Local Sweat Research Articles

Improved neural control of body temperature following heat acclimation in humans.

With the advent of more frequent extreme heat events, adaptability to hot environments will be crucial for the survival of many species, including humans. However, the mechanisms that mediate human heat adaptation have remained elusive. We tested the hypothesis that heat acclimation improves the neural control of body temperature. Skin sympathetic nerve activity, comprising the efferent neural signal that activates heat loss thermoeffectors, was measured in healthy adults exposed to passive heat stress before and after a 7day heat acclimation protocol. Heat acclimation reduced the activation threshold for skin sympathetic nerve activity, leading to an earlier activation of cutaneous vasodilatation and sweat production. These findings demonstrate that heat acclimation improves the neural control of body temperature in humans. Heat acclimation improves autonomic temperature regulation in humans. However, the mechanisms that mediate human heat adaptation remain poorly understood. The present study tested the hypothesis that heat acclimation improves the neural control of body temperature. Body temperatures, skin sympathetic nerve activity, cutaneous vasodilatation, and sweat production were measured in 14healthy adults (nine men and five women, aged 27±5 years) during passive heat stress performed before and after a 7day heat acclimation protocol. Heat acclimation increased whole-body sweat rate [+0.54Lh-1 (0.32, 0.75), P<0.01] and reduced resting core temperature [-0.29°C (-0.40, -0.18), P<0.01]. During passive heat stress, the change in mean body temperature required to activate skin sympathetic nerve activity was reduced [-0.21°C (-0.34, -0.08), P<0.01] following heat acclimation. The earlier activation of skin sympathetic nerve activity resulted in lower activation thresholds for cutaneous vasodilatation [-0.18°C (-0.35, -0.01), P=0.04] and local sweat rate [-0.13°C (-0.24, -0.01), P=0.03]. These results demonstrate that heat acclimation leads to an earlier activation of the neural efferent outflow that activates the heat loss thermoeffectors of cutaneous vasodilatation and sweating.

Differences in dry-bulb temperature do not influence moderate-duration exercise performance in warm environments when vapor pressure is equivalent.

Recent studies have determined that ambient humidity plays a more important role in aerobic performance than dry-bulb temperature does in warm environments; however, no studies have kept humidity constant and independently manipulated temperature. Therefore, the purpose of this study was to determine the contribution of dry-bulb temperature, when vapor pressure was matched, on the thermoregulatory, perceptual and performance responses to a 30-min cycling work trial. Fourteen trained male cyclists (age: 32 ± 12year; height: 178 ± 6cm; mass: 76 ± 9kg; [Formula: see text]: 59 ± 9mLkg-1min-1; body surface area: 1.93 ± 0.12m2; peak power output: 393 ± 53W) volunteered, and underwent 1 exercise bout in moderate heat (MOD: 34.9 ± 0.2°C, 50.1 ± 1.1% relative humidity) and 1 in mild heat (MILD: 29.2 ± 0.2°C, 69.4 ± 0.9% relative humidity) matched for vapor pressure (2.8 ± 0.1kPa), with trials counterbalanced. Despite a higher weighted mean skin temperature during MOD (36.3 ± 0.5 vs. 34.5 ± 0.6°C, p < 0.01), none of rectal temperature (38.0 ± 0.3 vs. 37.9 ± 0.4°C, p = 0.30), local sweat rate (1.0 ± 0.3 vs. 0.9 ± 0.4mgcm-2min-1, p = 0.28), cutaneous blood flow (283 ± 116 vs. 287 ± 105 PU, p = 0.90), mean power output (206 ± 37 vs. 205 ± 41W, p = 0.87) or total work completed (371 ± 64 vs. 369 ± 70kJ, p = 0.77) showed any difference between environments during the work trial. However, all perceptual measures (perceived exertion, thermal discomfort, thermal sensation, skin wettedness, pleasantness, all p < 0.05) were affected detrimentally during MOD compared to MILD. In a warm and compensable environment, dry-bulb temperature did not influence high-intensity cycling performance when vapor pressure was maintained, whilst the perceptual responses were affected.

Intradermal Administration of Atrial Natriuretic Peptide Attenuates Cutaneous Vasodilation but Not Sweating in Young Men during Exercise in the Heat

Introduction: Prolonged exercise in the heat stimulates plasma release of atrial natriuretic peptide (ANP) in association with dehydration-induced reductions in blood volume. Elevated plasma ANP levels under these conditions may indirectly attenuate cutaneous blood flow and sweating responses due to the effects of this hormone on central blood volume and plasma osmolality and the resulting stimulation of nonthermal reflexes. However, it remains unclear whether cutaneous blood flow and sweating are directly modulated by ANP at the level of the cutaneous end organs (cutaneous microvessels and eccrine sweat glands) during prolonged exercise in the heat. Objective: Therefore, we evaluated the effects of local ANP administration on forearm cutaneous vascular conductance (CVC) and local sweat rate (LSR) during rest and exercise in the heat. Methods: In 9 habitually active young men (26 ± 6 years) CVC and LSR were evaluated at 3 intradermal microdialysis sites continuously perfused with lactated Ringer solution (control) or ANP (0.1 or 1.0 μM). Participants rested in a non-heat-stress condition (25°C) for approximately 60 min followed by 70 min in the heat (35°C). They then performed 50 min of moderate-intensity cycling (approx. 55% VO_{2 peak}), with a 30-min recovery. Thereafter, 50 mM sodium nitroprusside was administered at all sites to elicit maximum CVC, which was subsequently used to normalize all values (CVC_%max). Results: No effects of ANP on CVC_%max were observed in the non-heat-stress resting condition compared to the untreated control site (both p > 0.05). Conversely during rest in the heat there was an 11% (5–17%) reduction in CVC_%max at the 1.0 μM ANP site relative to the untreated control site (p < 0.05). At the end of exercise CVC_%max was attenuated by 12% (1–23%) at the 0.1 μM ANP site and by 21% (7–35%) at the 1.0 μM ANP site relative to the untreated control site (all p < 0.05). Conversely, neither concentration of ANP influenced sweating at any time point (all p > 0.05). Conclusion: Intradermal ANP administration directly attenuated cutaneous blood flow, but not sweating, in habitually active young men during rest and exercise in the heat.

Regional contributions of nitric oxide synthase to cholinergic cutaneous vasodilatation and sweating in young men.

What is the central question of this study? We evaluated whether regional variations exist in NO-dependent cutaneous vasodilatation and sweating during cholinergic stimulation. What is the main finding and its importance? Peak cutaneous vasodilatation and sweating were greater on the torso than the forearm. Furthermore, we found that NO was an important modulator of cholinergic cutaneous vasodilatation, but not sweating, across body regions, with a greater contribution of NO to cutaneous vasodilatation in the limb compared with the torso. These findings advance our understanding of the mechanisms influencing regional variations in cutaneous vasodilator and sweating responses to pharmacological stimulation. Regional variations in cutaneous vasodilatation and sweating exist across the body. Nitric oxide (NO) is an important modulator of these heat loss responses in the forearm. However, whether regional differences in NO-dependent cutaneous vasodilatation and sweating exist remain uncertain. In 14 habitually active young men (23±4years of age), cutaneous vascular conductance (CVC%max ) and local sweat rates were assessed at six skin sites. On each of the dorsal forearm, chest and upper back (trapezius), sites were continuously perfused with either lactated Ringer solution (control) or 10mmNω -nitro-l-arginine (l-NNA; an NO synthase inhibitor) dissolved in Ringer solution, via microdialysis. At all sites, cutaneous vasodilatation and sweating were induced by co-administration of the cholinergic agonist methacholine (1, 10, 100, 1000 and 2000mm; 25min per dose) followed by 50mm sodium nitroprusside (20-25min) to induce maximal vasodilatation. The l-NNA attenuated CVC%max relative to the control conditions for all regions (all P<0.05), and NO-dependent vasodilatation was greater at the forearm compared with the back and chest (both P<0.05). Furthermore, maximal vasodilatation was higher at the back and chest relative to the forearm (both P<0.05). Conversely, l-NNA had negligible effects on sweating across the body (all P>0.05). Peak local sweat rate was higher at the back relative to the forearm (P<0.05), with a similar trend observed for the chest. In habitually active young men, NO-dependent cholinergic cutaneous vasodilatation varied across the body, and the contribution to cholinergic sweating was negligible. These findings advance our understanding of the mechanisms influencing regional variations in cutaneous vasodilatation and sweating during pharmacological stimulation.

Ultra-simple wearable local sweat volume monitoring patch based on swellable hydrogels.

Quantifiably monitoring sweat rate and volume is important to assess the stress level of individuals and/or prevent dehydration, but despite intense research, a convenient, continuous, and low-cost method to monitor sweat rate and total sweat volume loss remains an un-met need. We present here an ultra-simple wearable sensor capable of measuring sweat rate and volume accurately. The device continuously monitors sweat rate by wicking the produced sweat into hydrogels that measurably swell in their physical geometry. The device has been designed as a simple to fabricate, low-cost, disposable patch. This patch exhibits stable and predictable operation over the maximum variable chemistry expected for sweat (pH 4-9 and salinity 0-100 mM NaCl). Preliminary in vivo testing of the patch has been achieved during aerobic exercise, and the sweat rates measured via the patch accurately follow actual sweat rates.

Thermal Behavior Augments Heat Loss Following Low Intensity Exercise.

We tested the hypothesis that thermal behavior alleviates thermal discomfort and accelerates core temperature recovery following low intensity exercise. Methods: In a 27 ± 0 °C, 48 ± 6% relative humidity environment, 12 healthy subjects (six females) completed 60 min of exercise followed by 90 min of seated recovery on two occasions. Subjects wore a suit top perfusing 34 ± 0 °C water during exercise. In the control trial, this water continually perfused throughout recovery. In the behavior trial, the upper body was maintained thermally comfortable by pressing a button to receive cool water (3 ± 2 °C) perfusing through the top for 2 min per button press. Results: Physiological variables (core temperature, p ≥ 0.18; mean skin temperature, p = 0.99; skin wettedness, p ≥ 0.09; forearm skin blood flow, p = 0.29 and local axilla sweat rate, p = 0.99) did not differ between trials during exercise. Following exercise, mean skin temperature decreased in the behavior trial in the first 10 min (by −0.5 ± 0.7 °C, p < 0.01) and upper body skin temperature was reduced until 70 min into recovery (by 1.8 ± 1.4 °C, p < 0.05). Core temperature recovered to pre-exercise levels 17 ± 31 min faster (p = 0.02) in the behavior trial. There were no differences in skin blood flow or local sweat rate between conditions during recovery (p ≥ 0.05). Whole-body thermal discomfort was reduced (by −0.4 ± 0.5 a.u.) in the behavior trial compared to the control trial within the first 20 min of recovery (p ≤ 0.02). Thermal behavior via upper body cooling resulted in augmented cumulative heat loss within the first 30 min of recovery (Behavior: 288 ± 92 kJ; Control: 160 ± 44 kJ, p = 0.02). Conclusions: Engaging in thermal behavior that results in large reductions in mean skin temperature following exercise accelerates the recovery of core temperature and alleviates thermal discomfort by promoting heat loss.

Autonomic and perceptual thermoregulatory responses to voluntarily engaging in a common thermoregulatory behaviour

We examined whether partial clothing removal is an effective thermoregulatory behaviour to attenuate both thermoregulatory and perceptual strain in a moderate environment (23 °C, 65% RH) during and after exercise. Ten healthy males (age: 21.9 (0.9) years; height: 173.9 (6.2) cm; mass: 62.3 (8.2) kg; body surface area: 1.8 (0.1) m2; VO2max: 51.8 (13.3) mL.kg−1.min−1) wore a long sleeve polyester shirt and performed two randomized cycling trials for 40 min at 40% VO2max followed by 20 min recovery. In one trial, they were permitted to roll up their sleeves at any time they wanted (Roll) whereas in the other trial, they were instructed to remain with long sleeves (No Roll) until the end of the recovery. Thermoregulatory variables were measured continuously whilst thermal perceptions (forearm wettedness perception (WPForearm), forearm and whole-body thermal discomfort (TDForearm, TDWhole), local and whole-body thermal sensation (TSForearm, TSWhole) and whole-body wettedness perception (WPwhole)) were measured every 10 min. All subjects behaved by rolling up their sleeves at 21.6 (4.7) minutes. Tskin (32.3 (0.2) °C, vs 32.0 (0.1) °C, p = 0.03), local sweat rate on the forearm (0.24 (0.08) mg.cm−2.min−1 vs 0.2 (0.04) mg.cm−2.min−1, p = 0.05), WPForearm, TDForearm, TSForearm and WPWhole were all lower in Roll than No Roll (all p < 0.05) whilst Tcore and cutaneous vascular conductance (CVC) on the forearm were not different (all p > 0.7) throughout the entire trial. We conclude that this behavioural response is an effective thermoregulatory behaviour to modulate local sudomotor function and thermal perceptions, WPWhole during exercise but only Tsk, TDForearm WPForearm and WPWhole persisted throughout the recovery in a moderate environment.

Ad libitum water consumption off-sets the thermal and cardiovascular strain exacerbated by dehydration during a 3-h simulated heatwave.

To assess whether ad libitum water ingestion of different temperatures is sufficient to prevent dehydration-related exacerbations of thermal and cardiovascular strain, during exposure to conditions representative of a heatwave. Twelve participants (mean ± SD; 25 ± 4years) exercised for 180min at 3 METs in 40.1 ± 0.6°C, 40.4 ± 2.1%RH four times: (i) consuming 20°C water ad libitum (AL20); (ii) consuming 4°C water ad libitum (AL4); (iii) replacing no fluids (NOFR); (iv) replacing sweat losses (FULLFR). Fluid consumption (FC), dehydration (%DEH), rectal temperature (Tre), rate-pressure product (RPP), forearm blood flow (FBF), mean skin temperature (Tsk), and local sweat rate (LSR) were measured/determined. FC was greater in AL20 (1.30 ± 0.41 L) than AL4 (1.03 ± 0.32 L; P = 0.003). %DEH was lower (P < 0.001) in AL20 (0.11 ± 0.76%), AL4 (0.43 ± 0.64%), and FULLFR (0.01 ± 0.12%) compared to NOFR (1.93 ± 0.28%). %DEH was lower in AL20 than AL4 (P = 0.003). In NOFR, end-trial changes in Tre were greater (P < 0.001) (1.05 ± 0.27°C) compared to all other trials, but similar among AL20 (0.72 ± 0.30°C), AL4 (0.76 ± 0.25°C) and FULLFR (0.74 ± 0.35°C). End-trial RPP was higher (P < 0.001) in NOFR (12,389 ± 1578mmHg·bpm) compared to all other trials, but similar among FULLFR (11,067 ± 1292mmHg·bpm), AL20 (11,214 ± 2078mmHg·bpm) and AL4 (11,089 ± 1795mmHg·bpm). No differences in Tsk or LSR were observed among trials, but FBF was lower in NOFR compared to FULLFR (2.84 ± 0.69 vs. 3.52 ± 0.96ml/100ml/min; P = 0.029). 4°C or 20°C ad libitum water ingestion prevented dehydration levels that exacerbate thermal/cardiovascular strain, despite blunted fluid intake with 4°C water. Higher core temperatures with NOFR are attributed to impaired internal heat distribution secondary to a lower FBF.

TEA-sensitive K+ channels and human eccrine sweat gland output.

Cholinergic-activated sweating depends on an influx of Ca2+ from extracellular fluid. It is thought that the opening of K+ channels on secretory epithelial cells facilitates Ca2+ entry. We examined the hypothesis that tetraethylammonium (TEA)-sensitive K+ channels participate in sweat production. We used a pre-post experimental design and initiated cholinergic-mediated sweating with intradermal electrical stimulation, monitored local sweat rate (SR) with a small sweat capsule mounted on the skin, and delivered 50 mM TEA via intradermal microdialysis. Local SR was activated by intradermal stimulation frequencies of 0.2-64 Hz, and we generated a sigmoid-shaped stimulus-response curve by plotting the area under the SR-time curve versus log10 stimulus frequency. Peak local SR was reduced from 0.372 ± 0.331 to 0.226 ± 0.190 mg·min-1·cm-2 (P = 0.0001) during application of 50 mM TEA, whereas the EC50 and Hill slopes were not altered. The global sigmoid-shaped stimulus-response curves for control and 50 mM TEA were significantly different (P < 0.0001), and the plateau region was significantly reduced (P = 0.0023) with the TEA treatment. The effect of TEA on peak local SR was similar in male and female subjects. However, we did note a small effect of sex on the shape of the stimulus-response curves during intradermal electrical stimulation. Overall, these data support the hypothesis that cholinergic control of sweat gland activity is modulated by the presence of TEA-sensitive K+ channels in human sweat gland epithelial cells.NEW & NOTEWORTHY The contribution of various potassium channels to the process of cholinergic-mediated human eccrine sweat production is unclear. Using a novel model for cholinergic-mediated sweating in humans, we provide evidence that tetraethylammonium-sensitive K+ channels (KCa1.1 and Kv channels) contribute to eccrine sweat production.

Thermal behavior alleviates thermal discomfort during steady-state exercise without affecting whole body heat loss.

We tested the hypothesis that thermal behavior resulting in reductions in mean skin temperature alleviates thermal discomfort and mitigates the rise in core temperature during light-intensity exercise. In a 27 ± 0°C, 48 ± 6% relative humidity environment, 12 healthy subjects (6 men, 6 women) completed 60 min of recumbent cycling. In both trials, subjects wore a water-perfused suit top continually perfusing 34 ± 0°C water. In the behavior trial, subjects maintained their upper body thermally comfortable by pressing a button to perfuse cool water (2.2 ± 0.5°C) through the top for 2 min per button press. Metabolic heat production (control: 404 ± 52 W, behavior: 397 ± 65 W; P = 0.44) was similar between trials. Mean skin temperature was reduced in the behavior trial (by -2.1 ± 1.8°C, P < 0.01) because of voluntary reductions in water-perfused top temperature (P < 0.01). Whole body (P = 0.02) and local sweat rates were lower in the behavior trial (P ≤ 0.05). Absolute core temperature was similar (P ≥ 0.30); however, the change in core temperature was greater in the behavior trial after 40 min of exercise (P ≤ 0.03). Partitional calorimetry did not reveal any differences in cumulative heat storage (control: 554 ± 229, behavior: 544 ± 283 kJ; P = 0.90). Thermal behavior alleviated whole body thermal discomfort during exercise (by -1.17 ± 0.40 arbitrary units, P < 0.01). Despite lower evaporative cooling in the behavior trial, similar heat loss was achieved by voluntarily employing convective cooling. Therefore, thermal behavior resulting in large reductions in skin temperature is effective at alleviating thermal discomfort during exercise without affecting whole body heat loss.NEW & NOTEWORTHY This study aimed to determine the effectiveness of thermal behavior in maintaining thermal comfort during exercise by allowing subjects to voluntarily cool their torso and upper limbs with 2°C water throughout a light-intensity exercise protocol. We show that voluntary cooling of the upper body alleviates thermal discomfort while maintaining heat balance through convective rather than evaporative means of heat loss.

Normative data for sweating rate, sweat sodium concentration, and sweat sodium loss in athletes: An update and analysis by sport

ABSTRACTThe purpose of this study was to expand our previously published sweat normative data/analysis (n = 506) to establish sport-specific normative data for whole-body sweating rate (WBSR), sweat [Na+], and rate of sweat Na+ loss (RSSL). Data from 1303 athletes were compiled from observational testing (2000–2017) using a standardized absorbent sweat patch technique to determine local sweat [Na+] and normalized to whole-body sweat [Na+]. WBSR was determined from change in exercise body mass, corrected for food/fluid intake and urine/stool loss. RSSL was the product of sweat [Na+] and WBSR. There were significant differences between sports for WBSR, with highest losses in American football (1.51 ± 0.70 L/h), then endurance (1.28 ± 0.57 L/h), followed by basketball (0.95 ± 0.42 L/h), soccer (0.94 ± 0.38 L/h) and baseball (0.83 ± 0.34 L/h). For RSSL, American football (55.9 ± 36.8 mmol/h) and endurance (51.7 ± 27.8 mmol/h) were greater than soccer (34.6 ± 19.2 mmol/h), basketball (34.5 ± 21.2 mmol/h), and baseball (27.2 ± 14.7 mmol/h). After ANCOVA, significant between-sport differences in adjusted means for WBSR and RSSL remained. In summary, due to the significant sport-specific variation in WBSR and RSSL, American football and endurance have the greatest need for deliberate hydration strategies.Abbreviations: WBSR: whole body sweating rate; SR: sweating rate; Na+: sodium; RSSL: rate of sweat sodium loss

Thermal Behavior Does not Differ Between Sexes During and Following High Intensity Aerobic Exercise

Females utilize thermal behavior more than males during low intensity aerobic exercise. Core temperature is elevated during high vs. low intensity aerobic exercise because of greater heat production. Thus, thermal behavior is greater during high intensity exercise because of the heightened stimulus to behave. It is unknown if sex modulates thermal behavior during high intensity exercise. PURPOSE: Test the hypothesis that thermal behavior differs between males and females during high intensity exercise and recovery. METHODS: 10 males (M) and 10 females (F) (23±3y) underwent 30 min of cycling exercise at a power output that elicited 80±5% (F) and 78±4% (M) of VO2peak (P=0.28) followed by 120 min seated recovery in a 27±1°C, 21±2% relative humidity environment. Subjects were instructed to maintain a thermally comfortable neck temperature throughout using a custom-made neck device. Neck device temperature provided an index of thermal behavior. Mean skin (10 site) and core (intestinal) temperatures, mean skin wettedness (8 site), neck device temperature, skin blood flow (laser Doppler) and local sweat rate (ventilated capsule) were measured continually. RESULTS: There were no sex differences in heat production during exercise (F: 399±68, M: 429±62 W/m2, P=0.39). During exercise, core and mean skin temperatures, skin wettedness, skin blood flow and local sweat rate increased, while neck device temperature decreased (all P<0.01). There were no sex differences in core (F: 37.7±0.2, M: 37.9±0.3°C, P> 0.50), mean skin (F: 32.6±0.3, M: 32.6±0.3°C, P>0.99) or neck device (F: 12.1±10.6, M: 11.9±10.2°C, P>0.25) temperatures, mean skin wettedness (at 30 min: F: 0.50±0.06, M: 0.53±0.04 au, P>0.99), skin blood flow (F: 163±50, M: 172±36 PU, P>0.99) or local sweat rate (F: 0.72±0.20, M: 0.85±0.27 mg/cm2/min, P>0.33) during exercise (data reported at 30 min). During recovery, core and mean skin temperatures, mean skin wettedness, skin blood flow and local sweat rate decreased, and neck device temperature increased back towards pre-exercise levels (all P<0.01). There were no differences in the dynamics of these changes between sexes (all P>0.16). CONCLUSIONS: Thermal behavior during and following high intensity aerobic exercise does not differ between males and females. This study was funded by lululemon athletica inc.

Separate and combined effects of KCa and KATP channel blockade with NOS inhibition on cutaneous vasodilation and sweating in older men during heat stress.

Our objective in this study was to examine the separate and combined effects of potassium (K+) channels and nitric oxide synthase (NOS) on cutaneous vasodilation and sweating in older men during rest and exercise in the heat. In 13 habitually active men (61 ± 4 yr), cutaneous vascular conductance and local sweat rate were assessed at six dorsal forearm skin sites continuously perfused with either 1) lactated Ringer (control), 2) 10 mM NG-nitro-l-arginine methyl ester (l-NAME, NOS inhibitor), 3) 50 mM tetraethylammonium (TEA; Ca2+-activated K+ channel blocker), 4) 5 mM glybenclamide (GLY; ATP-sensitive K+ channel blocker), 5) 50 mM TEA + 10 mM l-NAME, and 6) 5 mM GLY + 10 mM l-NAME via microdialysis. Participants rested in non-heat stress (25°C) and heat stress (35°C) conditions for ∼60 min each, followed by 50 min of moderate-intensity cycling (∼55% V̇o2peak) and 30 min of recovery in the heat. During rest and exercise in the heat, l-NAME, TEA + l-NAME, and GLY + l-NAME attenuated CVC relative to control (all P ≤ 0.05), although l-NAME was not different from TEA + l-NAME or GLY + l-NAME (all P > 0.05). TEA attenuated CVC during rest, whereas GLY attenuated CVC during exercise (both P ≤ 0.05). Additionally, whereas neither l-NAME nor TEA altered sweating throughout the protocol (all P > 0.05), combined TEA + l-NAME attenuated sweating during exercise in the heat (P ≤ 0.05). We conclude that in habitually active older men blockade of KCa and KATP channels attenuates cutaneous vasodilation during rest and exercise in the heat, respectively, and these effects are NOS dependent. Furthermore, combined NOS inhibition and KCa channel blockade attenuates sweating during exercise in the heat.

No Thermoregulatory Impairment in Skin Graft Donor Sites during Exercise-Heat Stress.

To test the hypothesis that well-healed donor and noninjured sites demonstrate similar elevations in skin blood flow and sweating during exercise-induced hyperthermia. Twenty burn survivors (>1 yr postinjury; four females) cycled for 60 min in a 39.7°C ± 0.3°C and 21.1% ± 3.3% relative humidity environment at approximately 50% of maximal aerobic capacity. Core and mean skin temperatures were recorded throughout exercise. Skin blood flow (laser-Doppler imaging) was measured at baseline and after exercise within donor (LDFDON) and adjacent noninjured control (LDFCON) sites. At 45 min of exercise, local sweat rates (Technical Absorbents) were measured within the same donor (LSRDON) and noninjured (LSRCON) areas. After 60 min of exercise, core and skin temperatures reached 38.2°C ± 0.4°C and 35.5°C ± 1.2°C, respectively. The increase in skin blood flow from baseline to end-exercise (LDFDON, 91.6 ± 44.5 AU; LDFCON, 106.0 ± 61.6 AU; P = 0.17) and local sweat rates (LSRDON, 0.46 ± 0.26 mg·cm·min; LSRCON, 0.53 ± 0.25 mg·cm·min; P = 0.14) were not different between donor and noninjured control sites. Well-healed donor sites retain the ability to increase skin blood flow and sweating during exercise heat stress, providing evidence against the inclusion of donor sites when determining whether a burn injury meets the Army's Standards of Medical Fitness.

Role of K+ channels and NOS on human eccrine sweat gland function

The non‐selective NOS inhibitor L‐NAME has been shown to reduce cholinergic‐mediated sweating in humans. We tested the hypothesis that the effect of NOS inhibition on sweat gland out is mediated through the ability of NO to activate KCa1.1 channels. We generated stimulus response curves using: lactated‐Ringers, 50 mM TEA, 20 mM L‐NAME and a cocktail of 50 mM TEA plus 20 mM L‐NAME (n=10). Local sweat rate (SR) was measured by passing dry gas through a small sweat capsule mounted on the skin. The skin was stimulated at a constant current intensity of 2.5 mA for 30 s at frequencies of 0.2, 1, 2, 4, 6, 8, 12, 16, 32, and 64 Hz using two small stainless‐steel stimulating electrodes. We plotted the area under the SR‐time curve versus stimulus frequency. All data were expressed as the area under the local SR‐time curve (AUC) and normalize to the peak AUC response during Saline control trials (% AUC peak). During Ringers perfusion, peak local sweat output averaged 99.6 ± 5.7 AUC % peak which was significantly (p&lt;0.0001) reduced by application of 50 mM TEA to 61.7 ± 22.7 AUC %peak. Addition of 20 mM L‐NAME to the 50 mM TEA solution produced an additional 20% reduction in peak SR to 42.5 ± 21.1 %AUC peak (p &lt;0.05). These data support the hypothesis that sudomotor control of sweat gland activity is modulated by the presence of TEA sensitive K+ channels and the activity of an intrinsic NOS enzyme in the epithelial cells of the human sweat glands. Further, the ability of L‐NAME to produce an additional reduction in peak SR following 50 mM TEA indicates that the influence of NOS on local SR is not likely mediated via a modulation of TEA sensitive K+ channels.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Thermal Behavior During Exercise Alleviates Thermal Discomfort Despite Exacerbating Increases in Core Temperature

PurposeIncreases in metabolic heat production during exercise stimulate perceptions of thermal discomfort as core and skin temperatures, and skin wettedness increase. Thermal discomfort is the precursor to thermal behavior. Employing thermal behavior during exercise may reduce thermal discomfort by attenuating the rise in core temperature. However, this remains unknown. We tested the hypothesis that thermal behavior attenuates the rise in core temperature and alleviates thermal discomfort during exercise.MethodsTwelve healthy subjects (24 ± 3 y, 6 females) performed two trials in which they completed 60 min of recumbent cycling exercise at a fixed rate of metabolic heat production (217 ± 28 W/m2) in a 27 ± 0°C, 48 ± 6% relative humidity environment. In both trials subjects wore a water perfused suit top. In the control trial, 34 ± 0°C water circulated through the top during the trial (CON). The experimental trial allowed for thermal behavior (BEH) where subjects were instructed to maintain their upper body thermally comfortable throughout. In BEH, subjects thermally behaved by pressing a button to receive cool water (2 ± 1°C) through the water perfused suit top for 2 min, which was followed by a 1 min wash out period. Mean skin (10 site) and core (telemetry pill) temperatures, mean skin wettedness (8 site), skin blood flow (forearm, laser Doppler), and local sweat rate (ventilated capsule) were measured continually. Local sweat rate was measured under (on mid‐axillary line) and outside (on anterior thigh, n=7) of the water perfused suit top. Whole body thermal comfort was recorded every 10 min. Water perfused suit top temperature provided an index of thermal behavior. Data are presented as mean ± SD as the absolute change from the values acquired pre‐exercise.ResultsMetabolic heat production was not different between trials (P=0.44). The increase in core temperature was greater in BEH vs. CON at 50 and 60 min (both by +0.1 ± 0.3°C, P&lt;0.01). Mean skin temperature was reduced in BEH vs. CON from 20 min (by −0.5 ± 0.7°C, P&lt;0.01) onwards (P&lt;0.01). Mean skin wettedness was greater in BEH vs. CON from 30 min (by +0.01 ± 0.03 a.u., P&lt;0.01) onwards (P&lt;0.01). Water perfused suit top temperature was reduced in BEH vs. CON from 10 min (by −5.6 ± 7.0°C, P&lt;0.01) onwards (P&lt;0.01). Mid‐axillary sweat rate was attenuated in BEH vs. CON from 10 min (by −0.1 ± 0.12 g/cm2/min) onwards (P&lt;0.01), and thigh sweat rate was attenuated at min 20 (by: −0.1 ± 0.2 g/cm2/min) and 60 (by −0.2 ± 0.2 g/cm2/min). Forearm skin blood flow was not different between BEH and CON at any time (P=0.20). Increases in whole body thermal discomfort were attenuated in BEH vs. CON within the first 10 min (by −0.4 ± 0.4 a.u., P=0.04) onwards (P&lt;0.01).ConclusionsEmploying thermal behavior that reduces mean skin temperature during exercise alleviates thermal discomfort despite exacerbating the rise in core temperature and skin wettedness. Reductions in sweat rate may contribute to the greater rise in core temperature when employing thermal behavior. These findings may question the role of skin wettedness in stimulating thermal behavior during exercise.Support or Funding InformationSupported by lululemon athletica inc.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

The use of infrared thermal imaging to measure spatial and temporal sweat retention in clothing

In our previous laboratory study a ‘destructive’ gravimetric method was developed to quantify local garment sweat absorption. While this currently is the only methodology that permits direct and analytical measurements of garment regional sweat absorption, the latter approach is time-consuming and expensive, therefore, of limited applicability. As such, in this study, we wanted to assess whether infrared thermography could be used as an indirect method to estimate garment regional sweat absorption, right after exercise, in a ‘non-destructive’ fashion. Spatial and temporal sweat absorption data, obtained in our previous study, were correlated with spatial and temporal temperature data obtained in the same experiment with an infrared thermal camera. The data suggest that infrared thermography is a good tool to qualitatively predict regional sweat absorption in garments at separate individual time points; however, temporal changes are not predicted well, due to a moisture content threshold above which variations in sweat content cannot be discriminated by further temperature changes.

Independent Influence of Spinal Cord Injury Level on Thermoregulation during Exercise.

This study aimed to establish the true influence of spinal cord injury (SCI) level on core temperature and sweating during exercise in the heat independently of biophysical factors. A total of 31 trained males (8 with tetraplegia [TP; C5-C8], 7 with high paraplegia [HP; T1-T5], 8 with low paraplegia [LP; T6-L1], and 8 able bodied [AB]) performed 3 × 10 min of arm ergometry with 3-min rest at a metabolic heat production of (a) 4.0 W·kg (AB vs TP) or (b) 6.0 W·kg (AB vs HP vs LP), in 35°C, 50% relative humidity. Esophageal (Tes) and local skin temperatures and local sweat rate (LSR) on the forehead and upper back were measured throughout. Change in Tes was greatest in TP (1.86°C ± 0.32°C vs 0.29°C ± 0.07°C, P < 0.001) and greater in HP compared with LP and AB, reaching 1.20°C ± 0.50°C, 0.66°C ± 0.23°C, and 0.53°C ± 0.12°C, respectively (P < 0.001). Approximately half of the variability in end-trial ΔTes was described by SCI level in paraplegics (adjusted R = 0.490, P = 0.005). Esophageal temperature onset thresholds of sweating at the forehead and upper back were similar among HP, LP, and AB, whereas no sweating was observed in TP. Thermosensitivity (ΔTes vs ΔLSR) was also similar, except for LP demonstrating lower thermosensitivity than AB at the upper back (0.78 ± 0.26 vs 1.59 ± 0.89 mg·cm·min, P = 0.039). Change in skin temperature was greatest in denervated regions, most notably at the calf in all SCI groups (TP, 2.07°C ± 0.93°C; HP, 2.73°C ± 0.68°C; LP, 2.92°C ± 1.48°C). This study is the first to show the relationship between ΔTes and SCI level in athletes with paraplegia after removing variability arising from differences in metabolic heat production and mass. Individual variability in ΔTes is further reduced among athletes with TP because of minimal evaporative heat loss secondary to an absence of sweating.

Thermal Behavior Differs between Males and Females during Exercise and Recovery.

This study tested the hypothesis that females rely on thermal behavior to a greater extent during and after exercise, relative to males. In a 24°C ± 1°C; (45% ± 10% RH) environment, 10 males (M) and 10 females (F) (22 ± 2 yr) cycled for 60 min (metabolic heat production: M, 117 ± 18 W·m; F, 129 ± 21 W·m), followed by 60-min recovery. Mean skin and core temperatures, skin blood flow and local sweat rates were measured continually. Subjects controlled the temperature of their dorsal neck to perceived thermal comfort using a custom-made device. Neck device temperature provided an index of thermal behavior and mean body temperature provided an index of the stimulus for thermal behavior. Data were analyzed for total area under the curve for exercise and recovery time points. To further isolate the effect of exercise on thermal behavior during recovery, data were also analyzed the minute mean body temperature returned to preexercise levels within a subject. There were no sex differences in metabolic heat production (P = 0.71) or body temperatures (P ≥ 0.10) during exercise. Area under the curve for neck device temperature during exercise was greater for F (-98.4°C·min ± 33.6°C·min vs -64.5°C·min ± 47.8°C·min, P = 0.04), but did not differ during recovery (F, 86.8°C·min ± 37.8°C·min; M, 65.6°C·min ± 35.9°C·min; P = 0.11). In M, mean skin (P = 0.90), core (P = 0.70) and neck device (P = 0.99) temperatures had recovered by the time that mean body temperature had returned to preexercise levels. However, in F, neck device temperature (P = 0.04) was reduced while core temperature remained elevated (P < 0.01). Females use thermal behavior during exercise to a greater extent than M. During recovery, thermal behavior may compensate for elevated core temperatures in F despite mean body temperatures returning to preexercise levels.

Reliability of a wearable sweat rate monitor and routine sweat analysis techniques under heat stress in females

IntroductionThe aim of the study was to evaluate the reliability of five different sweat analysis techniques which measure; whole body sweat rate [WBSR], local sweat rate [LSR] (via technical absorbent [TA] method and KuduSmart® monitor), sweat conductivity [SC] and sweat gland activation [SGA] in a female population when exercising moderately under heat stress. MethodsFourteen females (age; 26 ± 7 years, body mass; 66.5 ± 7.6 kg, height; 167.1 ± 6.4 cm) completed a preliminary threshold walking test (to determine exercise intensity) and two main trials, separated by 2 days. Main trials consisted of 30-min seated rest in the environmental chamber (35 °C, 50% relative humidity) in an upper body sauna-suit, before its removal, and walking at a moderate intensity (4 metabolic equivalents) for 30-min (speeds ranged from 4.8 to 6.5 km h−1). WBSR was measured via nude mass pre and post exercise. The TA and Tegaderm patches (for sweat sodium chloride) were placed on the back, forearm and chest for the entire 60-min, replicated for all participants for both trials. SGA was assessed following the 60-min trial and the KuduSmart® monitor was placed on the left arm for the 30-min of exercise. ResultsWBSR, LSR methods and SC demonstrated no difference between trials (p > 0.05), good agreement (within limits), strong correlations (r ≥ 0.88) and low typical error of measurements [TEM] (< 0.04 L min−1, 0.13 mg min−1 cm−2 and 8 mmol L−1, respectively). SGA method showed moderate intra-class correlation (r = 0.80), with high TEM (5 glands) and large limits of agreement. ConclusionSudomotor function is reliable, as demonstrated by good reliability, small TEM and strong correlations. The use of these sweat techniques is appropriate and practical in females who are exercising at moderate intensity under heat stress, and so, may aid future interventions. SGA shows larger variation and should be used with caution.