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Distinct cellular mechanisms of cholinergic and beta-adrenergic sweat secretion.

The cholinergic and beta-adrenergic sweat secretions from human sweat glands differ with respect to secretory rates and their susceptibility to cystic fibrosis (CF). Using the cultured beta-adrenergic-sensitive sweat secretory cell, we sought to determine the intracellular electrophysiological mechanisms underlying these functional differences. We found that the cholinergic agonist methacholine (10(-6) M) induced a Ca(2+)-dependent biphasic membrane potential (Vm) response: an initial hyperpolarization and a secondary depolarization. The initial hyperpolarization was independent of bath Cl- and dependent on transmembrane K+ gradient. However, the secondary depolarization of Vm was dependent on bath Cl-. In contrast, the beta-adrenergic agonist isoproterenol (10(-5) M) induced a monophasic depolarization of Vm. This depolarization was 1) dependent on bath Cl-, 2) independent of K+ conductance (GK) blocker Ba2+ (5mM), 3) unaffected by the methacholine-induced secondary depolarization of Vm, and 4) absent in cells derived from CF subjects. These results indicated that the cholinergic agonist-induced secretion mainly involves the activation of Ca(2+)-dependent GK and Cl- conductance (GCl), whereas the beta-adrenergic secretion seems to mainly depend on the activation of cystic fibrosis transmembrane conductance regulator-GCl.

Adrenergic beta-Agonists↗

Calf sweat lactate in peripheral arterial occlusive disease.

The energy metabolism of sweat glands was studied to evaluate the reduction in oxygen delivery in the tissue of patients with peripheral arterial occlusive disease. We compared lactate concentration in pilocarpine-iontophoresis sweat collected from the middle calf area ([ L]sw) of 10 healthy subjects (group 1) and 84 patients suffering from intermittent claudications (group 2, n = 49), from rest pain (group 3, n = 21), and from severe ischemic skin changes (group 4, n = 14). In addition, the effect of a vasoactive drug (naftidrofuryl, 600 mg) or placebo infusion on [L]sw was investigated (n = 30). Results (means +/- SE) showed that 1) [L]sw (mmol/l) increased significantly with the severity of the symptoms: group 1 = 16.5 +/- 0.4, group 2 = 18.7 +/- 0.4, group 3 = 22.8 +/- 0.9, and group 4 = 27.5 +/- 2.0; and 2) [L]sw was reduced by 10% (P less than 0.01) after naftidrofuryl infusion, whereas there was no change after placebo infusion. We suggest that lactate in calf sweat is a good indicator in the evaluation of the severity of peripheral occlusive arterial disease and in assessing the efficiency of vasoactive drug treatment.

Aged↗

Circadian rhythm in sweating and cutaneous blood flow.

To characterize the changes in the control of the heat loss responses associated with the circadian variation in body temperature, we studied five men during 20 min of exercise in 25 degrees C on 6 separate days. Experiments were conducted at six times, equally spaced over the 24-h day. Esophageal temperature (Tes) and chest sweat rate (msw) were measured continuously, and forearm blood flow (FBF) was measured one to two times per minute. The thresholds for sweating and forearm vasodilation were significantly higher at 1600 and 2000 than at 2400 and 0400, averaging 0.57 and 0.65 degrees C higher, respectively, at 1600 than at 0400. Resting Tes and the Tes thresholds for cutaneous vasodilation and sweating during exercise all showed a similar circadian rhythm. The level at which core temperature is regulated therefore varies over the 24-h day with the zenith occurring around 1600 and the nadir at 0400. However, whereas the slope of the msw-to-Tes relation did not change over the 24-h day, the slope of the FBF-to-Tes relation tended to increase between 0400 and 2400, implying that the circadian rhythm may be more complex than just a shift in the central reference temperature.

Adult↗

Differing luminal potential difference of cystic fibrosis and control sweat secretory coils in vitro.

Transepithelial potential difference (PD) of isolated segments of the secretory coil of both human control and cystic fibrosis (CF) eccrine sweat glands was measured during stimulation with methacholine (MCh) and isoproterenol (ISO) in vitro. Negative luminal PD of about 10 and 16 mV developed across the secretory coil epithelium in control and CF secretory coil, respectively, during maximal MCh stimulation. ISO (10(-5) M) stimulation generated a mean of 1.9-mV negative luminal PD in control glands; however, ISO failed to enhance the luminal PD beyond the resting level of 0.9 mV in the CF secretory coil. The inhibition of ISO-induced (10(-5) M) luminal PD in control secretory coil by propranolol (5 X 10(-5) M) but not by atropine (10(-5) M) indicated its pharmacologic specificity. The possibility is discussed that this lack of electrical driving force during ISO stimulation could be one of the mechanisms for the absence of sweating response to beta-adrenergic stimulation in CF sweat glands reported recently (8). The mechanism for the higher MCh-induced luminal PD in the CF secretory coil remains to be studied.

Adult↗

Menstrual cycle phase and time of day alter reference signal controlling arm blood flow and sweating.

The changes occurring in the esophageal temperature (Tes) thresholds for initiation of heat loss responses as affected by the circadian period and menstrual cycle were studied. Four women exercised at 60% peak Vo2 in 35 degrees C (ambient water vapor pressure 1.73 kPa) for 30 min at 0400 and 1600 during the follicular (F) and luteal (L) phase. Tes, arm sweating rate (msw), and forearm blood flow (FBF) were measured frequently. At rest, Tes averaged 0.3 degrees C higher during L than F at both 0400 and 1600 and approximately 0.4 degrees C higher at 1600 than at 0400 during both phases. During exercise transients, the slopes of the FBF:Tes and the msw:Tes relationships were not different among treatments. The thresholds for initiation of sweating and cutaneous vasodilation were higher at 1600 than 0400 during both phases. Thresholds during F at 0400 averaged 36.44 degrees C for msw and 36.80 degrees C for vasodilation. The thresholds during L at 1600 averaged 37.46 and 37.53 degrees C for sweating and vasodilation, respectively. Our data indicate that the thermoregulatory effector activity during exercise is a function of numerous inputs, and one of these may be hormonal or hormonal-like in action. Controlling time of day and menstrual cycle phase are as important as controlling for aerobic power, age, and fitness in studying female thermoregulatory responses during exercise.

Adult↗

Morphology and development of an apoeccrine sweat gland in human axillae.

Evidence is presented that in adult human axillae there exists a third type of sweat gland tentatively designated as the apoeccrine sweat gland. This type of gland shows a segmental or diffuse apocrinelike dilatation of its secretory tubule but has a long and thin duct which does not open into a hair follicle. The electron microscopy of its dilated segment is often indistinguishable from that of the classical apocrine gland. The less remarkably dilated segment of the apoeccrine gland tends to retain intercellular canaliculi and/or dark cells. These apoeccrine glands are consistently present in adult human axillae regardless of sex or race. In the axillae of the two 6-yr-old subjects, both classical apocrine and eccrine glands were present but no apoeccrine glands were found. Between 8-14 yr of age, the number of large eccrine glands with or without partial segmental dilatation gradually increased. At 16-18 yr of age, the number of apoeccrine glands increased to as high as 45% of the total axillary glands. The data support the notion that apoeccrine glands develop during puberty in the axillae from eccrine or eccrinelike sweat glands.

Adolescent↗

Core temperature and sweating onset in humans acclimated to heat given at a fixed daily time.

The thermoregulatory functions of rats acclimated to heat given daily at a fixed time are altered, especially during the period in which they were previously exposed to heat. In this study, we investigated the existence of similar phenomena in humans. Volunteers were exposed to an ambient temperature (Ta) of 46 degrees C and a relative humidity of 20% for 4 h (1400-1800) for 9-10 consecutive days. In the first experiment, the rectal temperatures (Tre) of six subjects were measured over 24 h at a Ta of 27 degrees C with and without heat acclimation. Heat acclimation significantly lowered Tre only between 1400 and 1800. In the second experiment, six subjects rested in a chair at a Ta of 28 degrees C and a relative humidity of 40% with both legs immersed in warm water (42 degrees C) for 30 min. The Tre and sweating rates at the forearm and chest were measured. Measurements were made in the morning (0900-1100) and afternoon (1500-1700) on the same day before and after heat acclimation. Heat acclimation shortened the sweating latency and decreased the threshold Tre for sweating. However, these changes were significant only in the afternoon. The results suggest that repeated heat exposure in humans, limited to a fixed time daily, alters the core temperature level and thermoregulatory function, especially during the period in which the subjects had previously been exposed to heat.

Acclimatization↗

Evaporation of sweat from sedentary man in humid environments.

UNLABELLED: Physiological and sensory responses were observed in four male subjects while they were seated on a balance. The chamber temperature always equaled mean skin (Tsk)(34-36 degrees C), thus eliminating all sensible heat transfer. Ambient water vapor pressure (Pa) was increased in steps from 10 to 40 Torr. Tests at air velocities from 0.1 to 2.4 m/s were conducted with subjects nude and clothed. Esophageal temperature (Tes) and Tsk, heat rate (HR) and weight loss (M) were measured throughout the 2.5-h tests. After each 25-min humidity step subjects recorded their warm discomfort, sensation of sweating, and thermal sensation. RESULTS: Tsk, HR, and M were unaffected by humidity until critical Pa (P a crit) was reached above which M decreased and Tsk and HR increased rapidly. P a crit decreased with clothing and decreasing velocity. Tes remainded relatively constant throughout the tests. Sweating, discomfort and temperature sensations increased gradually with increasing Pa. Above P a crit sweating and discomfort sensations accelerated markedly. Mass transfer coefficients and clothing vapor conductance factors were evaluated. Skin wettedness at Pa crit decreased from 74% at 0.1 m/s to 35% at 2.4 m/s.

Adolescent↗

Skin blood flow and sweating changes following exercise training and heat acclimation.

Eight subjects underwent an exercise training program (10 days at 75% VO2max for 1 h/day at 25 degrees C db/13 degrees C wb) and a heat-acclimation program (10 days at 50% VO2max for 1 h/day at 35 degrees C db/32 degrees C wb). The relations of chest sweat rate and of forearm blood flow to internal temperature were determined for each subject at a 25 degrees C ambient temperature before training, between training and acclimation, and following acclimation. Training shifted the vasodilation and sweating thresholds toward lower internal temperatures, and acclimation further lowered these thresholds. All threshold shifts were statistically significant (P less than 0.05). Training and acclimation both appeared to increase the slope of the sweating relation, but these effects were not statistically significant. Changes in the slope of the blood flow relation were small and inconsistent. Since arm blood flow is higher at any given internal temperature after acclimation, the lower blood flow which is reported to accompany heat acclimation must result from the lower body temperatures.

Acclimatization↗

Sweating response in man during transient rises of air temperature.

Nude men were exposed to neutral environments (Ta = 28 degrees C, Pw = 20 mbar) changing to warm environments (Ta = 50 degrees C, Pw = 20 mbar). The transient period from neutral to warm environment lasted 4 min (dTA/DT = 5.50 degrees C/min) or 20 min (DTa/dt = 1.10 degrees C/min) or 40 min (dTa/dt = 0.55 degrees C/min) or 60 min (dTa/dt = 0.37 degrees C/min). Continuous measurements were made of rectal and mean skin temperatures and of body weigth loss. Sweating started before appreciable variation in rectal temperature. Onset of sweating could be explained by a peripheral proportional and rate control. Unsteady-state sweating can be predicted by summated stimulation of skin and rectal temperatures. This stimulation could be increased for some subjects by a multiplicative effect due to differences in local skin temperatures. This multiplicative effect occurred during the first transient period.

Adult↗

Local sweating and cutaneous blood flow during exercise in hypobaric environments.

The effect of acute hypobaric hypoxia on local sweating and cutaneous blood flow was studied in four men and four women (follicular phase of menstrual cycle), who exercised at 60% of their altitude-specific peak aerobic power for 35 min at barometric pressures (PB) of 770 Torr (sea level), 552 Torr (2,596 m), and 428 Torr (4,575 m) at an ambient temperature of 30 degrees C. We measured esophageal temperature (Tes), mean skin temperature (Tsk, 8 sites), and local sweating (ms) from dew-point sensors attached to the skin at the chest, arm, and thigh. Skin blood flow (SkBF) of the forearm was measured once each minute by venous occlusion plethysmography. There were no gender differences in the sensitivity (slope) or the threshold of either ms/Tes or SkBF/Tes at any altitude. No change in the Tes for sweating onset occurred with altitude. The mean slopes of the ms/Tes relationships for the three regional sites decreased with increasing altitude, although these differences were not significant between the two lower PBS. The slope of SkBF/Tes was reduced in five of the eight subjects at 428 Torr. Enhanced body cooling as a response to the higher evaporative capacity of the environment is suggested as a component of these peripheral changes occurring in hypobaric hypoxia.

Adult↗

Responses of sweating and body temperature to sinusoidal exercise.

This study determined the phase response and amplitude response (delta) of esophageal temperature (T(es)), mean skin temperature (Tsk), and forearm sweating rate (Msw) to sinusoidal work. Six healthy male subjects exercised on a cycle ergometer with a constant load (approximately 35% maximal O2 uptake) for a 30-min period; for the next 40 min they exercised with a sinusoidal load at 25 degrees C at 35% relative humidity. The sinusoidal load varied between approximately 10 and 60% maximal O2 uptake, and three different time periods (1.3, 4, and 8 min) were selected. Each subject performed three experiments that differed only in the timing of sinusoidal work. During the 4- and 8-min periods, T(es), Tsk, and Msw changed almost sinusoidally. The phase of Msw change significantly preceded those of T(es) and Tsk changes (P < 0.05). During the 1.3-min period, the level of T(es) and Tsk remained almost constant (delta T(es) 0.01 +/- 0.00 degrees C, delta Tsk 0.03 +/- 0.01 degrees C), whereas Msw showed a clear sinusoidal pattern. We conclude that the sweating response during sinusoidal work depends on both thermal and nonthermal factors, the latter being emotional, mental, or sensory stimulation. The contribution of the nonthermal factors to the general sweating response during exercise can be separated from that of the thermal factors by using sinusoidal work during a short period (e.g., 1.3 min).

Adult↗

Control of thermoregulatory sweating is altered by hydration level and exercise intensity.

The purpose of this study was to examine the thermoregulatory sweating control parameters of threshold temperature and sensitivity to determine whether 1) these variables were altered by hypohydration level and exercise intensity and 2) these alterations, if present, were additive and independent. Nine heat-acclimated men completed a matrix of nine trials: three exercise intensities of 25, 45, and 65% maximal O2 uptake and three hydration levels, i.e., euhydration and hypohydration (Hy) at 3 and 5% of body weight. During each trial, subjects attempted 50 min of treadmill exercise in a warm room (30 degrees C dry bulb, 50% relative humidity) while esophageal temperature and upper arm sweating rate were continuously measured. Hypohydration was achieved by exercise and fluid restriction the day preceding the trials. The following new findings were made: 1) threshold temperature increased in graded manner with hypohydration level (approximately 0.06 degree C/% Hy); 2) sensitivity decreased in a graded manner with hypohydration level (approximately 0.06 units/%Hy); 3) threshold temperature was not altered by exercise intensity; and 4) sensitivity increased from low- to moderate- and high-intensity exercise. We conclude that both hypohydration level and exercise intensity produce independent effects on control of thermoregulatory sweating.

Adult↗

Effects of exercise intensity on the sweating response to a sustained static exercise.

To investigate how the sweating response to a sustained handgrip exercise depends on changes in the exercise intensity, the sweating response to exercise was measured in eight healthy male subjects. Each subject lay in the supine position in a climatic chamber (35 degrees C and 50% relative humidity) for approximately 60 min. This exposure caused sudomotor activation by increasing skin temperature without a marked change in internal temperature. After this period, each subject performed isometric handgrip exercise [15, 30, 45, and 60% maximal voluntary contraction (MVC)] for 60 s. Although esophageal and mean skin temperatures did not change with a rise in exercise intensity and were similar at all exercise intensities, the sweating rate (SR) on the forearm increased significantly (P < 0.05) from baseline (0.094 +/- 0.021 mg. cm(-2). min(-1) at 30% MVC, 0.102 +/- 0.022 mg. cm(-2). min(-1) at 45% MVC, 0.059 +/- 0.009 mg. cm(-2). min(-1) at 60% MVC) in parallel with exercise intensity above exercise intensity at 30% MVC (0.121 +/- 0.023 mg. cm(-2). min(-1) at 30% MVC, 0.242 +/- 0.051 mg. cm(-2). min(-1) at 45% MVC, 0.290 +/- 0.056 mg. cm(-2). min(-1) at 60% MVC). Above 45% MVC, SR on the palm increased significantly from baseline (P < 0.05). Although SR on the forearm and palm tended to increase with a rise in exercise intensity, there was a difference in the time courses of SR between sites. SR on the palm showed a plateau after abrupt increase, whereas SR on the forearm increased progressively during exercise. These results suggest that the increase in SR with the increase in sustained handgrip exercise intensity is due to nonthermal factors and that the magnitude of these factors during the exercise may be responsible for the magnitude of SR.

Adult↗

Effect of local acetylcholinesterase inhibition on sweat rate in humans.

ACh is the neurotransmitter responsible for increasing sweat rate (SR) in humans. Because ACh is rapidly hydrolyzed by acetylcholinesterase (AChE), it is possible that AChE contributes to the modulation of SR. Thus the primary purpose of this project was to identify whether AChE around human sweat glands is capable of modulating SR during local application of various concentrations of ACh in vivo, as well as during a heat stress. In seven subjects, two microdialysis probes were placed in the intradermal space of the forearm. One probe was perfused with the AChE inhibitor neostigmine (10 microM); the adjacent membrane was perfused with the vehicle (Ringer solution). SR over both membranes was monitored via capacitance hygrometry during microdialysis administration of various concentrations of ACh (1 x 10(-7)-2 M) and during whole body heating. SR was significantly greater at the neostigmine-treated site than at the control site during administration of lower concentrations of ACh (1 x 10(-7)-1 x 10(-3) M, P < 0.05), but not during administration of higher concentrations of ACh (1 x 10(-2)-2 M, P > 0.05). Moreover, the core temperature threshold for the onset of sweating at the neostigmine-treated site was significantly reduced relative to that at the control site. However, no differences in SR were observed between sites after 35 min of whole body heating. These results suggest that AChE is capable of modulating SR when ACh concentrations are low to moderate (i.e., when sudomotor activity is low) but is less effective in governing SR after SR has increased substantially.

Acetylcholinesterase↗

Effect of training on zinc metabolism: changes in serum and sweat zinc concentrations in sportsmen.

The purpose of this research was to determine the effects of daily physical training on serum and sweat zinc concentrations in professional sportsmen between October and December, during the competing season. Twelve volleyball players and another 12 control subjects have participated in this study. Tests were made in October and December which consisted of a progressive bicycle ergometer test (increasing 30 W every 3 min to reach maximum tolerated power). Blood samples were obtained at rest and immediately after exercise. Total serum zinc increased significantly after maximal exercise in both sportsmen and control subjects. In athletes, the change after exercise was significantly higher in December than in October. The percentage of ultrafiltrable zinc (ZnUf) in October was similar in sportsmen and in controls. In December, however, after exercise, the percentage of ZnUf was higher in athletes. With respect to sweat zinc, it was in the same range both in controls and in sportsmen in October. In December, however, sweat zinc was significantly higher in athletes as compared with the situation in October and with respect to the control group. In October, the zinc concentration of urine was similar for sportsmen and controls. In December, the sportsmen showed an increase in urinary zinc excretion with respect to control subjects. Cortisol in athletes increased significantly after exercise in December. In conclusion, a daily and maintained practice of exercise is probably responsible for an alteration of zinc metabolism. The results suggest that ZnUf control, zinc supplementation and/or stress control appear to be indicated in athletes to prevent the diminution of active ZnUf. In our practical opinion we think that alterations in zinc metabolism with increases in zinc excretion and stress levels lead to a situation of latent fatigue with a decreased endurance.

Adult↗

Calcitonin gene-related peptide during sweating in young healthy women.

Calcitonin gene-related peptide (CGRP) concentrations are increased in postmenopausal women and castrated men with symptomatic flushing. We wanted to determine if a CGRP increase exists in the plasma of healthy fertile-age women during sweating. Plasma concentrations of CGRP were measured by radioimmunoassay at maximal sweating during a sauna session and during bicycle exercise both at maximal and 70% of maximal work capacity in 8 healthy women of fertile age. Plasma concentrations of CGRP were unaffected (>90% statistical power) during both experimental sessions. We suggest that sweating itself does not explain the rise in CGRP concentrations observed in flushing postmenopausal women.

Adult↗

Changes in sweat glands morphology in cattle before and during heat stimulation.

The morphology of apocrine sweat glands in two breeds of cattle, the White Fulani and Friesian was studied histologically using biopsy midside skin samples obtained from the animal at 6.00 a.m. (period 1), 2.30 p. m. (period 2) and 4.00 p. m. (period 3), respectively. Sweat glands with three morphologic types of epithelium were observed. Type 1 consisted of flattened low cuboidal epithelium. Type 2 had tall cuboidal epithelium with cell apical borders slightly indented and the gland lumen narrower than in type 1. A third group of glands had tall columnar epithelial cells (type 3) with bleb-like protuberances on their luminal surfaces. There were also corresponding changes in the morphology of myoepithelial cells from an elongated form in type 1 to a contracted form in types 2 and 3. The morphology of secretory cell surfaces was found to vary with the sampling period; a greater percentage of type 1 glands was seen in period 1 and a preponderance of types 2 and 3 glands (in varying proportions) in periods 2 and 3. Breed differences in the distribution of type of epithelium at various sampling periods were observed. These results are discussed in relation to the functional activity pattern of the sweat glands on stimulation by heat.

Animals↗