Activated Sweat Gland Density Research Articles

Sex-related differences in sudomotor function in healthy early twenties focused on activated sweat gland density.

The purpose of this study was to quantitatively assess the difference in sudomotor function between healthy males and females in their early twenties by measuring skin surface area and activated sweat gland density (ASGD). The quantitative sudomotor axon reflex test (QSART), a method for evaluating autonomic nervous system activity, was used for quantification. In QSART, the sweat glands are activated directly or indirectly by the subcutaneous application of neurotransmitters, such as acetylcholine, through iontophoresis. This series of mechanisms is called the sudomotor axon reflex. After recording age, height, weight, and several measurements of the forearm, QSART was performed on 101 healthy controls aged 21-26 years to measure ASGD. The mean temperature and humidity on the measurement days were 11.4°C and 58.1% on May 3, 2018, and 14.7°C and 70.3% on May 10, 2018. The result of independent sample t-test showed higher ASGD in women (P < 0.05). The body surface area and the surface area of the forearms were higher in men (P < 0.001), but the number of activated sweat glands was not significantly different according to sex. The activated sweat gland counts of the body and forearms were analyzed through linear regression by age for males and females. Except for the activated sweat gland count of the male body, the analysis showed a tendency to decrease with increasing age but was not statistically significant in any case (P > 0.05). Showing insufficient coefficient of determination (R2), multiple regression analyses with sex and ages did not correct this insignificance between age and activated sweat gland count.

Nicotinic receptors modulate skin perfusion during normothermia, and have a limited role in skin vasodilatation and sweating during hyperthermia.

What is the central question of this study? What is the role of nicotinic receptors in the regulation of normothermic cutaneous blood flow and cutaneous vasodilatation and sweating during whole-body heating induced following resting in a non-heat-stress condition? What is the main finding and its importance? Nicotinic receptors modulated cutaneous vascular tone during rest in a non-heat-stress condition and in the early stage of heating, but they had a limited role in mediating cutaneous vasodilatation when core temperature increased>0.4°C. Further, the contribution of nicotinic receptors to sweating was negligible during whole-body heating. Our findings provide new insights into the role of nicotinic receptors in end-organ function of skin vasculature and sweat glands in humans. Nicotinic receptors are present in human skin including cutaneous vessels and eccrine sweat glands as well as peripheral nerves. We tested the hypothesis that nicotinic receptors do not contribute to the control of cutaneous vascular tone in the normothermic state, but are involved in mediating cutaneous vasodilatation and sweating during a whole-body passive heat stress in humans. We first performed a nicotinic receptor blocker verification protocol in six young adults (one female) wherein increases in cutaneous vascular conductance and sweating elicited by 10mm nicotine were blocked by administration of 500µm hexamethonium to confirm effective blockade. Thereafter, 12 young males participated in a passive heating protocol. After an instrumentation period in a non-heat-stress condition, participants rested for a 10min baseline period. Thereafter, oesophageal temperature was increased by 1.0°C using water-perfusion suits. Cutaneous vascular conductance, sweat rate, active sweat gland density and sweat output per individual gland were assessed with and without 500µm hexamethonium administered via intradermal microdialysis. Hexamethonium reduced cutaneous vascular conductance by 22-34% during normothermia and the early stage of heating. However, this effect was diminished as oesophageal temperature increased >0.4°C. Active sweat gland density was reduced by hexamethonium when oesophageal temperature was elevated by 0.4-0.6°C above baseline resting. However, this was paralleled by a marginal increase in sweat gland output. Consequently, sweat rate remained unchanged. We showed that nicotinic receptors modulate cutaneous perfusion during normothermia and the early stage of heating, but not when core temperature increases >0.4°C. Additionally, they play a limited role in mediating sweating during heating.

Sweating distribution and active sweat glands on the scalp of young males in hot-dry and hot-humid environments

We investigated the effects of humidity on regional sweating secretion and active sweat gland density on the scalp during passive heating in hot environments. Eight male subjects shaved their heads prior to expose to dry (30%RH; H30%) and humid (85%RH; H85%) conditions at an air temperature of 32°C. Total sweat rate, local sweat rates (frontal, vertex, temporal, and occipital regions), active sweat glands on the scalp (2 frontal, 2 parietal, 2 temporal, 1 occipital, and 1 vertex), and rectal and skin temperatures were measured during leg immersion in 42°C water for 60min. (1) Total sweat rates were greater for H30% (179.4 ± 35.6gh-1) than for H85% (148.1 ± 27.2gh-1) (P < 0.05). (2) Scalp sweat secretion tended to be greater in the H85% than the H30%. (3) Head sweat rates were greater on the frontal than on the vertex for both humidity conditions (P < 0.05). (4) Active sweat gland density on the scalp was greater for H85% (82 ± 13glandscm-2) than for H30% (62 ± 17glandscm-2) (P < 0.05). (5) No significant difference was found in rectal temperature between H30% and H85%, whereas mean skin temperature was significantly lower for H30% (34.8 ± 0.7°C) than for the H85% condition (36.0 ± 0.3°C) (P < 0.05). These results indicate that the thermoregulatory sweating responses for the scalp region were significantly increased in the hot-humid condition compared to the hot-dry condition. Among the regions on the scalp surface, the vertex was the least sensitive to the change in humidity.

Maximum Skin Wettedness after Aerobic Training with and without Heat Acclimation.

To quantify how maximum skin wettedness (ωmax); that is, the determinant of the boundary between compensable and uncompensable heat stress, is altered by aerobic training in previously unfit individuals and further augmented by heat acclimation. Eight untrained individuals completed an 8-wk aerobic training program immediately followed by 8 d of hot/humid (38°C, 65%RH) heat acclimation. Participants completed a humidity ramp protocol pretraining (PRE-TRN), posttraining (POST-TRN), and after heat acclimation (POST-HA), involving treadmill marching at a heat production of 450 W for 105 min in 37.5°C, 2.0 kPa (35%RH). After attaining a steady-state esophageal temperature (Tes), humidity increased 0.04 kPa·min. An upward inflection in Tes indicated the upper limit of physiological compensability (Pcrit), which was then used to quantify ωmax. Local sweat rate, activated sweat gland density, and sweat gland output on the back and arm were simultaneously measured throughout. Peak aerobic capacity increased POST-TRN by approximately 14% (PRE-TRN: 45.8 ± 11.8 mL·kg·min; POST-TRN: 52.0 ± 11.1 mL·kg·min, P < 0.001). ωmax values became progressively greater from PRE-TRN (0.72 ± 0.06) to POST-TRN (0.84 ± 0.08; P = 0.02), to POST-HA (0.95 ± 0.05; P = 0.03). These shifts in ωmax were facilitated by a progressively greater local sweat rate and activated sweat gland density from PRE-TRN (0.84 ± 0.21 mg·cm·min; 67 ± 20 glands per square centimeter) to POST-TRN (0.96 ± 0.21 mg·cm·min, P = 0.03; 86 ± 27 glands per square centimeter; P = 0.009), to POST-HA (1.15 ± 0.21 mg·cm·min; P < 0.001; 98 ± 35 glands per square centimeter; P < 0.001). No differences in sweat gland output were observed. A greater ωmax occurred after 8 wk of aerobic training, but ωmax was further augmented with heat acclimation, indicating only a partially increased heat loss capacity with training. These ωmax values may assist future predictions of heat stress risk in untrained/trained unacclimated individuals and trained heat-acclimated individuals.

Effect of Intensive and Repetitive Heat Exposure on the Sudomotor Activity

The sweating response is modulated in two different ways depending on adaptation conditions. In this work, we examined sudomotor activities before and after intensive and repetitive heat exposure. Nine male volunteers were exposed to 30-min half-body immersion in hot water (42 ± 0.5°C) at the same time of day on alternate days for 3 weeks. All experiments were performed in an automated climate chamber. Tympanic (Tty) and skin (Ts) temperatures were measured. Mean body temperature (mTb) was calculated. Sudomotor activities, including sweat onset time, sweat rate and volume, activated sweat gland density (ASGD) and output (ASGO), were tested in four regions of the skin: chest, abdomen, upper back and thigh. Basal Tty and mTb were found to decrease by 0.15°C (P < 0.05) and 0.16°C (P < 0.05), respectively. As a typical data (upper back), sweat onset time increased by 33.6% (P < 0.05) after heat acclimation. After heat acclimation, sweat rate decreased by 14.7% (P < 0.05), sweat volume decreased by 15.5% (P < 0.05) and ASGO also decreased by 11.1% (P < 0.05). ASGD decreased by 4.1% after heat acclimation without statistical significance. The data suggest that intensive and repetitive heat exposure induces suppression of sudomotor activities within 3 weeks.

A Lower Heat Activated Sweat Gland Density in Larger Individuals Does Not Impair Local Sweat Rates During Hot and Humid Heat Stress

While the absolute number of sweat glands is primarily determined in utero, a larger body surface area (BSA) will naturally reduce the density of sweat glands per surface area which may compromise sweat rate per unit BSA, and consequently the maximal skin surface sweat coverage (i.e. skin wettedness: ωmax) during exercise in a hot/humid environment. The purpose of the present study was to compare the heat activated sweat gland density (HASGD), sweat gland output (SGO), local sweat rate (LSR) and ωmax between groups differing greatly in BSA during hot and humid active heat stress. Twelve participants separated into two groups based on body size (Small (SM): n=6, 65±6 kg, 1.8±0.1 m2; Large (LG): n=6, 102±13 kg, 2.3±0.1 m2) exercised on an upright cycle ergometer at an evaporative heat balance requirement (Ereq) of 240 W/m2 and 290 W/m2 for up to 75 min at 36°C, 70% RH. LSR of the upper back was measured throughout and expressed relative to surface area (mg/cm2/min). HASGD in number of sweat glands per cm2 (glands/cm2) was measured medially to LSR using the starch iodine technique every 15 minutes and averaged throughout the trial. Mean SGO was derived from the division of LSR and mean HASGD, and expressed as μg/gland/min. On a separate occasion ωmax was measured using a humidity‐ramp protocol (increase of 0.3 kPa from 2.3 kPa every 7.5‐min) during exercise at a fixed external workload of 100W at 36°C until an inflection of esophageal temperature was observed. LSR was similar at 240 W/m2 (SM: 1.24±0.24; LG: 1.40±0.47 mg/cm2/min, P=0.25) and 290 W/m2 (SM: 1.36±0.18; LG: 1.36±0.36 mg/cm2/min, P=0.48). HASGD was greater in SM compared to LG group at 240 W/m2 (SM: 67±12; LG: 55±6 glands/cm2, P=0.03) and 290 W/m2 (SM: 73±9; LG: 57±11 glands/cm2, P&lt;0.01). SGO was trending to be greater in the LG group at 240 W/m2 (SM: 18.6±5.0; LG: 25.2±10.2 μg/gland/min, P=0.10) while significantly greater in the LG group at 290 W/m2 (SM: 17.3±1.6; LG: 21.2±5.7 μg/gland/min, P=0.03). On the other hand, ωmax was not different between groups (SM: 0.82±0.16; LG: 0.72±0.07, P=0.13). In conclusion, a lower HASGD in people with a greater BSA is compensated by a greater SGO to yield a similar LSR up to an Ereq of 290 W/m2 and a similar ωmax. Future research should attempt to assess how even greater reductions in HASGD due to disproportionally larger differences in BSA (ie morbid obesity) compromise LSR, ωmax, and therefore the level of heat stress that can be physiologically compensated.Support or Funding InformationSupported by a NSERC Discovery Grant (P. Imbeault &amp; O. Jay)

Seasonal acclimation in sudomotor function evaluated by QSART in healthy humans.

The quantitative sudomotor axon reflex testing (QSART) is a classic test of routine postganglionic sudomotor function. We investigated sudomotor function by QSART after summer (July 2012) and winter (January 2013) seasonal acclimation (SA) in the Republic of Korea. QSART with acetylcholine (ACh) iontophoresis were performed to determine directly activated (DIR) and axon reflex-mediated (AXR1, 2) sweating rate. Onset time of axon reflex, activated sweat gland density (ASGD), activated sweat gland output (ASGO), tympanic and skin temperatures (Tty, Tsk), basal metabolic rate (BMR), and evaporative loss volume changes were measured. Tympanic and mean body temperature (Tb; calculated from Tty, Tsk) were significantly lower after summer-SA than that of winter-SA. Sweat onset time was delayed during winter-SA compared to that after summer-SA. BMR, AXR(1), AXR(2), and DIR sweat rates, ASGD and ASGO, and evaporative loss volume were significantly diminished after winter-SA relative to after summer-SA. In conclusion, changes in sweating activity measured by QSART confirmed the involvement of the peripheral nervous system in variation of sudomotor activity in seasonal acclimation.

EDARV370A associated facial characteristics in Uyghur population revealing further pleiotropic effects.

An adaptive variant of human Ectodysplasin receptor, EDARV370A, had undergone strong positive selection in East Asia. In mice and humans, EDARV370A was found to affect ectodermal-derived characteristics, including hair thickness, hair shape, active sweat gland density and teeth formation. Facial characteristics are also largely ectodermal derived. In this study, taking advantage of an admixed population of East Asian and European ancestry-the Uyghur, we aim to test whether EDARV370A is affecting facial characteristics and to investigate its pleiotropic nature and genetic model. In a sample of 1027 Uyghurs, we discover that EDARV370A is significantly associated with several facial characteristics, in particular shape of earlobe (P=3.64×10 (-6) ) and type of chin (P=9.23×10 (-5) ), with successful replication in other East Asian populations. Additionally, in this Uyghur population, we replicate previous association findings of incisors shoveling (P=1.02×10 (-7) ), double incisors shoveling (P=1.86×10 (-12) ) and hair straightness (P=3.99×10 (-16) ), providing strong evidence supporting an additive model for the EDARV370A associations. Partial least square path model confirms EDARV370A systematically affect these weakly related ectodermal-derived characteristics, suggesting the pleiotropic effect of EDARV370A mainly plays roles in early embryo development. This study extends our knowledge about the pleiotropic nature of EDARV370A and provides potential clues to its adaptation fitness in human evolution.

Effects of Topical Menthol on Skin Blood Flow and Active Sweat Gland Density during Hyperthermia

Topical application of menthol evokes cold sensation and cutaneous vasoconstriction without actual reduction in tissue temperature via the stimulation of a specific cold receptor family known as TRPM8. While being widely used to reduce joint pain, muscle inflammation, and soft tissue injuries in athletes and individuals with musculoskeletal disease, topical menthol may adversely affect body’s heat loss mechanisms. PURPOSE: To investigate if topical application of menthol reduces skin blood flow (SkBF) and active sweat gland density (ASGD) to the extent to which body heat loss is significantly reduced during recovery from exercise-induced hyperthermia. METHODS: Ten healthy male subjects (22±1 yrs) underwent two trials of cycle exercise at 50% VO2max in the heat (45°C, 50%) until their rectal temperatures (Tre) elevate 1.5°C above the baseline. Following the cessation of exercise, either 10g of 3.1% menthol gel (MEN) or placebo Lanolin cream (PBO) was applied on the limbs except hands and feet after which subjects recovered on a chair for 30min in thermoneutral condition (23°C, 50%). SkBF and ASGD were measured using a laser Doppler flowmetery and an iodine-impregnated cotton paper on ventral forearm and anterior thigh. Thermal measurements included Tre, 4-sites mean skin temperature (Tsk), and thermal sensation (TS: −4 very cold ~ 4 very hot). RESULTS: Cold TS in MEN was significantly greater than in PBO (F=29.22, P<.01) while reduction in SkBF and ASGD in MEN did not show significant difference compared to PBO. These slight alterations in vasomotor/sudomotor responses to topical menthol did not significantly impair Tre or Tsk recovery from hyperthermia.Table: No title available.CONCLUSION: Topical application of menthol does not adversely affect body heat loss during recovery from exercise-induced hyperthermia while significantly inducing cold TS.

Sweat gland density and response during high-intensity exercise in athletes with spinal cord injuries.

Sweat production is crucial for thermoregulation. However, sweating can be problematic for individuals with spinal cord injuries (SCI), as they display a blunting of sudomotor and vasomotor responses below the level of the injury. Sweat gland density and eccrine gland metabolism in SCI are not well understood. Consequently, this study examined sweat lactate (S-LA) (reflective of sweat gland metabolism), active sweat gland density (SGD), and sweat output per gland (S/G) in 7 SCI athletes and 8 able-bodied (AB) controls matched for arm ergometry VO2peak. A sweat collection device was positioned on the upper scapular and medial calf of each subject just prior to the beginning of the trial, with iodine sweat gland density patches positioned on the upper scapular and medial calf. Participants were tested on a ramp protocol (7 min per stage, 20 W increase per stage) in a common exercise environment (21±1°C, 45-65% relative humidity). An independent t-test revealed lower (p<0.05) SGD (upper scapular) for SCI (22.3 ±14.8 glands · cm−2) vs. AB. (41.0 ± 8.1 glands · cm−2). However, there was no significant difference for S/G between groups. S-LA was significantly greater (p<0.05) during the second exercise stage for SCI (11.5±10.9 mmol · l−1) vs. AB (26.8±11.07 mmol · l−1). These findings suggest that SCI athletes had less active sweat glands compared to the AB group, but the sweat response was similar (SLA, S/G) between AB and SCI athletes. The results suggest similar interglandular metabolic activity irrespective of overall sweat rate.

Beneficial effect of Oligonol supplementation on sweating response under heat stress in humans.

Oligonol is a low-molecular weight polyphenol that possesses antioxidant and anti-inflammatory properties. However, nothing is known regarding the impact of Oligonol on sudomotor activity. This study investigated the effects of Oligonol supplementation on sudomotor activity during heat load in humans. Initially, we conducted a placebo-controlled, cross-over trial where participants took a daily dose of Oligonol 200 mg or placebo for one week. After a 2 week washout period, the subjects were switched to the other study arm. As a heat load, half-body immersion into hot water (42 ± 0.5 °C for 30 min) was performed in an automated climate chamber. Tympanic and skin temperatures were measured. Sudomotor activity, including onset time, sweat rate (SR) and volume (SV), active sweat gland density (ASGD), and sweat gland output (SGO), was tested in four or eight areas of skin. When compared with placebo, Oligonol attenuated increases in tympanic and skin temperatures after the heat load. There was an increasing trend in local sweat onset time, but there was a decrease in local SR, SV, ASGD, and SGO for Oligonol compared to placebo. The mean ASGD was significantly higher in the Oligonol group than in the placebo group for 10, 20, and 30 min. This study demonstrates that Oligonol appears to be worthy of consideration as a natural supplement to support more economical use of body fluids against heat stress.

Age‐ and sex‐related differences in sudomotor function evaluated by the quantitative sudomotor axon reflex test (QSART) in healthy humans

The aim of the present study was to quantitatively investigate the age and sex-related differences in sudomotor function in healthy humans. The quantitative sudomotor axon reflex test (QSART) with iontophoresis (2mA for 5min) and 10% acetylcholine (ACh) was performed to determine axon reflex-mediated (AXR), with and without iotophoresis (AXR(1) and AXR(2), respectively), and directly activated (DIR) sweating. All experiments were conducted under thermoneutral conditions (temperature 24.0±0.5°C; relative humidity 40±3%). In general, men had enhanced values of onset time of AXR, sweat rates, activated sweat gland density (SGD) and activated sweat gland output (SGO) than women, but not in all cases. The onset time of AXR (r(2) =0.567; P<0.001) was positively correlated with advancing age, whereas sweat rates of AXR(1) and AXR(2) (r(2) =0.571 and r(2) =0.486, respectively; P<0.0001), DIR (r(2) =0.594; P<0.0001), SGD (r(2) =0.496; P<0.0001) and SGO (r(2) =0.551; P<0.0001) were negatively correlated in both men and women with advancing age. The results demonstrate that an attenuation of sudomotor function occurs with aging in both sexes. Moreover, the findings showed a progressive increase in onset time and a decrease in sweat rates, SGD and SGO with increasing age in both sexes. A variation in sweat function was found between sexes, but not in all age groups.

The Effects of Caffeine Ingestion Before Passive Heat Loading on Serum Leptin Levels in Humans

We assessed the effects of ingesting caffeine before passive heat loading (PHL) on serum leptin and sweating response, which are both physiological responses associated with energy expenditure. The subjects were nine male university students (age, 24.1 ± 3.5 years; height, 173.4 ± 7.6 cm; weight, 69.2 ± 5.7 kg; maximal oxygen consumption, 48.6 ± 4.7 ml [Symbol: see text] kg⁻¹ [Symbol: see text] min⁻¹). This study used a within-subject, random, crossover design. Tests were performed twice at the same time (2-5 p.m.) at a 1-week interval following 3 mg[Symbol: see text]kg(-1) caffeine ingestion (Caff-I) or not (No-Caff). PHL included a half bath in hot water (42 ± 0.5 °C for 30 min) in a thermoneutral climate chamber (25 ± 0.5 °C, 60 ± 3 % relative humidity, <1 m/s air velocity). After PHL, blood levels of leptin and free fatty acids were significantly higher in the Caff-I compared to those in the No-Caff after PHL (P < 0.01). Waist circumference and whole-body sweat loss volume were significantly higher in the Caff-I compared to those in the No-Caff (P < 0.001). Mean active sweat gland density was significantly higher in the Caff-I compared to those in the No-Caff at 10 min during PHL (P < 0.001). The results suggest that ingesting caffeine before PHL is more energy efficient than that of a single PHL.

The relationship between aerobic capacity and the recruitment of activated sweat gland density with passive heating

The relationship between aerobic capacity and the recruitment of activated sweat gland density with passive heating

Caffeine Increases Sweating Sensitivity via Changes in Sudomotor Activity During Physical Loading

We assessed the effect of caffeine on sudomotor activity and sweating sensitivity during physical loading. Both physiological responses could occur due to energy expenditure. Subjects were 13 athletically trained males (22.1 ± 3.7 years old, 174.2 ± 5.4 cm tall, and weighing 70.9 ± 4.6 kg, with maximal oxygen consumption [VO(2)max] of 53.6 ± 4.4 mL/kg/minute). The study involved a within-subject, random, crossover design. Tests were performed following the ingestion of 3 mg/kg caffeine. The physical loading involved running for 30 minutes at 60% VO(2)max (24.0 ± 0.5°C, 40 ± 3.0% relative humidity). Tympanic temperature (TYMP) was significantly higher in the caffeine-consuming group (Caffe-I) at pre-exercise (40 minutes after caffeine intake and immediately before running) (P<.05). Mean body temperature (mT(b)) was significantly higher in the Caffe-I group at pre- and post-exercise (30 min after start of running) (P<.05). Onset time of localized sweating was significantly shorter in the Caffe-I group (P<.01), but localized sweat volume and active sweat gland output (per single gland) was significantly higher in the Caffe-I group (P<.001). Activated sweat gland density was significantly increased in the Caffe-I group on the abdomen and thigh (P<.01). In conclusion, caffeine ingestion caused not only increases in TYMP and mT(b) through thermogenesis, but also an increased sweating sensitivity via changes in sudomotor activity.

자발적 온열유도부하 중 카페인이 활동한선밀도의 동원력에 미친 영향

This study investigated the effect of 3mg/kg caffeine on activated sweat gland density (ASGD) during active heat load (treadmill running at 60% V·O2max, AHL) in thermoneutral climate chamber (temperature, 25±0.5℃, 60±3% relative humidity and less than 1 m/sec air velocity). 10 college students (endurance trained, age, 21.0±2.5 yrs; height, 173.0±3.2 cm; weight, 72.5±4.3 kg; V·O2max, 54.3±3.5 ml/kg/min) volunteered for this investigation and randomized, crossover designed into either a no caffeine (Non-Caff) or intake caffeine (Caffeine). In the first 20 minutes of AHL, the ASGD were higher in the Caffeine on U-Arm (upper arm), L-Back (lowr back) and a significantly higher on Chest (P.05) and U-Back(upper back) (P.01), while at 80 min mark, ASGD were lower in Non-Caff on U-back (P.05) and L-back. The whole body toally loss volume(WBTLV) were higher in the Caffeine at 20 min (P.001) and 80 min (P.001). However, water intake volume were higher on Non-Caff at 20 min (p.001) and 80 min (p.001). In conclusion, caffeine stimulate the sympathetic nervous system result in increased ASGD (the lasting effect possible within 20 min) and WBTLV. In addition, caffeine has an effect on energy expenditure as well via stimulate sweating.

Effect of caffeine on the metabolic responses of lipolysis and activated sweat gland density in human during physical activity

This study measured caffeine-induced changes in activated sweat gland density (ASGD) and fat oxidation using a randomized crossover design with 10 healthy volunteers given caffeine (Caffe-I, 3 mg/kg ingested 30 min before experiment) and non-caffeine (No-Caff). Subjects were 173.0±3.2 cm in height, 72.5±4.3 kg in weight, and 21.5±2.5 years in age. All experiments were performed in an automated climate chamber (24.0±0.5°C, relative humidity 50±3%, air velocity less than 1 m/sec) between 2–5 p.m. The ASGD on the chest, upper arm, upper back, and lower back were measured (after 30 min running at 60% VO2max), and blood samples were taken (at 40 min before, immediately before and after 30 min running). Activated sweat gland density levels were higher in Caffe-I (Chest p<0.05 and U-Back p<0.01) and free fatty acids (FFA) were higher in Caffe-I compared to No-Caff immediately before (p<0.05) and after running (p<0.01). In summary, caffeine increases ASGD and FFA by stimulating the sympathetic nervous system and increasing of lipolysis.

Effect of the Heat-exposure on Peripheral Sudomotor Activity Including the Density of Active Sweat Glands and Single Sweat Gland Output

Tropical inhabitants are able to tolerate heat through permanent residence in hot and often humid tropical climates. The goal of this study was to clarify the peripheral mechanisms involved in thermal sweating pre and post exposure (heat-acclimatization over 10 days) by studying the sweating responses to acetylcholine (ACh), a primary neurotransmitter of sudomotor activity, in healthy subjects (n=12). Ten percent ACh was administered on the inner forearm skin for iontophoresis. Quantitative sudomotor axon reflex testing, after iontophoresis (2 mA for 5 min) with ACH, was performed to determine directly activated (DIR) and axon reflex-mediated (AXR) sweating during ACh iontophoresis. The sweat rate, activated sweat gland density, sweat gland output per single gland activated, as well as oral and skin temperature changes were measured. The post exposure activity had a short onset time (p<0.01), higher active sweat rate [(AXR (p<0.001) and DIR (p<0.001)], higher sweat output per gland (p<0.001) and higher transepidermal water loss (p<0.001) compared to the pre-exposure measurements. The activated sweat rate in the sudomotor activity increased the output for post-exposure compared to the pre-exposure measurements. The results suggested that post-exposure activity showed a higher active sweat gland output due to the combination of a higher AXR (DIR) sweat rate and a shorter onset time. Therefore, higher sudomotor responses to ACh receptors indicate accelerated sympathetic nerve responsiveness to ACh sensitivity by exposure to environmental conditions.

유산소성 훈련이 활동한선밀도 및 한선의 출력기능에 미치는 영향

The sweat volume of indirectly activated(AXR) and directly activated(DIR) of sweating that occurs in the aerobic exercise-trained as compared to the sedentary subjects has been attributed to differences in the peripheral sweating mechanisms, although such mechanisms have not been completely investigated in comparative terms. The aim of this study was to investigate quantitatively the peripheral sudomotor adaptive mechanisms attributed for AXR and DIR sweating that is found in the aerobic exercise- trained runner(Trainee) in contrast to the health control(HC) subjects. QSART by 2 mA for 5 min of 10% ACh were applied to determine AXR by nicotinic receptor mediated sweating activity(axon reflex-mediated) and DIR by muscarinic receptor mediated sweating activity sweating during ACh iontophoresis. The sweat volumes of AXR(1), AXR(2) and DIR were higher in the aerobic exercise-trained Trainees as compared to those for the sedentary subjects. Furthermore, number of activated sweat gland density was higher in the aerobic exercise-trained Trainees as compared to sedentary subjects(p0.001). The activated single sweat gland output was higher in the aerobic-trained Trainees as compared to the output for the sedentary subjects(p0.001). These findings suggest that aerobic exercise-trained Trainees had higher sweat volume due to the combinations of a higher sweat gland output per activated sweat gland and more increased density of activated sweat gland.

Tropical Malaysians and temperate Koreans exhibit significant differences in sweating sensitivity in response to iontophoretically administered acetylcholine

Natives of the tropics are able to tolerate high ambient temperatures. This results from their long-term residence in hot and often humid tropical climates. This study was designed to compare the peripheral mechanisms of thermal sweating in tropical natives with that of their temperate counterparts. Fifty-five healthy male subjects including 20 native Koreans who live in the temperate Korean climate (Temperate-N) and 35 native tropical Malaysian men that have lived all of their lives in Malaysia (Tropical-N) were enrolled in this study after providing written informed consent to participate. Quantitative sudomotor axon reflex testing after iontophoresis (2 mA for 5 min) with 10% acetylcholine (ACh) was used to determine directly activated (DIR) and axon reflex-mediated (AXR) sweating during ACh iontophoresis. The sweat rate, activated sweat gland density, sweat gland output per single gland activated, and oral and skin temperature changes were measured. The sweat onset time of AXR (nicotinic-receptor-mediated) was 56 s shorter in the Temperate-N than in the Tropical-N subjects (P < 0.0001). The nicotinic-receptor-mediated sweating activity AXR (1), and the muscarinic-receptor-mediated sweating activity DIR, in terms of sweat volume, were 103% and 59% higher in the Temperate-N compared to the Tropical-N subjects (P < 0.0001). The Temperate-N group also had a 17.8% (P < 0.0001) higher active sweat gland density, 35.4% higher sweat output per gland, 0.24 degrees C higher resting oral temperature, and 0.62 degrees C higher resting forearm skin temperature compared to the Tropical-N subjects (P < 0.01). ACh iontophoresis did not influence oral temperature, but increased skin temperature near where the ACh was administered, in both groups. These results suggest that suppressed thermal sweating in the Tropical-N subjects was, at least in part, due to suppressed sweat gland sensitivity to ACh through both recruitment of active sweat glands and the sweat gland output per each gland. This physiological trait guarantees a more economical use of body fluids, thus ensuring more efficient protection against heat stress.