Function of human eccrine sweat glands during dynamic exercise and passive heat stress.

The purpose of this study was to identify the pattern of change in the density of activated sweat glands (ASG) and sweat output per gland (SGO) during dynamic constant-workload exercise and passive heat stress. Eight male subjects (22.8 +/- 0.9 yr) exercised at a constant workload (117.5 +/- 4.8 W) and were also passively heated by lower-leg immersion into hot water of 42 degrees C under an ambient temperature of 25 degrees C and relative humidity of 50%. Esophageal temperature, mean skin temperature, sweating rate (SR), and heart rate were measured continuously during both trials. The number of ASG was determined every 4 min after the onset of sweating, whereas SGO was calculated by dividing SR by ASG. During both exercise and passive heating, SR increased abruptly during the first 8 min after onset of sweating, followed by a slower increase. Similarly for both protocols, the number of ASG increased rapidly during the first 8 min after the onset of sweating and then ceased to increase further (P > 0.05). Conversely, SGO increased linearly throughout both perturbations. Our results suggest that changes in forearm sweating rate rely on both ASG and SGO during the initial period of exercise and passive heating, whereas further increases in SR are dependent on increases in SGO.     

Localized β-adrenergic receptor blockade does not affect sweating during exercise

The purpose of the current study was to determine the effect of a locally administered nonselective β-adrenergic antagonist on sweat gland function during exercise. Systemically administered propranolol has been reported to increase, decrease, or not alter sweat production during exercise. To eliminate the confounding systemic effects associated with orally administered propranolol, we used iontophoresis to deliver it to the eccrine sweat glands within a localized area on one forearm prior to exercise. This allowed for determination of the direct effect of β-adrenergic receptor blockade on sweating during exercise. Subjects (n = 14) reported to the laboratory (23 ± 1°C, 35 ± 3% relative humidity) after having refrained from exercise for ≥12 h. Propranolol (1% solution) was administered to a 5-cm(2) area of the flexor surface of one forearm via iontophoresis (1.5 mA) for 5 min. A saline solution was administered to the opposing arm via iontophoresis. Each subject then exercised on a motor-driven treadmill at 75% of their age-predicted maximal heart rate for 20 min, while sweat rate was measured simultaneously in both forearms. Immediately after cessation of exercise, the number of active sweat glands was measured by application of iodine-impregnated paper to each forearm. The sweat rate for the control and propranolol-treated forearm was 0.62 ± 41 and 0.60 ± 0.44 (SD) mg·cm(-2)·min(-1), respectively (P = 0.86). The density of active sweat glands for the control and propranolol-treated forearm was 130 ± 6 and 134 ± 5 (SD) glands/cm(2), respectively, (P = 0.33). End-exercise skin temperature was 32.9 ± 0.2 and 33.1 ± 0.3°C for the control and propranolol-treated forearm, respectively (P = 0.51). Results of the current study show that when propranolol is administered locally, thus eliminating the potential confounding systemic effects of the drug, it does not directly affect sweating during the initial stages of high-intensity exercise in young, healthy subjects.     

Effect of age on heat-activated sweat gland density and flow during exercise in dry heat

Physiological responses of eight postmenopausal older women (age 52-62 yr) and eight younger women (age 20-30 yr) were compared during moderate intensity exercise in a hot dry environment (48 degrees C dry bulb, 25 degrees C wet bulb). The age groups were matched on the basis of maximal O2 consumption (VO2max), body surface area, and body fatness. After heat acclimation the women walked at 40% VO2max for up to 2 h in the hot dry environment while heart rate (HR), rectal temperature (Tre), mean skin temperature (Tsk), whole-body sweating rate (Msw), and local sweating rates (msw; forearm, chest, and scapula) were measured. Additionally, the density of heat-activated sweat glands (HASG) was determined and average sweat gland flow (SGF) was calculated for the scapular area. Although no differences between age groups were found in HR response (when analyzed as percent of maximal HR) or Tsk, the older women had a significantly higher Tre throughout the heat-exercise session. The greater heat storage of the older women may be explained by their significantly lower Msw and msw. There were no differences between the younger and older women in the density of HASG after 30 min; therefore, the lower msw reflects a diminished output per HASG rather than a decrease in the number of sweat glands recruited. The diminished thermoregulatory ability of the older women, unrelated to differences in VO2max, appears to reflect either 1) a diminished response of the sweat glands to central and/or peripheral stimuli, or 2) an age-related structural alteration in the eccrine glands or surrounding skin cells.     

Shivering onset, metabolic response, and convective heat transfer during cold air exposure

The onset and intensity of shivering of various muscles during cold air exposure are quantified and related to increases in metabolic rate and convective heat loss. Thirteen male subjects resting in a supine position and wearing only shorts were exposed to 10 degrees C air (42% relative humidity and less than 0.4 m/s airflow) for 2 h. Measurements included surface electromyogram recordings at six muscle sites representing the trunk and limb regions of one side of the body, temperatures and heat fluxes at the same contralateral sites, and metabolic rate. The subjects were grouped according to lean (LEAN, n = 6) and average body fat (NORM, n = 7) content. While the rectal temperatures fluctuated slightly but not significantly during exposure, the skin temperature decreased greatly, more at the limb sites than at the trunk sites. Muscles of the trunk region began to shiver sooner and at a higher intensity than those of the limbs. The intensity of shivering and its increase over time of exposure were consistent with the increase in the convective heat transfer coefficient calculated from skin temperatures and heat fluxes. Both the onset of shivering and the magnitude of the increase in metabolic rate due to shivering were higher for the LEAN group than for the NORM group. A regression analysis indicates that, for a given decrease in mean skin temperature, the increase in metabolic rate due to shivering is attenuated by the square root of percent body fat. Thus the LEAN group shivered at higher intensity, resulting in higher increases in metabolic heat production and convective heat loss during cold air exposure than did the NORM group.     

Regional differences in the sweating responses of older and younger men.

Ten older (60-71 yr) and nine younger (20-25 yr) active healthy men were exposed to passive heating [by placing the lower legs and feet in a 43 degrees C water bath for 60 min while sitting in a warm (35 degrees C, 45% relative humidity) chamber] in summer and winter. The increase in rectal temperature (Tre) was significantly (P less than 0.05) greater, and mean skin temperature and forearm blood flow were lower, for the older men in both seasons. Total sweating rate was lower in the older men, but significantly (P less than 0.05) so only in the summer. The Tre threshold for sweating was unaffected by either age or site (back vs. thigh). The local sweating rate (msw) on the thigh was significantly lower (P less than 0.05) for the older men throughout the exposure, whereas there were no significant age-related differences for the average or peak values of back msw, although lesser sweating on the back occurred during the first 30 min of exposure. The decreased msw on the thigh was due to a lower sweat output per heat-activated sweat gland rather than from recruitment of fewer glands. It was concluded that regional differences exist in the age-related decrement in sweat gland function. Furthermore, these findings suggest that aging leads to a decreased ability to maintain body temperature with passive heating of the extremities, which may be attributed in part to decreased regional sweat gland function.     

Rectal temperature, distal sweat rate, and forearm blood flow following mild exercise at two phases of the circadian cycle

Changes in rectal temperature during mild exercise in the middle of the rising (11:00 h) and falling (23:00 h) phases of the circadian rhythm of resting core temperature have been compared. Seven healthy males were studied at rest, while exercising on a cycle ergometer (60 min at 80 W), and during the first 30 min of recovery. Rectal temperature, forearm blood flow, and forearm sweat rate were measured at 1 min intervals throughout. During exercise, there were significant time-of-day differences in the profiles of all three variables, and in the thresholds for increases in forearm blood flow and sweating. Forearm blood flow and sweat rate were recruited more rapidly and to a greater extent with evening exercise, and rectal temperature rose less. Analysis of covariance, with rectal temperature as the covariate, indicated the associations between it and forearm blood flow or sweating were significantly different (p<0.05) between the two times of day. There were also significant (p<0.05) time-of-day effects for forearm blood flow and sweating that were independent of rectal temperature. During recovery, rectal temperature fell more quickly in the late evening than late morning. Forearm blood flow and sweating also showed time-of-day differences, but these did not co-vary with rectal temperature. Control of rectal temperature during exercise and recovery appears to be more effective in the late evening than late morning, and differences in forearm blood flow and sweating, as well as factors independent of these two variables, contribute to this difference. The results support our "heat-gain/heat-loss modes" hypothesis.     

Rectal temperature,distal sweat rate,and forearm blood flow following mild exercise at two phases of the circadian cycle

Changes in rectal temperature during mild exercise in the middle of the rising (11:00 h) and falling (23:00 h) phases of the circadian rhythm of resting core temperature have been compared. Seven healthy males were studied at rest, while exercising on a cycle ergometer (60 min at 80 W), and during the first 30 min of recovery. Rectal temperature, forearm blood flow, and forearm sweat rate were measured at 1 min intervals throughout. During exercise, there were significant time‐of‐day differences in the profiles of all three variables, and in the thresholds for increases in forearm blood flow and sweating. Forearm blood flow and sweat rate were recruited more rapidly and to a greater extent with evening exercise, and rectal temperature rose less. Analysis of covariance, with rectal temperature as the covariate, indicated the associations between it and forearm blood flow or sweating were significantly different (p<0.05) between the two times of day. There were also significant (p<0.05) time‐of‐day effects for forearm blood flow and sweating that were independent of rectal temperature. During recovery, rectal temperature fell more quickly in the late evening than late morning. Forearm blood flow and sweating also showed time‐of‐day differences, but these did not co‐vary with rectal temperature. Control of rectal temperature during exercise and recovery appears to be more effective in the late evening than late morning, and differences in forearm blood flow and sweating, as well as factors independent of these two variables, contribute to this difference. The results support our “heat‐gain/heat‐loss modes” hypothesis.     

Modified iodine-paper technique for the standardized determination of sweat gland activation

Quantifying sweat gland activation provides important information when explaining differences in sweat rate between populations and physiological conditions. However, no standard technique has been proposed to measure sweat gland activation, while the reliability of sweat gland activation measurements is unknown. We examined the interrater and internal reliability of the modified-iodine paper technique, as well as compared computer-aided analysis to manual counts of sweat gland activation. Iodine-impregnated paper was pressed against the skin of 35 participants in whom sweating was elicited by exercise in the heat or infusion of methylcholine. The number of active glands was subsequently determined by computer-aided analysis. In total, 382 measurements were used to evaluate: 1) agreement between computer analysis and manual counts; 2) the interrater reliability of computer analysis between independent investigators; and 3) the internal reliability of sweat gland activation measurements between duplicate samples. The number of glands identified with computer analysis did not differ from manual counts (68 ± 29 vs. 72 ± 24 glands/cm(2); P = 0.27). These measures were highly correlated (r = 0.77) with a mean bias ± limits of agreement of -4 ± 38 glands/cm(2). When comparing computer analysis measures between investigators, values were highly correlated (r = 0.95; P < 0.001) and the mean bias ± limits of agreement was 4 ± 18 glands/cm(2). Finally, duplicate measures of sweat gland activation were highly correlated (r = 0.88; P < 0.001) with a mean bias ± limits of agreement of 3 ± 29 glands/cm(2). These results favor the use of the modified-iodine paper technique with computer-aided analysis as a standard technique to reliably evaluate the number of active sweat glands.     

Pilocarpine-induced sweat gland function in individuals with multiple sclerosis.

This investigation tested the hypothesis that cholinergic sweat function of individuals with multiple sclerosis (MS) (MS-Con; n = 10) is diminished relative to matched healthy control subjects (Con; n = 10). In addition, cholinergic sweat function was determined before and after 15 wk of aerobic training in a subgroup of individuals with MS (MS-Ex; n = 7). Cholinergic sweating responses were assessed via pilocarpine iontophoresis on ventral forearm skin. A collection disk placed over the stimulated area collected sweat for 15 min. Sweat rate (SR) was calculated by dividing sweat collector volume by collection area and time. Iodine-treated paper was applied to the stimulated area to measure number of activated sweat glands (ASG). Sweat gland output (SGO) was calculated by dividing SR by density of glands under the collector. Sweat gland function was determined in MS-Ex to test the hypothesis that exercise training would increase sweating responses. No differences in ASG were observed between MS-Con and Con. SR and SGO in MS-Con [0.18 mg.cm(-2).min(-1) (SD 0.08); 1.74 microg.gland(-1).min(-1) (SD 0.79), respectively] were significantly lower (P < or = 0.05) than in Con [0.27 mg.cm(-2).min(-1) (SD 0.10); 2.43 microg.gland(-1).min(-1) (SD 0.69)]. Aerobic exercise training significantly (P < or = 0.05) increased peak aerobic capacity in MS-Ex [1.86 (SD 0.75) vs. 2.10 (SD 0.67) l/min] with no changes in ASG, SR, and SGO. Sweat gland function in individuals with MS is impaired relative to healthy controls. Fifteen weeks of aerobic training did not increase stimulated sweating responses in individuals with MS. Diminished peripheral sweating responses may be a consequence of impairments in autonomic control of sudomotor function.     

Predictors of sweat loss in man during prolonged exercise

Nineteen healthy male subjects, differing in training status and Vo2max (52 +/- 1 ml.min-1.kg-1, mean +/- SEM; 43-64 ml.min-1.kg-1, range), exercised for 1 h at an absolute workload of 192 +/- 8 W (140-265 W); this was equivalent to 70 +/- 1% Vo2max (66-74%). Each exercise test was performed on an electrically braked cycle ergometer at a constant ambient temperature (22.5 +/- 0.0 degrees C) and relative humidity (85 +/- 0%). Nude body weight was recorded prior to and after each exercise test. Absolute sweat loss (body weight loss corrected for respiratory weight loss) during each test was 910 +/- 82 g (426-1665 g); this was equivalent to 1.3 +/- 0.1% (0.7-2.2%) of pre-exercise body weight (relative sweat loss). Weighted mean skin temperature and rectal temperature increased after 5 min of exercise from 30.5 +/- 0.3 degrees C and 37.2 +/- 0.1 degrees C respectively to 32.5 +/- 0.2 degrees C and 38.8 +/- 0.1 degrees C respectively, recorded immediately prior to the end of exercise. Bivariate linear regression and Pearson's correlation demonstrated absolute sweat loss was related to Vo2max (r = 0.72, p less than 0.001), absolute exercise workload (r = 0.66, p less than 0.01), body surface area (r = 0.62, p less than 0.01), weight (r = 0.60, p less than 0.01) and height (r = 0.53, p less than 0.05). Relative sweat loss was related to VO2max (r = 0.77, P less than 0.001) and absolute exercise workload (R = 0.59, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Maturation- and aging-related changes in heat loss effector function

This paper addresses the ways in which heat loss effector functions change with maturation and aging, using data obtained in our laboratory. Prepubertal children have an underdeveloped sweat function compared with young adults; this is compensated by a greater surface area-to-mass ratio and relatively greater heat loss from cutaneous vasodilation on the head and trunk when the air temperature is lower than the skin temperature. As the heat dissipation depends greatly on the evaporation of sweat, the core temperature of prepubertal children is greater than that of young adults owing to the underdevelopment of sweating. In the elderly the heat loss effector function decreases with aging. The decrease may first involve cutaneous vasodilation, then sweat output per gland, and finally active sweat gland density; and it may proceed from the lower limbs to the back of the upper body, the front of the upper body, then the upper limbs and finally to the head.     

Postnatal expression and denervation induced up-regulation of aquaporin-5 protein in rat sweat gland

The evolution of aquaporin-5 (AQP5) expression during postnatal development has not been defined in the sweat gland. Previous studies have suggested that AQP isoforms in several peripheral targets are regulated by a neural mechanism. We have examined, in rat sweat glands, the expression of AQP5 during postnatal development and the effects of denervation on AQP5 expression. Both AQP5 mRNA and protein begin to be expressed at postnatal day 10, before sweat-secretory responsiveness first appears; this expression coincides with the occurrence of vasoactive intestinal peptide (VIP) immunoreactivity. Early noradrenergic and later cholinergic interaction between sweat glands and their innervation are disrupted by neonatal chemical sympathectomy or postnatal severance of the sciatic nerve. Examination of such denervated developing rats has shown that secretory responsiveness fails to arise later in the adults, and AQP5 immunostaining increases in the denervated glands, whereas gland morphogenesis and the occurrence of AQP5 expression proceed normally. Immunobloting has revealed an increase of AQP5 abundance after the denervated mature glands lose their secretory ability. These findings suggest that AQP5 protein is necessary for sweat secretion, and that the expression of AQP5 in rat sweat glands is independent of sympathetic innervation. Our data also indicate that factor(s) regulating the normal morphological development of sweat gland might be responsible for controlling AQP5 expression.     

Functional and morphological changes in the eccrine sweat gland with heat acclimation

Three adult male patas monkeys (11-15 kg) were heat acclimated by continuous exposure to an ambient temperature of 33 +/- 1 degree C at 13% relative humidity for 9 mo. During the last month, they were also exposed to 45 degrees C at 10% relative humidity for 4 h/day and 5 days/wk. Before and after 3 wk of acclimation, the animals were given a heat-tolerance test in which rectal (Tre) and mean skin (Tsk) temperatures, heart rate, and sweat rate (msw) were monitored during a 90-min exposure to 45 degrees C heat with 24% relative humidity under lenperone (1.0-1.4 mg/kg im) tranquilization. Maximal in vivo msw was also determined in response to subcutaneous injections (1 and 10% solutions) of methacholine (MCh). Before and after 9 wk and 9 mo of acclimation, sweat glands were dissected from biopsy specimens of the lateral calf, cannulated, and stimulated in vitro with MCh. Morphological measurements of isolated tubules were compared with maximal secretory rates produced by MCh stimulation. Three weeks of acclimation 1) reduced Tre and Tsk and increased msw during the heat tolerance test and 2) significantly increased maximal msw in response to MCh stimulation. Acclimation also increased (P less than 0.05) sweat gland size, as measured by tubular length and tubular volume. Maximal in vitro msw produced by MCh stimulation and msw per unit length of secretory coil also increased significantly. We conclude that heat acclimation increases the size of eccrine sweat glands and that these larger glands produce more sweat. They are also more efficient because they produce more sweat per unit length of secretory coil.     

Influence of training on sweating responses during submaximal exercise in horses.

Sweating responses were examined in five horses during a standardized exercise test (SET) in hot conditions (32-34 degrees C, 45-55% relative humidity) during 8 wk of exercise training (5 days/wk) in moderate conditions (19-21 degrees C, 45-55% relative humidity). SETs consisting of 7 km at 50% maximal O(2) consumption, determined 1 wk before training day (TD) 0, were completed on a treadmill set at a 6 degrees incline on TD0, 14, 28, 42, and 56. Mean maximal O(2) consumption, measured 2 days before each SET, increased 19% [TD0 to 42: 135 +/- 5 (SE) to 161 +/- 4 ml. kg(-1). min(-1)]. Peak sweating rate (SR) during exercise increased on TD14, 28, 42, and 56 compared with TD0, whereas SRs and sweat losses in recovery decreased by TD28. By TD56, end-exercise rectal and pulmonary artery temperature decreased by 0.9 +/- 0.1 and 1.2 +/- 0.1 degrees C, respectively, and mean change in body mass during the SET decreased by 23% (TD0: 10.1 +/- 0.9; TD56: 7.7 +/- 0.3 kg). Sweat Na(+) concentration during exercise decreased, whereas sweat K(+) concentration increased, and values for Cl(-) concentration in sweat were unchanged. Moderate-intensity training in cool conditions resulted in a 1.6-fold increase in sweating sensitivity evident by 4 wk and a 0.7 +/- 0.1 degrees C decrease in sweating threshold after 8 wk during exercise in hot, dry conditions. Altered sweating responses contributed to improved heat dissipation during exercise and a lower end-exercise core temperature. Despite higher SRs for a given core temperature during exercise, decreases in recovery SRs result in an overall reduction in sweat fluid losses but no change in total sweat ion losses after training.     

Effects of bromocriptine on sweat gland function during heat acclimatization

This study examined the involvement of the hormones aldosterone and prolactin in sweat gland function during heat acclimatization. Two groups of male subjects (n = 8) were tested - one receiving a placebo (control), the other receiving bromocriptine. Both groups performed cycle ergometer exercise at 50% of maximal oxygen uptake over 10 consecutive days in an environmental chamber maintained at 39 degrees C and 30% relative humidity. Duration of exercise was 90 min on days 2-4 and 6-9, and 45 min on test days 1, 5 and 10. Electrolyte concentrations were determined by total body washdown. Prolactin increased (p less than 0.001) during exercise on day 1 in the control group but not on days 5 and 10. In contrast, prolactin was suppressed by bromocriptine and did not rise in response to exercise or heat exposure. Plasma aldosterone increased during exercise in both groups, showing no differences between groups. The sodium concentration in sweat decreased significantly (p less than 0.05) in the control group from day 1 to 10 but was unchanged in the treatment group. These data suggest that acclimatization-related changes in sweat gland function may be attenuated by increases in central dopaminergic activity and implicate prolactin in control of sweat gland function.     

Human Core Temperature Responses during Exercise and Subsequent Recovery: An Important Interaction between Diurnal Variation and Measurement Site

Chronobiological investigations into core temperature during and after exercise can involve ambulatory measurements of intestinal temperature during actual competitions, esophageal temperature measurements in laboratory simulations, or rectal temperature, which can be measured in both the field and laboratory. These sites have yet to be compared during both morning and afternoon exercise and subsequent recovery. At 08∶00 and 17∶00 h, seven recreationally active males exercised at 70% peak oxygen uptake for 30 min and then recovered passively for 30 min. During the experiment, esophageal, rectal, intestinal, and skin temperatures, plus sweat loss, heart rate, and ratings of perceived exertion (RPE), were monitored. We found that the diurnal variation in intestinal temperature responses (0.45±0.32°C; mean±SD) was significantly larger compared with rectal (0.33±0.24°C) and, particularly, esophageal temperature responses (0.21±0.20°C; p= 0.019). This reflected a greater difference of 0.25–0.40°C between the esophagus and the other two sites in the afternoon, compared to inter‐site differences of only 0.13–0.16°C in the morning. Diurnal variation was small for skin temperature, heart rate, sweat loss, and RPE responses during exercise (p>0.05). Our data suggest that the relative differences between intestinal, rectal, and esophageal temperature during exercise and subsequent recovery depend on time of day to the extent that inferences from studies on experimental and applied chronobiology will be affected.     

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.     

Plasma aldosterone and sweat sodium concentrations after exercise and heat acclimation

This investigation was designed to determine the relationship between the levels of plasma aldosterone and eccrine sweat gland sodium excretion following exercise and heat acclimation. Ten subjects exercised at 45% of their maximal O2 uptake in a hot (40 degrees C), moderately humid (45% relative humidity) environment for 2 h/day on ten consecutive days. Acclimation was verified by significant reductions in exercise heart rate, rectal temperature, and heat storage, as well as significant elevation of resting plasma volume (12%, P less than 0.05) and exercise sweat rate on day 10 compared with day 1 of acclimation. During exercise, the concentration and total content of sodium in sweat as well as plasma aldosterone were significantly decreased from day 1 to day 10. The ratio of sweat sodium reabsorbed to plasma aldosterone concentration was significantly increased from day 1 to day 10 after both 1 and 2 h of exercise. These data indicate that plasma aldosterone concentrations decrease following heat acclimation; and eccrine gland responsiveness to aldosterone, as represented by sweat sodium reabsorption, may be augumented through exercise and heat acclimation.     

Thermogenic and psychogenic recruitment of human eccrine sweat glands: Variations between glabrous and non-glabrous skin surfaces

Human eccrine sweat-gland recruitment and secretion rates were investigated from the glabrous (volar) and non-glabrous hand surfaces during psychogenic (mental arithmetic) and thermogenic stimuli (mild hyperthermia). It was hypothesised that these treatments would activate glands from both skin surfaces, with the non-thermal stimulus increasing secretion rates primarily by recruiting more sweat glands. Ten healthy men participated in two seated, resting trials in temperate conditions (25–26 °C). Trials commenced under normothermic conditions during which the first psychogenic stress was applied. That was followed by passive heating (0.5 °C mean body temperature elevation) and thermal clamping, with a second cognitive challenge then applied. Sudomotor activity was evaluated from both hands, with colourimetry used to identify activated sweat glands, skin conductance to determine the onset of precursor sweating and ventilated sweat capsules to measure rates of discharged sweating. From glandular activation and sweat rate data, sweat-gland outputs were derived. These psychogenic and thermogenic stimuli activated sweat glands from both the glabrous and non-glabrous skin surfaces, with the former dominating at the glabrous skin and the latter at the non-glabrous surface. Indeed, those stimuli individually accounted for ~90% of the site-specific maximal number of activated sweat glands observed when both stimuli were simultaneously applied. During the normothermic psychological stimulation, sweating from the glabrous surface was elevated via a 185% increase in the number of activated glands within the first 60 s. The hypothetical mechanism for this response may involve the serial activation of additional eccrine sweat glands during the progressive evolution of psychogenic sweating.     

Thermoregulatory responses of lower limb amputees during exercise in a hot environment

Lower limb amputees (LLAs) have less skin surface required for sweating; thus, the ability to dissipate heat from the body may decrease and the risk of heat illness may increase during exercise in a hot environment. However, no study has compared the thermoregulatory responses during exercise between LLAs and able-body (AB) individuals with different body surface areas. This study aimed to compare the thermoregulatory responses of LLAs with those of AB individuals during exercise in a hot environment. Seven LLAs (LLA group) and 7 able-body individuals (AB group) participated in the study. A 60% peak power output of arm crank upper-body exercise was performed for 60 min in a hot environment (32 °C, 50% relative humidity). There was no difference in the increase in rectal temperature (LLA: 0.8 ± 0.2 °C, AB: 0.8  ± 0.2 °C) and mean skin temperature between the groups during the 60-min exercise. In the LLA group, the accumulated local sweat rate of the thigh during exercise was significantly higher on the non-cut side than on the cut side (64.6 ± 43.0 mg/h vs. 37.0 ± 27.2 mg/h, p < 0.05). The total sweat rate was significantly higher in the LLA group than in the AB group (1.18 ± 0.37 kg/h vs. 0.84 ± 0.10 kg/h, p < 0.05). Thermal sensation and comfort were lower in the LLA group than in the AB group. Different heat loss responses were observed in the AB and LLA groups during exercise in the heat. The LLA group compensates for sweating on the cut side due to an increase in sweat loss on the intact limb, thereby preserving appropriate thermoregulation during exercise.