Humid heat acclimation does not elicit a preferential sweat redistribution toward the limbs

2004 ◽  
Vol 286 (3) ◽  
pp. R512-R518 ◽  
Author(s):  
Mark J. Patterson ◽  
Jodie M. Stocks ◽  
Nigel A. S. Taylor

We tested the hypothesis that local sweat rates would not display a systematic postadaptation redistribution toward the limbs after humid heat acclimation. Eleven nonadapted males were acclimated over 3 wk (16 exposures), cycling 90 min/day, 6 days/wk (40°C, 60% relative humidity), using the controlled-hyperthermia acclimation technique, in which work rate was modified to achieve and maintain a target core temperature (38.5°C). Local sudomotor adaptation (forehead, chest, scapula, forearm, thigh) and onset thresholds were studied during constant work intensity heat stress tests (39.8°C, 59.2% relative humidity) conducted on days 1, 8, and 22 of acclimation. The mean body temperature (T̄b) at which sweating commenced (threshold) was reduced on days 8 and 22 ( P < 0.05), and these displacements paralleled the resting thermoneutral T̄b shift, such that the T̄b change to elicit sweating remained constant from days 1 to 22. Whole body sweat rate increased significantly from 0.87 ± 0.06 l/h on day 1 to 1.09 ± 0.08 and 1.16 ± 0.11 l/h on days 8 and 22, respectively. However, not all skin regions exhibited equivalent relative sweat rate elevations from day 1 to day 22. The relative increase in forearm sweat rate (117 ± 31%) exceeded that at the forehead (47 ± 18%; P < 0.05) and thigh (42 ± 16%; P < 0.05), while the chest sweat rate elevation (106 ± 29%) also exceeded the thigh ( P < 0.05). Two unique postacclimation observations arose from this project. First, reduced sweat thresholds appeared to be primarily related to a lower resting T̄b, and more dependent on T̄b change. Second, our data did not support the hypothesis of a generalized and preferential trunk-to-limb sweat redistribution after heat acclimation.

Author(s):  
Puck Alkemade ◽  
Nicola Gerrett ◽  
Thijs M. H. Eijsvogels ◽  
Hein A. M. Daanen

Abstract Purpose The magnitude of heat acclimation (HA) adaptations varies largely among individuals, but it remains unclear what factors influence this variability. This study compared individual characteristics related to fitness status and body dimensions of low-, medium-, and high responders to HA. Methods Twenty-four participants (9 female, 15 male; maximum oxygen uptake [$$\dot{{V}}$$ V ˙ O2peak,kg] 52 ± 9 mL kg−1 min−1) completed 10 daily controlled-hyperthermia HA sessions. Adaptations were evaluated by heat stress tests (HST; 35 min cycling 1.5 W  kg−1; 33 °C, 65% relative humidity) pre- and post-HA. Low-, medium-, and high responder groups were determined based on tertiles (n = 8) of individual adaptations for resting rectal temperature (Tre), exercise-induced Tre rise (ΔTre), whole-body sweat rate (WBSR), and heart rate (HR). Results Body dimensions (p > 0.3) and $$\dot{{V}}$$ V ˙ O2peak,kg (p > 0.052) did not differentiate low-, medium-, and high responders for resting Tre or ΔTre. High WBSR responders had a larger body mass and lower body surface area-to-mass ratio than low responders (83.0 ± 9.3 vs 67.5 ± 7.3 kg; 249 ± 12 vs 274 ± 15 cm2 kg−1, respectively; p < 0.005). Conversely, high HR responders had a smaller body mass than low responders (69.2 ± 6.8 vs 83.4 ± 9.4 kg; p = 0.02). $$\dot{{V}}$$ V ˙ O2peak,kg did not differ among levels of responsiveness for WBSR and HR (p > 0.3). Conclusion Individual body dimensions influenced the magnitude of sudomotor and cardiovascular adaptive responses, but did not differentiate Tre adaptations to HA. The influence of $$\dot{{V}}$$ V ˙ O2peak,kg on the magnitude of adaptations was limited.


2015 ◽  
Vol 309 (1) ◽  
pp. R36-R42 ◽  
Author(s):  
Nicole E. Moyen ◽  
Hannah M. Anderson ◽  
Jenna M. Burchfield ◽  
Matthew A. Tucker ◽  
Melina A. Gonzalez ◽  
...  

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.


2019 ◽  
Vol 316 (1) ◽  
pp. R13-R20 ◽  
Author(s):  
Nathan B. Morris ◽  
Georgia K. Chaseling ◽  
Anthony R. Bain ◽  
Ollie Jay

This study sought to determine whether the temperature of water ingested before exercise alters the onset threshold and subsequent thermosensitivity of local vasomotor and sudomotor responses after exercise begins. Twenty men [24 (SD 4) yr of age, 75.8 (SD 8.1) kg body mass, 52.3 (SD 7.7) ml·min−1·kg−1peak O2consumption (V̇o2peak)] ingested 1.5°C, 37°C, or 50°C water (3.2 ml/kg), rested for 5 min, and then cycled at 50% V̇o2peakfor 15 min at 23.0 (SD 0.9) °C and 32 (SD 10) % relative humidity. Mean body temperature (Tb), local sweat rate (LSR), and skin blood flow (SBF) were measured. In a subset of eight men [25 (SD 5) yr of age, 78.6 (SD 8.3) kg body mass, 48.9 (SD 11.1) ml·min−1·kg−1V̇o2peak], blood pressure was measured and cutaneous vascular conductance (CVC) was determined. The change in Tbwas greater at the onset of LSR measurement with ingestion of 1.5°C than 50°C water [ΔTb= 0.19 (SD 0.15) vs. 0.11 (SD 0.12) °C, P = 0.04], but not 37°C water [ΔTb= 0.14 (SD 0.14) °C, P = 0.23], but did not differ between trials for SBF measurement [ΔTb= 0.18 (SD 0.15) °C, 0.11 (SD 0.13) °C, and 0.09 (SD 0.09) °C with 1.5°C, 37°C, and 50°C water, respectively, P = 0.07]. Conversely, the thermosensitivity of LSR and SBF was not different [LSR = 1.11 (SD 0.75), 1.11 (SD 0.75), and 1.34 (SD 1.11) mg·min−1·cm−2·°C−1with 1.5°C, 37°C, and 50°C ingested water, respectively ( P = 0.46); SBF = 717 (SD 882), 517 (SD 606), and 857 (SD 904) %baseline arbitrary units (AU)/°C with 1.5°C, 37°C, and 50°C ingested water, respectively ( P = 0.95)]. After 15 min of exercise, LSR and SBF were greater with ingestion of 50°C than 1.5°C water [LSR = 0.40 (SD 0.17) vs. 0.31 (SD 0.19) mg·min−1·cm−2( P = 0.02); SBF = 407 (SD 149) vs. 279 (SD 117) %baseline AU ( P < 0.001)], but not 37°C water [LSR = 0.50 (SD 0.22) mg·min−1·cm−2; SBF = 324 (SD 169) %baseline AU]. CVC was statistically unaffected [275 (SD 81), 340 (SD 114), and 384 (SD 160) %baseline CVC with 1.5°C, 37°C, and 50°C ingested water, respectively, P = 0.30]. Collectively, these results support the concept that visceral thermoreceptors modify the central drive for thermoeffector responses.


2009 ◽  
Vol 297 (4) ◽  
pp. R1082-R1085 ◽  
Author(s):  
Michael J. Buono ◽  
Travis R. Numan ◽  
Ryan M. Claros ◽  
Stephanie K. Brodine ◽  
Fred W. Kolkhorst

We investigated whether the eccrine sweat glands must actively produce sweat during heat acclimation if they are to adapt and increase their capacity to sweat. Eight volunteers received intradermal injections of BOTOX, to prevent neural stimulation and sweat production of the sweat glands during heat acclimation, and saline injections as a control in the contralateral forearm. Subjects performed 90 min of moderate-intensity exercise in the heat (35°C, 40% relative humidity) on 10 consecutive days. Heat acclimation decreased end-exercise heart rate (156 ± 22 vs. 138 ± 17 beats/min; P = 0.0001) and rectal temperature (38.2 ± 0.3 vs. 37.9 ± 0.3°C; P = 0.0003) and increased whole body sweat rate (0.70 ± 0.29 vs. 1.06 ± 0.50 l/h; P = 0.030). During heat acclimation, there was no measurable sweating in the BOTOX-treated forearm, but the control forearm sweat rate during exercise increased 40% over the 10 days ( P = 0.040). Peripheral sweat gland function was assessed using pilocarpine iontophoresis before and after heat acclimation. Before heat acclimation, the pilocarpine-induced sweat rate of the control and BOTOX-injected forearms did not differ (0.65 ± 0.20 vs. 0.66 ± 0.22 mg·cm−2·min−1). However, following heat acclimation, the pilocarpine-induced sweat rate in the control arm increased 18% to 0.77 ± 0.21 mg·cm−2·min−1 ( P = 0.021) but decreased 52% to 0.32 ± 0.18 mg·cm−2·min−1 ( P < 0.001) in the BOTOX-treated arm. Using complete chemodenervation of the sweat glands, coupled with direct cholinergic stimulation via pilocarpine iontophoresis, we demonstrated that sweat glands must be active during heat acclimation if they are to adapt and increase their capacity to sweat.


2016 ◽  
Vol 41 (8) ◽  
pp. 816-824 ◽  
Author(s):  
Martin P. Poirier ◽  
Daniel Gagnon ◽  
Glen P. Kenny

The purpose of this study was to examine if local changes in sweat rate following 14 days of heat acclimation reflect those that occur at the whole-body level. Both prior to and following a 14-day traditional heat acclimation protocol, 10 males exercised in the heat (35 °C, ∼20% relative humidity) at increasing rates of heat production equal to 300 (Ex1), 350 (Ex2), and 400 (Ex3) W·m−2. A 10-min recovery period followed Ex1, while a 20-min recovery period separated Ex2 and Ex3. The exercise protocol was performed in a direct calorimeter to measure whole-body sweat rate and, on a separate day, in a thermal chamber to measure local sweat rate (LSR), sweat gland activation (SGA), and sweat gland output (SGO) on the upper back, chest, and mid-anterior forearm. Post-acclimation, whole-body sweat rate was greater during each exercise bout (Ex1: 14.3 ± 0.9; Ex2: 17.3 ± 1.2; Ex3: 19.4 ± 1.3 g·min−1, all p ≤ 0.05) relative to pre-acclimation (Ex1: 13.1 ± 0.6; Ex2: 15.4 ± 0.8; Ex3: 16.5 ± 1.3 g·min−1). In contrast, only LSR on the forearm increased with acclimation, and this increase was only observed during Ex2 (Post: 1.32 ± 0.33 vs. Pre: 1.06 ± 0.22 mg·min−1·cm−2, p = 0.03) and Ex3 (Post: 1.47 ± 0.41 vs. Pre: 1.17 ± 0.23 mg·min−1·cm−2, p = 0.05). The greater forearm LSR post-acclimation was due to an increase in SGO, as no changes in SGA were observed. Overall, these data demonstrate marked regional variability in the effect of heat acclimation on LSR, such that not all local measurements of sweat rate reflect the improvements observed at the whole-body level.


Author(s):  
Leigh Arlegui ◽  
James W. Smallcombe ◽  
Damien Fournet ◽  
Keith Tolfrey ◽  
George Havenith

Abstract Purpose To determine sweating responses of pre-pubertal children during intermittent exercise in a warm environment and create whole-body maps of regional sweat rate (RSRs) distribution across the body. Methods Thirteen pre-pubertal children; six girls and seven boys (8.1 ± 0.8 years) took part. Sweat was collected using the technical absorbent method in the last 5 min of a 30-min intermittent exercise protocol performed at 30 ℃, 40% relative humidity and 2 m·s−1 frontal wind. Results Mean gross sweat loss (GSL) was 126 ± 47 g·m−2·h−1 and metabolic heat production was 278 ± 50 W·m2. The lower anterior torso area had the lowest RSR with a median (IQR) sweat rate (SR) of 40 (32) g·m−2·h−1. The highest was the forehead with a median SR of 255 (163) g·m−2·h−1. Normalised sweat maps (the ratio of each region’s SR to the mean SR for all measured pad regions) showed girls displayed lower ratio values at the anterior and posterior torso, and higher ratios at the hands, feet and forehead compared to boys. Absolute SRs were similar at hands and feet, but girls sweated less in most other areas, even after correction for metabolic rate. Conclusion Pre-pubertal children have different RSRs across the body, also showing sex differences in sweat distribution. Distributions differ from adults. Hands and feet RSR remain stable, but SR across other body areas increase with maturation. These data can increase specificity of models of human thermoregulation, improve the measurement accuracy of child-sized thermal manikins, and aid companies during product design and communication.


2015 ◽  
Vol 309 (5) ◽  
pp. R623-R627 ◽  
Author(s):  
Jonathan E. Wingo ◽  
David A. Low ◽  
David M. Keller ◽  
Kenichi Kimura ◽  
Craig G. Crandall

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.


1985 ◽  
Vol 59 (6) ◽  
pp. 1911-1917 ◽  
Author(s):  
V. Hessemer ◽  
K. Bruck

Ten women [mean maximal O2 uptake (VO2max), 2.81 l X min-1] exercised for 15 min on a cycle ergometer in the middle of the luteal phase (L) and in the early follicular phase (F) of the menstrual cycle at the same constant work rates (mean 122 W) and an ambient temperature of 18 degrees C. Serum progesterone averaged 44.7 nmol X l-1 in L and 0.7 nmol X l-1 in F. After a 4-h resting period, exercise was performed between 3 and 4 A.M., when the L-F core temperature difference is maximal. Preexercise esophageal (Tes), tympanic (Tty), and rectal (Tre) temperatures averaged 0.6 degrees C higher in L. During exercise Tes, Tty, and Tre averaged 0.5 degrees C higher. The thresholds for chest sweating and cutaneous vasodilation (heat clearance technique) at the thumb and forearm were elevated in L by an average of 0.47 degrees C, related to mean body temperature (Tb(es) = 0.87Tes + 0.13Tskin), Tes, Tty, or Tre. The above-threshold chest sweat rate and cutaneous heat clearances were also increased in L. The mean exercise heart rate was 170.0 beats X min-1 in L and 163.8 beats X min-1 in F. The mean exercise VO2 in L (2.21 l X min-1) was 5.2% higher than in F (2.10 l X min-1), the metabolic rate was increased in L by 5.6%, but the net efficiency was 5.3% lower. No significant L-F differences in the respiratory exchange ratio and postexercise plasma lactate were demonstrated.


2007 ◽  
Vol 103 (3) ◽  
pp. 990-994 ◽  
Author(s):  
Michael J. Buono ◽  
Kimberly D. Ball ◽  
Fred W. Kolkhorst

The purpose of this study was to determine the effect of active heat acclimation on the sweat osmolality and sweat sodium ion concentration vs. sweat rate relationship in humans. Eight healthy male volunteers completed 10 days of exercise in the heat. The mean exercising heart rate and core temperature were significantly decreased ( P < 0.05) by 18 beats/min and 0.6°C, respectively, following heat acclimation. Furthermore, sweat osmolality and the sweat sodium ion concentration vs. sweat rate relationships were shifted to the right. Specifically, the slopes of the relationships were not affected by heat acclimation. Rather, heat acclimation significantly reduced the y-intercepts of the sweat osmolality and sweat sodium relationships with sweat rate by 28 mosmol/kgH2O and 15 mmol/l, respectively. Thus there was a significantly lower sweat sodium ion concentration for a given sweat rate following heat acclimation. These results suggest that heat acclimation increases the sodium ion reabsorption capacity of the human eccrine sweat gland.


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