sweating response was monitored by resistance hygrometry for onset, a platform balance for whole-body sweat rate, and five individual capsules for regional sweat rate. Other variables measured included forearm blood flow, heart rate (HR), mean skin (Tsk) and rectal (Tre) temperatures, sweat electrolytes (Na+ and K+), oxygen uptake, and plasma volume changes. Preliminary tests included maximal aerobic power (VO2max) and percent body fat. Heat stress did not elicit any significant differences in sweating response between age groups. Indices of heat strain, Tre and HR, were also similar for both groups. The only significant difference between younger and older women was a higher Na+ concentration in the forearm sweat of postmenopausal women. No thermoregulatory responses were related to age, but both sweat rate (r = 0.48) and peak Tsk (r = -0.43) were related to VO2max. For healthy, active, older women aging did not diminish the functional capacity of the sweating mechanism to cope with heat stress while resting in this specific thermal environment.

Download Full-text

Cutaneous vascular responses to isometric handgrip exercise during local heating and hyperthermia

Journal of Applied Physiology ◽

10.1152/japplphysiol.00888.2004 ◽

2005 ◽

Vol 98 (6) ◽

pp. 2011-2018 ◽

Cited By ~ 18

Author(s):

Gregg R. McCord ◽

Christopher T. Minson

Keyword(s):

Blood Flow ◽

Heat Stress ◽

Skin Blood Flow ◽

Sweat Rate ◽

Local Heating ◽

Whole Body ◽

Handgrip Exercise ◽

Isometric Handgrip ◽

Hyperthermic Condition ◽

Isometric Handgrip Exercise

The dramatic increase in skin blood flow and sweating observed during heat stress is mediated by poorly understood sympathetic cholinergic mechanisms. One theory suggests that a single sympathetic cholinergic nerve mediates cutaneous active vasodilation (AVD) and sweating via cotransmission of separate neurotransmitters, because AVD and sweating track temporally and directionally when activated during passive whole body heat stress. It has also been suggested that these responses are regulated independently, because cutaneous vascular conductance (CVC) has been shown to decrease, whereas sweat rate increases, during combined hyperthermia and isometric handgrip exercise. We tested the hypothesis that CVC decreases during isometric handgrip exercise if skin blood flow is elevated using local heating to levels similar to that induced by pronounced hyperthermia but that this does not occur at lower levels of skin blood flow. Subjects performed isometric handgrip exercise as CVC was elevated at selected sites to varying levels by local heating (which is independent of AVD) in thermoneutral and hyperthermic conditions. During thermoneutral isometric handgrip exercise, CVC decreased at sites in which blood flow was significantly elevated before exercise (−6.5 ± 1.8% of maximal CVC at 41°C and −10.5 ± 2.0% of maximal CVC at 43°C; P < 0.05 vs. preexercise). During isometric handgrip exercise in the hyperthermic condition, an observed decrease in CVC was associated with the level of CVC before exercise. Taken together, these findings argue against withdrawal of AVD to explain the decrease in CVC observed during isometric handgrip exercise in hyperthermic conditions.

Download Full-text

TRPV4 channel blockade does not modulate skin vasodilation and sweating during hyperthermia or cutaneous post-occlusive reactive and thermal hyperemia

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00123.2020 ◽

2020 ◽

Author(s):

Naoto Fujii ◽

Glen P. Kenny ◽

Gregory W. McGarr ◽

Tatsuro Amano ◽

Yasushi Honda ◽

...

Keyword(s):

Young Adults ◽

Heat Stress ◽

Sweat Rate ◽

Reactive Hyperemia ◽

Body Core Temperature ◽

Whole Body ◽

Secretory Cells ◽

Transient Receptor Potential Vanilloid ◽

Cutaneous Vasodilation ◽

Trpv4 Channel

Transient receptor potential vanilloid 4 (TRPV4) channels exist on vascular endothelial cells and eccrine sweat gland secretory cells in human skin. Here, we assessed if TRPV4 channels contribute to cutaneous vasodilation and sweating during whole-body passive heat stress (protocol 1) and to cutaneous vasodilation during post-occlusive reactive hyperemia and local thermal hyperemia (protocol 2). Intradermal microdialysis was employed to locally deliver pharmacological agents to forearm skin sites where cutaneous vascular conductance (CVC) and sweat rate were assessed. In protocol 1 (twelve young adults), CVC and sweat rate were increased by passive whole-body heating resulting in a body core temperature elevation of 1.2±0.1ºC. The elevated CVC and sweat rate assessed at sites treated with TRPV4 channel antagonist (either 200 µM HC-067047 or 125 µM GSK2193874) were not different from the vehicle control site (5 % dimethyl sulfoxide). After whole-body heating, a TRPV4 channel agonist (100 µM GSK1016790A) was administered to each skin site, eliciting elevations in CVC. Relative to control, this response was partly attenuated by both TRPV4 channel antagonists, confirming drug efficacy. In protocol 2 (ten young adults), CVC was increased following a 5-min arterial occlusion and during local heating from 33 to 42ºC. These responses did not differ between the control and the TRPV4 channel antagonist sites (200 µM HC-067047). We show that TRPV4 channels are not required for regulating cutaneous vasodilation or sweating during a whole-body passive heat stress. Further, they are not required for regulating cutaneous vasodilation during post-occlusive reactive hyperemia and local thermal hyperemia.

Download Full-text

Exercise-Induced Trace Mineral Element Concentration in Regional Versus Whole-Body Wash-Down Sweat

International Journal of Sport Nutrition and Exercise Metabolism ◽

10.1123/ijsnem.21.3.233 ◽

2011 ◽

Vol 21 (3) ◽

pp. 233-239 ◽

Cited By ~ 20

Author(s):

Lindsay B. Baker ◽

John R. Stofan ◽

Henry C. Lukaski ◽

Craig A. Horswill

Keyword(s):

Element Concentration ◽

Sweat Rate ◽

Sulfate Solution ◽

Skin Surface ◽

Cycle Ergometer ◽

Whole Body ◽

Air Chamber ◽

Local Sweat Rate ◽

Exercise Induced ◽

Sweat Composition

Simultaneous whole-body wash-down (WBW) and regional skin surface sweat collections were completed to compare regional patch and WBW sweat calcium (Ca), magnesium (Mg), copper (Cu), manganese (Mn), iron (Fe), and zinc (Zn) concentrations. Athletes (4 men, 4 women) cycled in a plastic open-air chamber for 90 min in the heat. Before exercise, the subjects and cycle ergometer (covered in plastic) were washed with deionized water. After the onset of sweating, sterile patches were attached to the forearm, back, chest, forehead, and thigh and removed on saturation. After exercise, the subjects and cycle ergometer were washed with 5 L of 15-mM ammonium sulfate solution to collect all sweat minerals and determine the volume of unevaporated sweat. Control trials were performed to measure mineral contamination in regional and WBW methods. Because background contamination in the collection system was high for WBW Mn, Fe, and Zn, method comparisons were not made for these minerals. After correction for minimal background contamination, WBW sweat [Ca], [Mg], and [Cu] were 44.6 ± 20.0, 9.8 ± 4.8, and 0.125 ± 0.069 mg/L, respectively, and 5-site regional (weighted for local sweat rate and body surface area) sweat [Ca], [Mg], and [Cu] were 59.0 ± 15.9, 14.5 ± 4.8, and 0.166 ± 0.031 mg/L, respectively. Five-site regional [Ca], [Mg], and [Cu] overestimated WBW by 32%, 48%, and 33%, respectively. No individual regional patch site or 5-site regional was significantly correlated with WBW sweat [Ca] (r = –.21, p = .65), [Mg] (r = .49, p = .33), or [Cu] (r = .17, p = .74). In conclusion, regional sweat [Ca], [Mg], and [Cu] are not accurate surrogates for or significantly correlated with WBW sweat composition.

Download Full-text

Effect of hypohydration on postsynaptic cutaneous vasodilation and sweating in healthy men

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00525.2016 ◽

2017 ◽

Vol 312 (5) ◽

pp. R637-R642 ◽

Cited By ~ 5

Author(s):

Matthew A. Tucker ◽

Ashley Six ◽

Nicole E. Moyen ◽

Alf Z. Satterfield ◽

Matthew S. Ganio

Keyword(s):

Heat Stress ◽

Sweat Rate ◽

Local Heating ◽

Maximal Response ◽

Fluid Restriction ◽

Doppler Flowmetry ◽

Healthy Men ◽

Cutaneous Vasodilation ◽

Stress Changes ◽

Local Sweat Rate

Hypohydration decreases cutaneous vasodilation and sweating during heat stress, but it is unknown if these decrements are from postsynaptic (i.e., sweat gland/blood vessel) alterations. The purpose of this study was to determine if hypohydration affects postsynaptic cutaneous vasodilation and sweating responses. Twelve healthy men participated in euhydrated (EU) and hypohydrated (HY) trials, with hypohydration induced via fluid restriction and passive heat stress. Changes in cutaneous vascular conductance (CVC; %max) in response to incremental intradermal infusion of the endothelium-independent vasodilator sodium nitroprusside (SNP) and the endothelium-dependent vasodilator methacholine chloride (MCh) were assessed by laser Doppler flowmetry. Local sweat rate (LSR) was simultaneously assessed at the MCh site via ventilated capsule. At the end of the last dose, maximal CVC was elicited by delivering a maximal dose of SNP (5 × 10−2 M) for 30 min to both sites with simultaneous local heating (~44°C) at the SNP site. The concentration of drug needed to elicit 50% of the maximal response (log EC50) was compared between hydration conditions. The percent body mass loss was greater with HY vs. EU (−2.2 ± 0.7 vs. −0.1 ± 0.7%, P < 0.001). Log EC50 of endothelium-dependent CVC was lower with EU (−3.62 ± 0.22) vs. HY (−2.93 ± 0.08; P = 0.044). Hypohydration did not significantly alter endothelium-independent CVC or LSR (both P > 0.05). In conclusion, hypohydration attenuated endothelium-dependent CVC but did not affect endothelium-independent CVC or LSR responses. These data suggest that reductions in skin blood flow accompanying hypohydration can be partially attributed to altered postsynaptic function.

Download Full-text

Local arginase inhibition does not modulate cutaneous vasodilation or sweating in young and older men during exercise

Journal of Applied Physiology ◽

10.1152/japplphysiol.00657.2018 ◽

2019 ◽

Vol 126 (4) ◽

pp. 1129-1137 ◽

Cited By ~ 6

Author(s):

Robert D. Meade ◽

Naoto Fujii ◽

Gregory W. McGarr ◽

Lacy M. Alexander ◽

Pierre Boulay ◽

...

Keyword(s):

Heat Stress ◽

Sweat Rate ◽

Exercise Bout ◽

Older Men ◽

Whole Body ◽

Moderate Intensity ◽

No Production ◽

Passive Heating ◽

Cutaneous Vasodilation ◽

Age Related

Age-related impairments in cutaneous vascular conductance (CVC) and sweat rate (SR) during exercise may result from increased arginase activity, which can attenuate endogenous nitric oxide (NO) production. We therefore evaluated whether arginase inhibition modulates these heat-loss responses in young ( n = 9, 23 ± 3 yr) and older ( n = 9, 66 ± 6 yr) men during two 30-min bouts of moderate-intensity cycling (Ex1 and Ex2) in the heat (35°C). CVC and SR were measured at forearm skin sites perfused with 1) lactated Ringer’s (control), 2) NG-nitro-L-arginine methyl ester (L-NAME; NO synthase-inhibited), or 3) Nω-hydroxy-nor-arginine and S-(2-boronoethyl)-l-cysteine (Nor-NOHA + BEC; arginase-inhibited). In both groups, CVC was reduced at L-NAME relative to control and Nor-NOHA + BEC (both P < 0.01). Likewise, SR was attenuated with L-NAME compared with control and Nor-NOHA + BEC during each exercise bout in the young men (all P ≤ 0.05); however, no influence of treatment on SR in the older men was observed ( P = 0.14). Based on these findings, we then evaluated responses in 7 older men (64 ± 7 yr) during passively induced elevations in esophageal temperature (∆Tes) equal to those in Ex1 (0.6°C) and Ex2 (0.8°C). L-NAME reduced CVC by 18 ± 20% CVCmax at a ∆Tes of 0.8°C ( P = 0.03) compared with control, whereas Nor-NOHA + BEC augmented CVC by 20 ± 18% CVCmax, on average, throughout heating (both P ≤ 0.03). SR was not influenced by either treatment ( P = 0.80) Thus, arginase inhibition does not modulate CVC or SR during exercise in the heat but, consistent with previous findings, does augment CVC in older men during passive heating. NEW & NOTEWORTHY In the current study, we demonstrate that local arginase inhibition does not influence forearm cutaneous vasodilatory and sweating responses in young or older men during exercise-heat stress. Consistent with previous findings, however, we observed augmented cutaneous blood flow with arginase inhibition during whole-body passive heat stress. Thus, arginase differentially affects cutaneous vasodilation depending on the mode of heat stress but does not influence sweating during exercise or passive heating.

Download Full-text

Combined facial heating and inhalation of hot air do not alter thermoeffector responses in humans

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00018.2015 ◽

2015 ◽

Vol 309 (5) ◽

pp. R623-R627 ◽

Cited By ~ 1

Author(s):

Jonathan E. Wingo ◽

David A. Low ◽

David M. Keller ◽

Kenichi Kimura ◽

Craig G. Crandall

Keyword(s):

Heat Stress ◽

Respiratory Tract ◽

Sweat Rate ◽

Whole Body ◽

Facial Skin ◽

Mean Body Temperature ◽

Doppler Flowmetry ◽

Hot Air ◽

Cutaneous Vasodilation ◽

The Face

The influence of thermoreceptors in human facial skin on thermoeffector responses is equivocal; furthermore, the presence of thermoreceptors in the respiratory tract and their involvement in thermal homeostasis has not been elucidated. This study tested the hypothesis that hot air directed on the face and inhaled during whole body passive heat stress elicits an earlier onset and greater sensitivity of cutaneous vasodilation and sweating than that directed on an equal skin surface area away from the face. Six men and two women completed two trials separated by ∼1 wk. Participants were passively heated (water-perfused suit; core temperature increase ∼0.9°C) while hot air was directed on either the face or on the lower leg (counterbalanced). Skin blood flux (laser-Doppler flowmetry) and local sweat rate (capacitance hygrometry) were measured at the chest and one forearm. During hot-air heating, local temperatures of the cheek and leg were 38.4 ± 0.8°C and 38.8 ± 0.6°C, respectively ( P = 0.18). Breathing hot air combined with facial heating did not affect mean body temperature onsets ( P = 0.97 and 0.27 for arm and chest sites, respectively) or slopes of cutaneous vasodilation ( P = 0.49 and 0.43 for arm and chest sites, respectively), or the onsets ( P = 0.89 and 0.94 for arm and chest sites, respectively), or slopes of sweating ( P = 0.48 and 0.65 for arm and chest sites, respectively). Based on these findings, respiratory tract thermoreceptors, if present in humans, and selective facial skin heating do not modulate thermoeffector responses during passive heat stress.

Download Full-text

Impaired sweating responses to a passive whole body heat stress in individuals with multiple sclerosis

Journal of Neurophysiology ◽

10.1152/jn.00897.2016 ◽

2017 ◽

Vol 118 (1) ◽

pp. 7-14 ◽

Cited By ~ 9

Author(s):

Dustin R. Allen ◽

Mu Huang ◽

Iqra M. Parupia ◽

Ariana R. Dubelko ◽

Elliot M. Frohman ◽

...

Keyword(s):

Multiple Sclerosis ◽

Heat Stress ◽

Core Temperature ◽

Sweat Rate ◽

Whole Body ◽

Healthy Controls ◽

Cutaneous Vasodilation ◽

Whole Body Heat Stress ◽

Reflex Control ◽

Body Heat

Multiple sclerosis (MS) is an autoimmune disease that affects the central nervous system (CNS), disrupting autonomic function. The aim of this study was to test the hypothesis that individuals with MS have blunted control of thermoregulatory reflex increases in sweat rate (SR) and cutaneous vasodilation compared with controls during a passive whole body heat stress (WBH). Eighteen individuals with relapsing-remitting MS and 18 healthy controls (Con) participated in the study. Core temperature (Tcore), skin temperature, heart rate, arterial blood pressure (10-min intervals), skin blood flow (laser-Doppler flux, LDF), and SR were continuously measured during normothermic baseline (34°C water perfusing a tube-lined suit) and WBH (increased Tcore 0.8°C via 48°C water perfusing the suit). Following WBH, local heaters were warmed to 42°C, inducing peak cutaneous vasodilation at the site of LDF collection. Cutaneous vascular conductance (CVC) was calculated as the ratio of LDF to mean arterial pressure and expressed as a percentage of peak achieved during local heating. Individuals with MS had attenuated SR responses to WBH (ΔSR from baseline: Con, 0.65 ± 0.27; MS, 0.42 ± 0.17 mg·cm−2·min−1, P = 0.003), whereas Δ%CVC42C from baseline was similar between groups (Con, 42 ± 16%; MS, 38 ± 12%, P = 0.39). SR responses were blunted as a function of Tcore in MS (interaction: group × Tcore, P = 0.03), of which differences were evident at ΔTcore 0.7°C and 0.8°C ( P < 0.05). No interaction was observed in Δ%CVC42C. Taken together, the findings show MS blunts sweating responses, whereas control of the cutaneous vasculature is preserved, in response to WBH. NEW & NOTEWORTHY This study is the first to assess the reflex control of the thermoregulatory system in individuals living with multiple sclerosis (MS). The novel findings are twofold. First, attenuated increases in sweat rate in subjects with MS compared with healthy controls were observed in response to a moderate increase (0.8°C) in core temperature via passive whole body heat stress. Second, it appears the reflex control of the cutaneous vasculature is preserved in MS.

Download Full-text