Local Sweat Rate Research Articles

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

Aspirin ingestion does not alter the onset or slope of local sweat rate during whole‐body passive heat stressStephen J. Carter, Robert L. Herron, S. Zeb Akers, Ann B. Collins, Jonathan E. Wingo. Department of Kinesiology, The University of Alabama, Tuscaloosa, AL 35487Aspirin (acetylsalicylic acid; ASA) is a commonly prescribed over‐the‐counter drug. As a fever suppressant ASA may interfere with normal hypothalamic‐mediated temperature regulation. We sought to determine if varying doses of ASA would alter the onset and slope (i.e., sensitivity) of local sweat rate during whole‐body passive heating. Seven healthy men (mean ± SD; 28 ± 3 y) completed a counter‐balanced design to compare ASA treatments (single dose of non‐enteric coated 325‐mg ASA vs. 4 days of 81‐mg ASA) to a control trial. A 10 day washout period was given between ASA treatments. Participants were physically active, free from cardiovascular disease and refrained from vigorous physical activity 24 h prior to testing. Upon arrival, participants were outfitted with a heart rate monitor, rectal thermocouple, 6 skin thermocouples, and a ventilated capsule placed on the dorsal forearm to measure local sweat rate via capacitance hygrometry. To raise mean body temperature (Tb) participants rested supine while hot water (~49 °C) circulated through a tube‐lined suit. Body heating ensued until participants reached a 1.0 °C increase above baseline Tb. ASA did not affect Tb at baseline (P=0.14). The onset and slopes were unaffected by ASA use (P=0.33 and P=0.87, respectively). Additionally, ASA treatments did not alter peak sweat output (P=0.87). Aspirin ingestion did not appear to affect sweat responses in this cohort of men.

Thermoregulatory responses to heat stress and hypoxia (1104.19)

The aim of this study was to examine the thermoregulatory responses to combined heat stress and hypoxia. Seven healthy male subjects (22±3 yr, 80±11 kg, 180±7 cm), dressed in a water‐perfused suit, underwent moderate passive heating (Δ core temperature ~0.8 °C) on 2 separate occasions. In 1 trial subjects breathed normoxic air (NORMOXIA) and in the other subjects breathed balanced 13% O2 air (HYPOXIA). Skin blood flow (SkBF; laser Doppler flowmetry), expressed as cutaneous vascular conductance (CVC; flux/blood pressure), and local sweat rate (SR; capacitance hygrometry) were recorded on the forearm. Core (Tcore; intestinal pill) and local skin temperatures (Tsk), as well as blood pressure (BP; automated sphygmomanometry and digital photoplethysmography), heart rate (HR; ECG) oxygen saturation (SpO2; pulse oximetry) were also monitored. Tcore and mean body temperature (Tbody) thresholds for heat stress‐induced elevations in SkBF and SR, as well as the SkBF/SR: Tcore/Tbody slopes were calculated. At normothermic baseline HYPOXIA reduced SpO2 (98±1 vs 90±6 %, P<0.01) and slightly elevated forearm SkBF (9±6 vs 13±12 % CVC max, P=0.10) and HR (67±10 vs 74±7 beats.min‐1, P<0.01). Tcore (37.0±0.3 vs 37.0±0.3 °C, P=0.30) was unchanged. During heating the forearm SkBF Tcore threshold (36.9±0.3 vs 37.0±0.2 °C, P=0.30) and the forearm SR Tbody threshold (36.7±0.3 vs 36.7±0.2 °C, P=0.90) were not different between trials. The forearm SkBF:Tcore slope was slightly reduced during HYPOXIA (1.04±1.17 vs 0.59±1.19 CVC units·°C, P=0.07) whereas the forearm SR:Tbody slope (0.17±0.09 vs 0.22±0.11 ml.cm2.min‐1·°C, P=0.04) was increased by HYPOXIA. These results indicate that moderate hypoxia does not affect central thermoregulatory function but alters peripheral thermoregulatory effector function via blunted skin blood flow and accentuated sweating slopes possibly via baseline hypoxia‐induced cutaneous vasodilation.Grant Funding Source: European Commission FP7

Evidence that transient changes in sudomotor output with cold and warm fluid ingestion are independently modulated by abdominal, but not oral thermoreceptors

Two studies were performed to 1) characterize changes in local sweat rate (LSR) following fluid ingestion of different temperatures during exercise, and 2) identify the potential location of thermoreceptors along the gastrointestinal tract that independently modify sudomotor activity. In study 1, 12 men cycled at 50% Vo2peak for 75 min while ingesting 3.2 ml/kg of 1.5°C, 37°C, or 50°C fluid 5 min before exercise; and after 15, 30, and 45-min of exercise. In study 2, 8 men cycled at 50% Vo2peak for 75 min while 3.2 ml/kg of 1.5°C or 50°C fluid was delivered directly into the stomach via a nasogastric tube (NG trials) or was mouth-swilled only (SW trials) after 15, 30, and 45 min of exercise. Rectal (Tre), aural canal (Tau), and mean skin temperature (Tsk); and LSR on the forehead, upper-back, and forearm were measured. In study 1, Tre, Tau, and Tsk were identical between trials, but after each ingestion, LSR was significantly suppressed at all sites with 1.5°C fluid and was elevated with 50°C fluid compared with 37°C fluid (P < 0.001). The peak difference in mean LSR between 1.5°C and 50°C fluid after ingestion was 0.29 ± 0.06 mg·min(-1)·cm(-2). In study 2, LSR was similar between 1.5°C and 50°C fluids with SW trials (P = 0.738), but lower at all sites with 1.5°C fluid in NG trials (P < 0.001) despite no concurrent differences in Tre, Tau, and Tsk. These data demonstrate that 1) LSR is transiently altered by cold and warm fluid ingestion despite similar core and skin temperatures; and 2) thermoreceptors that independently and acutely modulate sudomotor output during fluid ingestion probably reside within the abdominal area, but not the mouth.

Selecting the correct exercise intensity for unbiased comparisons of thermoregulatory responses between groups of different mass and surface area

We assessed whether comparisons of thermoregulatory responses between groups unmatched for body mass and surface area (BSA) should be performed using a metabolic heat production (prod) in Watts or Watts per kilogram for changes in rectal temperature (ΔTre), and an evaporative heat balance requirement (Ereq) in Watts or Watts per square meter for local sweat rates (LSR). Two groups with vastly different mass and BSA [large (LG): 91.5 ± 6.8 kg, 2.12 ± 0.09 m(2), n = 8; small (SM): 67.6 ± 5.6 kg, 1.80 ± 0.09 m(2), n = 8; P < 0.001], but matched for heat acclimation status, sex, age, and with the same onset threshold esophageal temperatures (LG: +0.37 ± 0.12°C; SM: +0.41 ± 0.17°C; P = 0.364) and thermosensitivities (LG: 1.02 ± 0.54, SM: 1.00 ± 0.38 mg·cm(-2)·min(-1)·°C(-1); P = 0.918) for sweating, cycled for 60 min in 25°C at different levels of prod (500 W, 600 W, 6.5 W/kg, 9.0 W/kg) and Ereq (340 W, 400 W, 165 W/m(2), 190 W/m(2)). ΔTre was different between groups at a prod of 500 W (LG: 0.52 ± 0.15°C, SM: 0.92 ± 0.24°C; P < 0.001) and 600 W (LG: 0.78 ± 0.19°C, SM: 1.14 ± 0.24°C; P = 0.007), but similar at 6.5 W/kg (LG: 0.79 ± 0.21°C, SM: 0.85 ± 0.14°C; P = 0.433) and 9.0 W/kg (LG: 1.02 ± 0.22°C, SM: 1.14 ± 0.24°C; P = 0.303). Furthermore, ΔTre was the same at 9.0 W/kg in a 35°C environment (LG: 1.12 ± 0.30°C, SM: 1.14 ± 0.25°C) as at 25°C (P > 0.230). End-exercise LSR was different at Ereq of 400 W (LG: 0.41 ± 0.18, SM: 0.57 ± 0.13 mg·cm(-2)·min(-1); P = 0.043) with a trend toward higher LSR in SM at 340 W (LG: 0.28 ± 0.06, SM: 0.37 ± 0.15 mg·cm(-2)·min(-1); P = 0.057), but similar at 165 W/m(2) (LG: 0.28 ± 0.06, SM: 0.28 ± 0.12 mg·cm(-2)·min(-1); P = 0.988) and 190 W/m(2) (LG: 0.41 ± 0.18, SM: 0.37 ± 0.15 mg·cm(-2)·min(-1); P = 0.902). In conclusion, when comparing groups unmatched for mass and BSA, future experiments can avoid systematic differences in ΔTre and LSR by using a fixed prod in Watts per kilogram and Ereq in Watts per square meter, respectively.

Moderate-Intensity Intermittent Work in the Heat Results in Similar Low-Level Dehydration in Young and Older Males

Older individuals may be more susceptible to the negative thermal and cardiovascular consequences of dehydration during intermittent work in the heat. This study examined the hydration, thermal, and cardiovascular responses to intermittent exercise in the heat in 14 Young (Y, Mean ± SE; 25.8 ± 0.8 years), Middle-age (MA, 43.6 ± 0.9 years), and Older (O, 57.2 ± 1.5 years) healthy, non-heat acclimated males matched for height, mass, body surface area, and percent body fat. Rectal temperature (Tre), heart rate (HR), local sweat rate (LSR), and hydration indices were measured during 4 × 15-min moderate to heavy cycling bouts at 400 W heat production, each followed by a 15-min rest period, in Warm/Dry (35°C, 20% relative humidity [RH]) and Warm/Humid (35°C, 60% RH) heat. No differences were observed between the age groups for Tre, Tre change, HR, LSR, mass change, urine specific gravity, and plasma protein concentration in either condition, irrespective of the greater level of thermal and cardiovascular strain experienced in the Warm/Humid environment. Plasma volume changes (Dry Y: −5.4 ± 0.7, MA: −6.2 ± 0.9, O: −5.7 ± 0.9%, Humid Y: −7.3 ± 1.0, MA: −7.9 ± 0.8, O: −8.4 ± 1.0%) were similar between groups, as were urine specific gravity and plasma protein concentrations. Thus, physically active Young, Middle-age, and Older males demonstrate similar hydration, thermal, and cardiovascular responses during moderate- to high-intensity intermittent exercise in the heat.

Higher sweating rate and skin blood flow during the luteal phase of the menstrual cycle.

Evaporation by sweating is the most effective way to remove heat from the body. Sweat rates increase under both local and whole-body heat stress. Men and women differ in how they respond to heat, because sexual steroids alter resting body core temperature and the threshold for sweating and skin blood flow (SBF) during heating. The purpose of the present study was to compare local sweat rates and cutaneous vasodilatation during heat exposure in women with a regular menstrual cycle. The cutaneous vasodilatation was judged by measuring the SBF. Eight female and nine male subjects participated in this study, and their age range was 24-29 years. Female subjects were tested twice throughout one full menstrual cycle: once during the middle follicular phases and once during the luteal phase. Subjects remained in a temperature-regulated room at 41°C and 21% of relative humidity for 40 minutes. Sweat rate was recorded from the forehead, forearm, and thigh, and skin temperature and SBF were measured on the thigh and forehead. We found that the sweating rate and SBF were greater in the luteal phase compared to follicular phase (p<0.05). Since both SBF and sweating were controlled by the sympathetic nerve system, the sympathetic outflow was greater during whole body heat exposure in the luteal phase. In contrast, for men, there was no significant difference in sweating and SBF over the same calendar period (p>0.05). We propose the enhanced sympathetic activity in the luteal phase with a regular menstrual cycle.

Do Older Firefighters Show Long-Term Adaptations to Work in the Heat?

Older experienced firefighters may show signs of heat adaptation, and thus reduced physiological strain, due to repeated occupational heat stress exposure. The aim was to examine physiological and perceptual strain, and hydration, responses to intermittent exercise in the heat in 12 older Non-Firefighter (Non-FF) and experienced Firefighter (FF) males, pair matched for age (Group mean ± SE: Non-FF = 51.7 ± 1.5, FF = 49.8 ± 1.1 years), VO2peak (Non-FF = 39.4 ± 2.2, FF = 40.7 ± 1.8 mL·kg−1·min−1), body surface area (Non-FF = 1.94 ± 0.04, FF = 2.03 ± 0.03 m2), and percent body fat (Non-FF = 24.4 ± 2.3, FF = 19.3 ± 1.8%). Rectal (Tre) and mean skin (MTsk) temperatures, heart rate (HR), local sweat rate (LSR), hydration indices, and ratings of thermal sensation and perceived exertion were measured during 4 ×15-min (rest 15-min) moderate-to-heavy cycling bouts (400 W heat production) in Dry and Humid heat (35°C, ∼20 and ∼60% relative humidity, respectively). No differences were observed between the Non-FF and FF for Tre, Tre change, MTsk, HR,% max HR, LSR, physiological strain index (PhSI), or % plasma volume change. Plasma protein concentration was reduced at baseline for the Non-FF (7.6 ± 0.1 g·100 mL−1) than FF (8.0 ± 0.1 g·100 mL−1). The Perceptual Strain Index overestimated PhSI for Non-FF and FF in both thermal conditions. At the end of exercise, the Non-FF showed a greater Tre difference between thermal conditions (0.27 ± 0.05°C) compared to the FF (0.10 ± 0.09°C). Although the Non-Firefighters and Firefighters demonstrate similar cardiovascular and hydration responses during moderate-to-heavy intensity exercise within each of the thermal conditions, the attenuated thermal effects between the two heat stress conditions in the Firefighters suggests a protective adaptation.

Body Fatness, Body Core Temperature, and Heat Loss During Moderate-Intensity Exercise

This study examined the influence of body fatness on body core temperature and heat loss responses during moderate-intensity exercise. Nine men with lower body fat and eight men with higher body fat, matched for aerobic fitness, completed 1 h of recumbent cycling at the same absolute intensity in a warm environment (30 degrees C, 40% RH). Percent body fat was measured by hydrostatic weighing, using oxygen dilution to determine residual volume. Esophageal temperature (T(es)), mean skin temperature (T(sk)), and local sweat rate (m(sw)) were measured at rest and continuously during exercise while forearm blood flow (FBF) was measured at rest and every 10 min during exercise. The lower body fat and higher body fat groups were successfully matched for aerobic fitness, removing the influence of body fatness, given that V/O2(peak) was 50.72 +/- 7.34 and 50.43 +/- 5.01 ml x kg LBM(-1) x min(-1), respectively. When compared to lower body fat individuals, % body fat, body surface area (A(D)), and body mass were higher and A(D)/ mass was lower in higher body fat individuals. T(es), T(sk), FBF, m(sw), and the slope of m(sw):T(es) were not different between groups. Metabolic heat production was similar between the lower body fat (299.7 +/- 40.5 W x m(-2)) and higher body fat (288.1 +/- 30.6 W x m(-2)) subjects, respectively. Dry and evaporative heat loss, as well as heat storage during exercise, were not different between groups. These data suggest that there is no effect of body fatness on body core temperature or heat loss responses during moderate-intensity exercise in a warm environment.

Whole-Body Heat Loss during Exercise in the Heat Is Not Impaired in Type 1 Diabetes

The objective of this study is to determine whether individuals with type 1 diabetes exhibit impairments in local and whole-body heat loss responses that could affect core temperature regulation during exercise in the heat compared with matched, nondiabetic individuals. Twelve otherwise healthy individuals with type 1 diabetes (HbA1c = 7.7% ± 0.3%) and 12 controls matched for age, sex, body surface area, and physical fitness cycled continuously for 60 min at a set rate of metabolic heat production (approximately 400 W) in a whole-body direct calorimeter (35°C and 20% relative humidity). Local sweat rate (ventilated capsule) was measured on the back and skin blood flow (laser Doppler velocimetry) on the forearm. Core (rectal and esophageal) and mean skin temperatures and heart rate were measured continuously. Whole-body heat exchange and change in body heat content were measured using simultaneous direct whole-body and indirect calorimetry. The change (mean ± SE) in body heat content was similar between groups during exercise (diabetes, 409 ± 27 kJ; control, 386 ± 33 kJ; P = 0.584) and recovery (diabetes, -115 ± 16 kJ; control, -93 ± 24 kJ; P = 0.457). Local heat loss responses of sweating (P = 0.783) and skin blood flow (P = 0.078) as well as rectal temperature (diabetes, 37.87°C ± 0.10°C; control, 37.85°C; ± 0.13°C; P = 0.977) and heart rate (diabetes, 130 ± 9 beats·min, vs control, 126 ± 8 beats·min, P = 0.326) were comparable at the end of the exercise period. During light-to-moderate-intensity exercise performed under conditions permitting full sweat evaporation, otherwise healthy type 1 diabetic individuals did not show impaired heat loss responses during heat exposure when compared with matched individuals without diabetes.

Sweating the details: what really drives eccrine output during exercise‐heat stress

Copious sweating observed during passive or exercise-induced heat stress (exercise-heat stress) is the primary outcome of the sophisticated eccrine-dependent cooling system that has evolved in humans. One can speculate as to why sweating, with its large ability to liberate heat (580 kcal l-1), would be advantageous for a ‘naked ape’ ambulating in a warm savanna environment. Despite this grand role of sweating in human thermoregulation and evolution, it is humbling how little we know of its control and regulation. Recent work is beginning to detect the precise brain areas involved (Shafton & McAllen, 2013), but imprecise systemic factors are reported in the literature to be the primary drivers of eccrine sweating. In this issue of The Journal of Physiology, Gagnon and colleagues (Gagnon et al. 2013) challenge the notion that relative workload (current workload compared to maximum work capacity) is the primary determinant of sweat output during exercise-heat stress. In their experiment, human subjects performed exercise-heat stresses in a direct calorimeter at a fixed workload (290 W) in variable thermal environments (30, 35, 40 and 45°C) or at a variable workload (200, 350, or 500 W) in a fixed 30°C thermal environment. Using this direct method of measuring heat emitted, the evaporative requirement for heat balance was superior to relative workload in predicting whole-body sweat rate, and when relative workload was combined with the evaporative requirement for heat balance, predictions did not improve. Authors interpret these data as definitive evidence against the use of relative workload in experiments when the primary determinant is sweat rate. Rather, authors indicate that matching evaporative requirements to what is needed to maintain heat balance in both steady-state and non-steady-state exercise-heat stress is a superior experimental approach. Do these interpretations make sense? Using Occam's razor (the most direct hypothesis being most likely correct), it is logical that the evaporative requirement to maintain a regulated internal temperature would be the driving force for eccrine sweat output rather than a less direct measure such as relative workload. As one can see from a traditional heat balance equation (eqn (1)), relative workload is located within the M–Wk component vs. the more direct E: (1) where S is heat storage (balance); M is metabolism and Wk is external work; R+C+K is dry heat exchange via radiation, convection, and conduction; and E is evaporative heat loss. Relative workload has an inherent fitness bias. This can be observed with similar whole-body and local sweat rates when comparing high fitness (∼60 ml kg−1 min−1) and average fitness (∼40 ml kg−1 min−1) groups at fixed workload (100–110 W). In contrast, at a relative workload (60% of maximal), the same high fitness group had greater whole-body and local sweat rates compared to the average fitness group (Jay et al. 2011). What are the potential mechanisms of the fitness-induced increase in sweat output? Whole-body sweating mechanisms are difficult to determine and remain elusive. However, locally perfusing the sudorific agonist acetylcholine (ACh) via intradermal microdialysis stimulates muscarinic type-3 receptors on eccrine sweat glands, and if water vapour is collected via capacitance hygrometry just above the skin containing the microdialysis membrane, agonist to sweating dose–response relations can be determined in small areas of skin. Using this limited but better controlled approach, increasing maximal work capacity via 8 weeks of aerobic exercise training causes an increase in the in vivo maximal sweating responses (Wilson et al. 2010). Inactivity, such as 14 days of bedrest, decreases maximal work and sweating capacity and importantly, aerobic exercise training during bedrest rescues this response (Crandall et al. 2003). However, neither of these changes in work capacity changes the in vivo eccrine sweat gland cholinergic sensitivity. This indicates that for a given amount of ACh release from cholinergic sudomotor nerves there is not more sweating, but if the amount of ACh released increases, more eccrine sweating results. These data combined with this new study (Gagnon et al. 2013) suggest that trained individuals may release more ACh at a given relative workload, which may be responsible for their higher sweat rate. Gagnon et al. (2013) provide a long list of previous studies that compared independent groups at a relative workload rather than the more predictive evaporative requirement for heat balance. Are all these previous studies flawed? Not necessarily. Many, but not all, of these studies were fitness-matched to maximal work capacity and thus relative workloads would be similar. That said, the authors of this new study (Gagnon et al. 2013) give the field pause to consider what actually drives the sweating response during exercise-heat stress. Although more work needs to be completed to determine these precise driving forces and what can be used to compare experimental groups, future studies should be cautioned against using relative workload as a between-groups standardization when eccrine sweating is the main variable of interest.

Thermoreceptors in the upper gastrointestinal tract independently influence sudomotor activity

Warm and cool fluid ingestion during exercise has been previously shown to alter local sweat rate independently of core and skin temperatures. This study strove to identify the location of the thermoreceptors responsible. Six males cycled at 50% VO2max for 75 min in a 24.8 ± 0.7°C and 33.4 ± 3.5% RH environment, while either mouth‐swilling (SW) 1.5°C or 50°C water; or ingesting 1.5°C or 50°C water through a nasogastric (NG) tube in three 3.2 mL·kg−1 boluses after 15, 30, and 45 min of exercise. Mean skin temperature (Tsk), mean local sweat rate (MLSR) and rectal temperature (Tre) were measured continuously. For all trials, Tre and Tskwere similar throughout. In the NG trials, MLSR with 1.5°C water was lower than with 50°C water, after 30, 45, and 60 min (P&lt;0.05), but not after 15 or 75 min (P&gt;;0.05) of exercise. In contrast, during the SW trials, MLSR with 1.5°C and 50°C water was almost identical throughout exercise (P&gt;;0.05). In conclusion, thermoreceptors in the stomach region, rather than thermoreceptors in the mouth, are responsible for the transient alterations of sudomotor activity previously observed following the ingestion of warm and cool water. Supported by NSERC Discovery Grant #386143–2010.

Role of nitric oxide synthase on local sweat rate in older adults during intermittent exercise in the heat

Studies suggest that nitric oxide (NO) has a role in sweating. Older adults have a lower production of and sensitivity to NO which may explain why older adults have lower local sweat rates (LSR) compared with their younger counterparts during exercise. We examined the role of NO synthase (NOS) on LSR during intermittent exercise in the heat. Ten young (Y) and ten older (O) participants completed 3 × 15 min of cycling (rate of metabolic heat production of 600 W) separated by 15 min recovery in the heat (35ºC, 30% RH). Intradermal microdialysis probes were inserted in the forearm and perfused with either 0.9% saline (CON) or 10 mM L‐NAME (a NOS inhibitor). LSR was measured directly over each membrane. LSR was similar between Y and O during the exercise bouts at the CON (average of the 3 exercise bouts: Y; 0.96 ± 0.20 vs. O; 0.87 ± 0.25 mg·min−1·cm−2 p=0.327) and the LNAME (Y: 0.74 ± 0.18 vs. O: 0.83 ± 0.27 mg·min−1·cm−2 p=0.327) sites. However, the relative contribution of NO to the sweating response was reduced in Y (CON: 0.96 ± 0.20 vs. L‐NAME: 0.74 ± 0.18 mg·min−1·cm−2, p=0.017), but not O (CON: 0.87 ± 0.25 vs. L‐NAME: 0.83 ± 0.27 mg·min−1·cm−2, p=0.965). We conclude that the exercise‐induced increase in sweating is influenced by NO in younger adults. However, it appears that the level of influence is blunted in older individuals during high intensity exercise in the heat.This research was funded by Natural Sciences and Engineering Research Council (RGPIN‐298159–2009, held by Dr. Kenny).

Quantitative assessment of cutaneous C‐fiber function in human skin via direct sudomotor activation

Small sympathetic cholinergic C‐fiber function was examined using intradermal electrical stimulation to activate sudomotor nerves in the forearm skin of healthy humans. We measured local sweat rate (SR) with a 0.7 cm2 capsule containing a humidity sensor and a thermocouple and flushed with dry gas. Two small stainless steel needles were place into the skin (7 mm apart, 2 mm deep) and stimulated at a constant current intensity of 2.5 mA for 30 s and 120 s at frequencies of 0.2, 1, 2, 4, 8, 16, 32, and 64 Hz. The stimulus‐response characteristics were evaluated using a non‐linear four‐parameter logistic curve fitting equation. Peak local SR occurred between 32 and 64 Hz and was similar for 30 and 120 s stimulus duration averaging 0.46 ± 0.2 and 0.49 ± 0.2 mg • min−1 • cm−2, respectively. The EC50 averaged 8.3 ± 0.3 Hz during the 30 sec stimulus but decreased to 3.6 ± 0.05 Hz (p&lt;0.05) during the 120 s stimulus. The area under the SR‐time curve following atropine sulfate (2 μg/ml) was lower than control (p&lt;0.05) and not different from zero. These data support the hypothesis that the SR response to intradermal electrical stimulation reflects, exclusively, the effect of direct depolarization of sympathetic cholinergic C‐fibers and release of acetylcholine. As such, this model can be used to provide a quantifiable assessment of small C‐fiber function in human skin.

Seasonal acclimatization to the hot summer over 60 days in the Republic of Korea suppresses sweating sensitivity during passive heating

The main objective of this study was to determine the central mechanisms involved in suppression of thermal sweating after seasonal acclimatization (SA) during passive heating (immersing the legs in 43°C hot water for 30min). Testing was performed in July (before-SA) and August (after-SA) [25.2±2.2°C, 73.9±10.3% relative humidity (RH), Cheonan (Chungnam,126° 52′N, 33.38′E), in the Republic of Korea. All experiments were carried out in an automated climatic chamber (25.0±0.5°C and RH 60.0±3.00%). Twelve healthy men (height, 174.6±5.40cm; weight, 65.4±5.71kg; age, 22.7±2.90yr) participated. The local sweat onset time was delayed in the after-SA compared to that in the before-SA (p<0.001). The local sweat rate and whole body sweat loss volume decreased in the after-SA compared to those in the before-SA (p<0.001). In addition, evaporative loss volume decreased significantly in the after-SA compared to that in the before-SA [chest, upper-back, thigh and forearm (p<0.001)]. Changes in tympanic temperature and mean body temperature were significantly lower (p<0.05) and the basal metabolic rate decreased significantly in the after-SA compared to those in the before-SA (p<0.001). These results suggest that maintenance of a lower body temperature and basal metabolic rate can occur and blunt the central sudomotor mechanisms following seasonal acclimatization, which suppresses sweating sensitivity.

A comparison between the technical absorbent and ventilated capsule methods for measuring local sweat rate

This study assessed the accuracy of the technical absorbent (TA) method for measuring local sweat rate (LSR) relative to the well-established ventilated capsule (VC) method during steady-state and nonsteady-state sweating using large and small sample surface areas on the forearm and midback. Forty participants (38 males and two females) cycled at 60% peak oxygen consumption for 75 min in either a temperate [22.3 ± 0.9°C, 32 ± 17% relative humidity (RH)] or warm (32.5 ± 0.8°C, 29 ± 7% RH) environment. Simultaneous bilateral comparisons of 5-min LSR measurements using the TA and VC methods were performed for the back and forearm after 10, 30, 50, and 70 min. LSR values, measured using the TA method, were highly correlated with the VC method at all time points, irrespective of sample surface area and body region (all P < 0.001). On average, ≈ 79% of the variability observed in LSR measured with the VC method was described by the TA method. The mean difference in absolute LSR using the TA method (TA-VC with 95% confidence intervals) was -0.23 [-0.30,-0.16], -0.11 [-0.21,0.00], -0.03 [-0.14,+0.08], and +0.02 [-0.07,+0.11] mg · cm(-2) · min(-1) after 10, 30, 50, and 70 min of exercise, respectively. Duplicate LSR measurements within each method during steady-state sweating were highly correlated (TA: r = 0.96, P < 0.001, n = 20; VC: r = 0.97, P < 0.001, n = 20) with a mean bias of +0.07 ± 0.14 and +0.01 ± 0.10 mg · cm(-2) · min(-1) for TA and VC methods, respectively. The mean smallest detectable difference in LSR was 0.12 and 0.05 mg · min(-1) · cm(-2) for TA and VC methods, respectively. These data support the TA method as a reliable alternative for measuring the rate of sweat appearance on the skin surface.

Design data for footwear: sweating distribution on the human foot

PurposeThe purpose of this paper is to provide footwear designers, manikin builders and thermo‐physiological modellers with sweat distribution information for the human foot.Design/methodology/approachIndependent research from two laboratories, using different techniques, is brought together to describe sweat production of the foot. In total, 32 individuals were studied. One laboratory used running at two intensities in males and females, and measured sweat with absorbents placed inside the shoe. The other used ventilated sweat capsules on a passive, nude foot, with sweating evaluated during passive heating and incremental exercise to fatigue.FindingsResults from both laboratories are in agreement. Males secreted more than twice the volume of sweat produced by the females (p&lt;0.01) at the same relative work rate. Both genders demonstrated a non‐uniform sweat distribution, though this was less variable in females. Highest local sweat rates were observed from the medial ankles (p&lt;0.01). The dorsal foot sweated substantially more than the plantar (sole) areas (p&lt;0.01). Sweating on the plantar side of the foot was uniform. Wearing shoes limited the increase in sweat production with increasing load, while the sweat rate of uncovered feet kept increasing with work and thermal load.Practical implicationsThe observed variation in sweat rate across the foot shows that footwear design should follow the body mapping principle. Fabrics and materials with different properties can be used to improve comfort if applied to different foot surfaces. The data also demonstrate that foot models, whether physical (manikins) or mathematical, need to incorporate the observed variation across the foot to provide realistic simulation/testing of footwear.Originality/value

Regional variations in transepidermal water loss, eccrine sweat gland density, sweat secretion rates and electrolyte composition in resting and exercising humans

Literature from the past 168 years has been filtered to provide a unified summary of the regional distribution of cutaneous water and electrolyte losses. The former occurs via transepidermal water vapour diffusion and secretion from the eccrine sweat glands. Daily insensible water losses for a standardised individual (surface area 1.8 m2) will be 0.6–2.3 L, with the hands (80–160 g.h−1) and feet (50–150 g.h−1) losing the most, the head and neck losing intermediate amounts (40–75 g.h−1) and all remaining sites losing 15–60 g.h−1. Whilst sweat gland densities vary widely across the skin surface, this same individual would possess some 2.03 million functional glands, with the highest density on the volar surfaces of the fingers (530 glands.cm−2) and the lowest on the upper lip (16 glands.cm−2). During passive heating that results in a resting whole-body sweat rate of approximately 0.4 L.min−1, the forehead (0.99 mg.cm−2.min−1), dorsal fingers (0.62 mg.cm−2.min−1) and upper back (0.59 mg.cm−2.min−1) would display the highest sweat flows, whilst the medial thighs and anterior legs will secrete the least (both 0.12 mg.cm−2.min−1). Since sweat glands selectively reabsorb electrolytes, the sodium and chloride composition of discharged sweat varies with secretion rate. Across whole-body sweat rates from 0.72 to 3.65 mg.cm−2.min−1, sodium losses of 26.5–49.7 mmol.L−1 could be expected, with the corresponding chloride loss being 26.8–36.7 mmol.L−1. Nevertheless, there can be threefold differences in electrolyte losses across skin regions. When exercising in the heat, local sweat rates increase dramatically, with regional glandular flows becoming more homogeneous. However, intra-regional evaporative potential remains proportional to each local surface area. Thus, there is little evidence that regional sudomotor variations reflect an hierarchical distribution of sweating either at rest or during exercise.

Improved Procedure for Estimating Time-dependent Changes in Local Sweat Rates by Measuring Local Sweat Volumes

Sweat distribution over 21 body sites in 8 young males was described by determining the local sweat volume (LSRap), measured using absorbent pads throughout 3 different bicycle exercises performed at 35, 50, and 60% VO2max for 40 min, at 30°C and 50% relative humidity. The local upper back sweat rate was concurrently measured by the ventilated capsule method (LSRvc) in parallel with the absorbent method. The LSRap at the upper back correlated strongly with mean LSRvc at the position immediately above the absorbent pad (p<0.05). There were significant differences in LSRap among the 21 body sites within each exercise intensity (p<0.05). Regional comparisons showed a greater LSRap at the chest and back and lower LSRap at the flank, thighs, and legs. Moreover, LSRap was distributed symmetrically and was greater in the middle compared to the adjoining lateral sites. LSRvc data reanalysis of our previous studies on prepubertal boys, men, and women across a range of ages revealed that during passive and/or active heating, the LSRvc were arranged in order of lower limbs.

Effects of duration of stay in temperate area on thermoregulatory responses to passive heat exposure in tropical south-east Asian males residing in Japan

BackgroundIn this study, we investigated the effects of duration of stay in a temperate area on the thermoregulatory responses to passive heat exposure of residents from tropical areas, particularly to clarify whether they would lose their heat tolerance during passive heat exposure through residence in a temperate country, Japan.MethodsWe enrolled 12 males (mean ± SE age 25.7 ± 1.3 years) from south-east Asian countries who had resided in Japan for a mean of 24.5 ± 5.04 months, and 12 Japanese males (age 24.1 ± 0.9 years). Passive heat exposure was induced through leg immersion in hot water (42°C) for 60 minutes under conditions of 28°C air temperature and 50% relative humidity.ResultsCompared with the Japanese group, the tropical group displayed a higher pre-exposure rectal temperature (P < 0.01) and a smaller increase in rectal temperature during 60 minutes of leg immersion (P = 0.03). Additionally, the tropical group showed a tendency towards a lower total sweat rate (P = 0.06) and lower local sweat rate on the forehead (P = 0.07). The tropical group also had a significantly longer sweating onset time on the upper back (P = 0.04) compared with the Japanese groups. The tropical group who stayed in Japan for > 23 months sweated earlier on the forehead and upper back than those who stayed in Japan < 11 months (P < 0.01 and P = 0.03 for the forehead and upper back, respectively). There was a positive correlation between duration of stay in Japan and total sweat rate (r = 0.58, P <0.05), and negative correlations between duration of stay and sweating onset time on the forehead (r = −0.73, P = 0.01) and on the upper back (r = −0.66, P = 0.02). Other physiological indices measured in this study did not show any difference between the subjects in the tropical group who had lived in Japan for a shorter time and those who had lived there for a longer time.ConclusionsWe conclude that the nature of heat acclimatization of the sweating responses to passive heat exposure that are acquired from long-term heat acclimatization is decayed by a stay in a temperate area, as shown by the subjects in our tropical group. We did not find any evidence of a decay in the other physiological indices, indicating that heat tolerance acquired from long-term heat acclimatization is not completely diminished through residence in a temperate area for less than 4 years, although some aspects of this heat tolerance may be decayed.

Sex differences in thermoeffector responses during exercise at fixed requirements for heat loss

To assess potential mechanisms responsible for the lower sudomotor thermosensitivity in women during exercise, we examined sex differences in sudomotor function and skin blood flow (SkBF) during exercise performed at progressive increases in the requirement for heat loss. Eight men and eight women cycled at rates of metabolic heat production of 200, 250, and 300 W/m(2) of body surface area, with each rate being performed sequentially for 30 min. The protocol was performed in a direct calorimeter to measure evaporative heat loss (EHL) and in a thermal chamber to measure local sweat rate (LSR) (ventilated capsule), SkBF (laser-Doppler), sweat gland activation (modified iodine-paper technique), and sweat gland output (SGO) on the back, chest, and forearm. Despite a similar requirement for heat loss between the sexes, significantly lower increases in EHL and LSR were observed in women (P ≤ 0.001). Sex differences in EHL and LSR were not consistently observed during the first and second exercise periods, whereas EHL (348 ± 13 vs. 307 ± 9 W/m(2)) and LSR on the back (1.61 ± 0.07 vs. 1.20 ± 0.09 mg · min(-1) · cm(-2)), chest (1.33 ± 0.06 vs. 1.08 ± 0.09 mg · min(-1) · cm(-2)), and forearm (1.53 ± 0.07 vs. 1.20 ± 0.06 mg · min(-1) · cm(-2), men vs. women) became significantly greater in men during the last exercise period (P < 0.05). At each site, differences in LSR were solely due to a greater SGO in men, as opposed to differences in sweat gland activation. In contrast, no sex differences in SkBF were observed throughout the exercise period. The present study demonstrates that sex differences in sudomotor function are only evidenced beyond a certain requirement for heat loss, solely through differences in SGO. In contrast, the lower EHL and LSR in women are not paralleled by a lower SkBF response.