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PubMed1987

Lactate and bicarbonate uptake in the sweat duct of cystic fibrosis and normal subjects.

The sweat of single sweat glands of healthy individuals and cystic fibrosis patients was analyzed for differences in bicarbonate, lactate, and pH. These values were monitored as a function of sweat rate simultaneously with 1) the electrical potential difference at the duct orifice (with respect to the interstitial fluid) and 2) the concentrations of sodium, potassium, and chloride in surface sweat. Sweat in both groups contained about equal concentrations of lactate and bicarbonate at similar sweat rates. Similarly, the pH of sweat secreted at similar rates in the two populations was not significantly different. Acidification of sweat increased with decreasing sweat rate. In both populations, lactate and bicarbonate may be absorbed passively in the distal sweat duct in their nonionic form and, thus, not influenced by the increased electrical potential difference in the cystic fibrosis sweat duct. The uptake of these ions may involve active proton secretion by sweat duct cells.

Bicarbonates↗

PubMed2002

The interaction between epidermal growth factor and matrix metalloproteinases induces the development of sweat glands in human fetal skin.

BACKGROUND: The development of sweat glands is a very complicated biological process involving many factors. In this study, we explore the interrelationship among epidermal growth factor (EGF), matrix metalloproteinase 2 (MMP-2), matrix metalloproteinase 7 (MMP-7), and the development of sweat glands in human embryos. Furthermore, we hope to elucidate the mechanism(s) underlying the induction of epidermal stem cells into sweat gland cells. MATERIALS AND METHODS: Skin biopsies of human embryos obtained from spontaneous abortions at different gestational ages from 11 to 31 weeks were used in this study. The dynamic expression of EGF, MMP-2, MMP-7, and keratin-7 (K7) in developing sweat gland cells or extracellular stroma surrounding the sweat gland cells was examined with SP immunohistochemical methods. The localization of the cellular sources of MMP-2 and MMP-7 was examined with in situ hybridization. RESULTS: At 14-20 weeks of gestation, a gradual increase in EGF immunoreactivity was observed not only in developing sweat gland buds but also in extracellular stroma surrounding the buds, and the expression intensity of EGF peaked at 20-22 weeks of gestational age. All mRNA-positive buds or cells in developing sweat glands contained corresponding immunoreactive proteins. Positive immunostaining for K7 appeared in early sweat gland buds at 14-16 weeks of gestation, and from then on, the positive signal of K7 was concentrated in developing sweat gland cords or cells. CONCLUSIONS: The morphogenesis of sweat glands in human fetal skin begins at 14-16 weeks of gestational age, and is essentially complete by 24 weeks. There is a close relationship among EGF, extracellular matrix remodeling, and morphogenesis of the sweat glands. EGF is one of the inducers in the development and maturity of sweat gland buds or cells.

Embryonic and Fetal Development↗

PubMed1984

Rodent eccrine sweat glands: a case of multiple efferent innervation.

The sweat territories of peripheral nerves to the hind-paw of the mouse were defined by a silastic impression mold method that allowed identification of every secreting sweat gland. It was found that the tibial, sural, saphenous and peroneal nerves all contribute to the innervation of foot pad sweat glands, and there is extensive overlapping of the sweat territories of the different peripheral nerves. Most sweat glands could be activated by electrical stimulation of axons in two or three peripheral nerves or in separate fascicles of one nerve. This was interpreted to indicate that these sweat glands receive multiple innervation and that sweat glands in the overlap regions between autonomous zones of adjacent cutaneous nerves can receive axons from each nerve. Partial denervation of sweat glands by section of one source of innervation did not prevent the gland from sweating during stimulation of intact axons to the gland, or after pilocarpine treatment. Totally denervated glands did not exhibit denervation hypersensitivity; they became unresponsive to pilocarpine, acetylcholine and adrenaline. These characteristics allowed detection of the appearance and progression of reinnervation (and reactivation) of denervated sweat glands by collateral branching from sudomotor fibers. Not only do these results increase our basic understanding of the anatomical relations between peripheral nerves and the sweat glands they innervate, but they also demonstrate that the mouse sweat gland provides a useful model system for studying neuropathology of the sympathetic nervous system.

Animals↗

PubMed2002

Changes in mouse sudomotor function and sweat gland innervation with ageing.

Age-related changes in sudomotor neuroeffector function have been evaluated in mice aged 2 (young), 6, 12 (adult) and 18 (old) months. We evaluated sudomotor function by determining the number of sweat glands reactive to pilocarpine and the sweat output per gland on the plantar surface of the hindpaws with the impression mould technique. Protein gene product 9.5 (PGP) and vasoactive intestinal polypeptide (VIP) were immunohistochemically localised in footpads. A marked decrease (44%) in sweat output per gland was observed in old mice as well as a slight (17%), not significant decline in the number of secreting sweat glands. The sudomotor innervation, expressed as the area of sweat gland occupied by VIP and PGP immunoreactive nerve profiles, showed an initial increase from 2 to 6 months and a significant decline (35%) in 18- vs. 6-month-old mice. These results indicate that, in contrast to the number of secreting sweat glands, sweat output per gland does not reach the maximum in adult mouse until 6 months old and that sweating decreases in aged mice mainly due to a decline of sweat output per gland and to a lesser extent to a decrease in number of secreting glands. A reduction of sweat glands size in aged mice was also found, suggesting that the diminished sweat gland responsiveness with ageing may be attributed to sweat gland atrophy as well as to loss of innervation.

Acetylcholine↗

PubMed1994

Sweat testing for heroin, cocaine, and metabolites.

Although a variety of drugs have been detected in sweat, little information is available on the characteristics of drug excretion in sweat under controlled-dosing conditions. A series of clinical studies were designed to determine the identity, concentration, time course, dose dependency, and variability of drug and metabolite excretion in sweat following administration of single doses of cocaine and heroin to human subjects. Sweat was collected by means of a sweat patch that could be worn for a period of several days to several weeks at a time, resulting in accumulation of drug in the patch. Sweat patches were removed at specified times and frozen until analyzed by gas chromatography--mass spectrometry. Cocaine and heroin were the major analytes excreted in sweat following their administration. Smaller amounts of cocaine metabolites were also detected following cocaine administration. 6-Acetylmorphine appeared rapidly after heroin administration and continued to increase while heroin content decreased, suggesting that heroin was undergoing hydrolysis in the sweat patch. Cocaine appeared in sweat within 1-2 hours and peaked within 24 hours in an apparent dose-dependent manner. Analysis of duplicate adjacent patches from individual subjects who had been administered cocaine provided similar quantitative results, suggesting that intrasubject variability was relatively low, whereas intersubject variability was high. These observations regarding the excretion of cocaine and heroin analytes in sweat have important forensic implications to other fields such as hair analysis. Sweat excretion could be an important mechanism by which drugs enter hair. These data also suggest that the sweat patch could serve as a useful monitoring device in surveillance of individuals in treatment and probation programs.

Administration, Inhalation↗

PubMed1989

Free fatty acids and sterols in human eccrine sweat.

The lipid content of human sweat was determined in thermally induced sweat collected over a Vaseline or silicone barrier placed on the skin (clean sweat) and in sweat scraped from the skin surface without a barrier coating (scraped sweat). Lipids were extracted from concentrated sweat samples into chloroform:methanol and estimated by thin-layer chromatography in conjunction with photodensitometry. Scraped sweat contained 4 to 10 times more lipid than clean sweat and included cholesterol sulphate and ceramides resembling those found in the stratum corneum. In contrast, clean sweat contained only small amounts of free fatty acids and sterol. A marked individual and daily variation in sweat lipid content was also noted. The study indicates the importance of avoiding epidermal contamination when collecting sweat and the usefulness of our sweat collection method.

Adolescent↗

PubMed1989

Effects of dehydration and rehydration on thermoregulatory sweating in goats.

1. Measurement of rectal temperature (Tr), sweat rate, respiratory frequency (f) and respiratory evaporation (Eresp) were made in one Nubian and four Alpine-Toggenberg goats while they stood for 90 min in a climate chamber at 40 degrees C ambient temperature (Ta). The animals were studied when they were hydrated, when they had been dehydrated by 48 h water deprivation, and when they were rehydrated by voluntary drinking of water or saline or by intraruminal water administration. Plasma osmolality (Posm), plasma protein concentration (PP) and haematocrit (Hct) were measured before every experiment and before and after voluntary drinking. 2. Hydrated animals increased evaporation by panting and sweating during heat exposure and Tr rose about 1 degree C. The rate of sweating was as high or higher than Eresp. Dehydrated animals had lower sweat rates and higher Tr than hydrated animals, but f and Eresp were the same in hydrated and dehydrated animals. 3. When dehydrated goats were allowed to drink after 60 min of heat exposure, sweating began abruptly within 3 min of the start of drinking in every animal whether water or saline was drunk. Sweat rate returned to hydrated levels or higher before any change occurred in Posm, PP or Hct. Respiratory frequency was higher after drinking than in dehydrated animals which were not allowed to drink. 4. When water was administered by rumen tube after 60 min of heat exposure, sweating in the Nubian occurred with a short latency, similar to the onset after drinking. In the other four animals, sweating onset occurred on average at 13 min 42 s after intraruminal water administration. 5. It is concluded that sweating is a significant avenue of evaporative heat loss in these goats when they are hydrated and exposed to high Ta. Sweat rate is markedly reduced after water deprivation but returns to hydrated levels within 3 min after the start of drinking. The rapid recovery of sweating after voluntary drinking is not initiated by changes in Posm or in blood volume and does not appear to depend upon osmoreceptors in the mouth or gastrointestinal tract since it occurs after drinking either water or saline. The arrival of water in the rumen may be sufficient to initiate immediate sweating in some goats, but the act of drinking is necessary in others.

Animals↗

PubMed1987

Sweat lactate secretion during exercise in relation to women's aerobic capacity.

The purpose of this investigation was to determine whether sweat lactate secretion during exercise [approximately 70% maximum O2 consumption (VO2max), 60 min] differed in active vs. sedentary female subjects. Sweat rate, total sweat lactate secretion, and sweat lactate concentration were monitored in a group of sedentary (VO2max = 41.0 +/- 1.62 ml X kg-1 X min-1) and active (VO2max = 51.2 +/- 3.20 ml X kg-1 X min-1) women. Sweat rate was significantly (P less than 0.05) greater in the active subjects. There was a significant difference between groups in total amount of sweat lactate secreted (P less than 0.05), with the active group secreting less lactate (29.8 +/- 5.03 mmol, mean +/- SE) than the sedentary group (50.2 +/- 6.61 mmol). Concomitant with the lower total sweat lactate secretion in the active subjects was a significantly (P less than 0.05) more dilute sweat lactate concentration (42.6 +/- 14.08 vs. 100.4 +/- 32.37 mM). In these female subjects, sweat lactate concentration was inversely correlated (r = -0.79, P less than 0.01, n = 10) to sweat rate. It is concluded that total sweat lactate loss is significantly less in active than in sedentary women and that the active subjects secrete a greater quantity of lactate dilute sweat.

Adult↗

PubMed1982

Occurrence of mental and thermal sweating on the human axilla.

Sweat responses to mental arithmetic were recorded simultaneously on the axilla, palm, and general body surface (chest and forearm) by resistance or capacitance hygrometry at different ambient temperatures. Sweat expulsions observed on the axilla were fully synchronized with those on the general body surface, but not always with those on the palm. In some subjects the sweat responses to mental arithmetic on the general body surface were different in pattern from those on the palm. In such subjects the sweat response pattern on the axilla was similar to that on the general body surface. The sweat response to mental arithmetic occurred at a considerably lower environmental temperature on the axilla than on the general body surface. The occurrence of the sweat response on the axilla can be related to the peculiar feature of axillary thermal sweating: a lower threshold temperature and less responsiveness to thermal load compared with thermal sweating on the general body surface. This suggests that mental sweating on the axilla occurs due to the characteristic feature of thermal sweating on the axilla. Axillary eccrine sweating is not different qualitatively from sweating on the general body surface.

Adult↗

PubMed1988

Variable reduction in beta-adrenergic sweat secretion in cystic fibrosis heterozygotes.

Because patients with cystic fibrosis (CF) consistently lack sweating response to isoproterenol (ISO) in vivo and in vitro, we studied to what extent beta-adrenergic defect is expressed in CF heterozygotes. To improve the sensitivity and accuracy of determining the sweating response to intradermal ISO (also containing theophylline and atropine), a water vapor analyzer was used, and the peak sweat rates attained after intradermal injection in the forearm of optimal concentrations of ISO and methacholine (MCH) were determined. The peak ISO sweat rate was further normalized by the peak MCH sweat rate in each individual and expressed as the relative ISO sweat ratemax (in percent). The relative ISO sweat ratemax was determined independent of age and sex and was unchanged after brief acclimatization. The mean relative ISO sweat ratemax of CF heterozygotes was significantly lower than that of controls (10.1% vs 19.5%); however, 21 of the 54 CF heterozygotes overlapped with controls, and the remainder of the CF heterozygotes fell below the arbitrary demarcation line drawn at the relative sweat rate of around 10%. Thus, although the ISO sweat test may not be a practical discrimination test for CF heterozygotes, knowledge of the diversity of beta-adrenergic sweating responses in CF heterozygotes will provide a useful data base for further understanding the possible linkage (or its absence) between the abnormal CF gene(s) (which may be identified by molecular biologists in the near future) and the abnormal intracellular process(es) that takes place during beta-adrenergic stimulation of the CF eccrine sweat gland.

Acclimatization↗

PubMed2005

Video assisted thoracoscopic re-sympathetic surgery in the treatment of re-sweating hyperhidrosis.

OBJECTIVE: The characteristics and causes of re-sweating after sympathetic surgery in hyperhidrosis patients have yet to be clearly documented due primarily to low incidence of re-sympathetic surgery. The purpose of this study is to identify the causes of re-sweating following sympathetic surgery, and to assess the outcomes of re-sympathetic surgery. METHODS: From February 1997 to July 2003, 36 patients underwent re-sympathetic surgery in order to treat re-sweating. Patients originally underwent sympathetic surgery due to facial (14 cases), palmar (21 cases), and axillary (1 case) hyperhidrosis. RESULTS: Sympathectomy was performed as a primary surgical intervention in 7 cases (19.4%), sympathicotomy in 12 cases (33.3%), and sympathetic clipping in 17 cases (47.3%). Thirteen patients complained of re-sweating on both sides, and 23 patients exhibited unilateral re-sweating. The onset of re-sweating occurred after an average of 3.1+/-3.4 months (range, 1-12 months) after the operation. The causes of re-sweating after sympathetic surgery included an intact sympathetic chain in 4 cases (11.1%), incomplete resection in 6 cases (16.7%), partial reattachment in 6 cases (16.7%), improper ganglion location in 4 cases (11.1%), clip slipping out in 11 cases (30.5%), and unknown in 5 cases (13.9%). Twenty-seven patients (75.0%) exhibited re-sweating within 3 months, and 9 patients (25.0%) experienced re-sweating after 6 months. During the second operation, sympathicotomy was performed in 20 cases (55.6%) and sympathetic clipping in 16 cases (44.4%) in which 32 patients (88.9%) reported decreased sweating. CONCLUSIONS: Surgical errors during the initial operation constituted the main cause of re-sweating following sympathetic surgery. Re-sympathetic surgery was necessary in order to treat re-sweating, and was associated with favorable outcomes.

Adolescent↗

PubMed1983

Volume and composition of hand sweat of White and Black men and women in desert walks.

Many investigators have sought, but failed to find, ethnic differences in the number and regional distribution of active sweat glands. In this study measurements have been made of sweat secreted on one hand and also on the whole body of Whites and Blacks walking in desert heat. Whites numbered 31 men and 27 women, ages 30 to 88 years; there were 21 Black men and 31 Black women, ages 16 to 61 years. Each walked on three occasions for 1 hour at a rate that required an oxygen consumption of about 40% of aerobic capacity. Ambient temperature ranged from 32 to 44 degrees C in 1979 and 1980; means were 38.4 degrees C in 1979 and 36.7 degrees C in 1980. There was no sweat in the gloves of many Blacks; this was true of only a few Whites. Volume of body sweat increased in both races with rate of walking; volume of hand sweat increased more in Whites than in Blacks. The Mann-Whitney test revealed that volumes of hand sweat were significantly greater for Whites than for Blacks. It was concluded that in desert walks most Whites and few Blacks sweat freely on their hands. In samples of hand sweat, Na+, K+, and Cl- were determined. Concentrations of each ion varied widely in both races, and were unrelated to race. Concentrations of Na+ and Cl- generally are somewhat higher in hand sweat than in body sweat; concentrations of K+ are much higher. It follows that the values for concentration of Na+ and Cl- reported in Table 3 probably are somewhat higher than would have been found in body sweat, and concentrations of K+ are probably much higher.

Adult↗

PubMed1980

Effect of hidromeiosis on sweat drippage during acclimation to humid heat.

Sweat rate and the rate of change in sweat drippage were studied during the acclimation of eight healthy male subject during exposure to heat during 10 consecutive days. During acclimation to hot humid conditions, the increase in total body sweat rate results in an increase in the rate of sweat drippage. We found, however, that on each day the drippage rate markedly decreased with time after the 1st h of heat exposure. This hidromeiosis was investigated as a function of the heat exposure time. No shortening of the onset time of hidromeiosis occurred with acclimation. With repeated heat exposures, the initial sweat rates in response to stress increased, and the subsequent decline became larger with higher sweat rates at the time of onset of hidromeiosis. Hidromeiosis appears to be a function of the degree of skin wettedness reached in the various local skin areas which determine the overall body skin wettedness upon which evaporative adjustments depend. Thus, the observed overshoot in total sweat rate as indicated by sweat drippage, and the subsequent hidromeiosis, result from initial oversweating in the poorly ventilated areas of skin. This sweat decline seems to be due to a reduction in output of the active sweat glands rather than to a reduction in active sweat gland number.

Acclimatization↗

PubMed1997

Effects of non-pharmacological sympathetic sudomotor denervation on sweating in humans with essential palmar hyperhidrosis.

OBJECTIVE: Quantitative sweat production and -ionic composition in Essential Hyperhidrosis (EH), and the effects of T2-T3 thoracoscopic sympathicolysis (TS) hereon, are unknown. Standardised pilocarpine iontophoresis sweat tests were performed before and after TS in order to study these issues. DESIGN AND METHODS: Pilocarpine iontophoretic sweat tests measuring maximal sweat production (mg) and sweat Na+, K+ and Cl- concentrations (mMol/L) were performed on both forearms of 10 EH patients, before and six weeks after TS, and in normal volunteers. RESULTS: As compared to normals, preoperative maximal sweat production was 30% higher (199.4 +/- 68.8 (SD) vs. 150.6 +/- 45.6 mg) in EH patients; due to type II error, however, statistical significance was not reached. Na+ and Cl- concentrations were similar, and K+ concentration was slightly lower in EH patients. After TS, sweat production had decreased to equal levels as in normals (149.1 +/- 52.1 mg), whereas the Na+ (from 33.6 +/- 6.9 to 51.0 +/- 6.4 mMol/L), Cl- (from 21.5 +/- 6.6 to 37.2 +/- 7.1 mMol/L) and K+ (from 7.5 +/- 1.3 to 8.6 +/- 2.2 mMol/L) concentrations had increased. CONCLUSIONS: EH patients present 30% higher maximal sweat production at their forearms. This increase may be due to an increased activity of the adrenergic component of sweat gland innervation. The post-TS increase in Na+, Cl- and K+ concentrations suggests that the adrenergic component of sweat gland innervation in itself decreases sweat ion concentrations.

Adult↗

PubMed1969

The response of the sweat glands of the newborn baby to thermal stimuli and to intradermal acetylcholine.

1. Measurements of evaporative sweat loss were made on fifty-six premature and full-term babies 1-67 days after birth with an infra-red analyser and a ventilated capsule placed on the thigh. Measurements were also made of total evaporative water loss while in a closed metabolic chamber and of the regional distribution of sweating with starch-iodine paper.2. No sweating to thermal stimuli could be detected in infants of less than 210 days post-conceptual age, even when rectal temperature rose as high as 37.8 degrees C. In older infants sweat was detected first on the forehead and temple, later on the chest, and usually by 240-260 days post-conceptual age on the legs (term approximately 268 days). Generalized sweating on the limbs appeared at an earlier post-conceptual age in the more prematurely born infants.3. The response of sweat glands on the thigh to an intradermal injection of 2 mug acetylcholine (ACh) was tested. No sweat response was detected in infants under 225 days post-conceptual age, while all infants born within 2 weeks of term responded. The response was often augmented after 2-5 tests at 5-10 min intervals; all the eight infants born within 2 weeks of term who were examined twice in the first 2 weeks of life showed a greater response on the second occasion.4. An average of 414 active sweat glands/cm(2) were detected on the thigh in eight babies 7-10 days old born within 2 weeks of term. This was 6(1/2) times the number found in adults. The mean peak sweat rate to chemical stimulation was however only 2.4 nl./gland.min, which was 3 times lower than the maximum rate recorded in adults.5. In five infants with congenital defects of the brain and complete absence of temperature control there was no sweat response to thermal or direct chemical stimulation of the glands.6. Functional maturation appears to depend on intact central innervation and is marginally hastened by post-natal factors. Immaturity of the sweat glands can account for the lack of any response to thermal stimuli in premature babies, but not for the modest thermal response obtained in babies at term.

Acetylcholine↗

PubMed1981

Role of calcium in cholinergic and adrenergic mechanisms of eccrine sweat secretion.

The role of Ca2+ in eccrine sweat secretion was studied using isolated cannulated monkey palm eccrine sweat glands in vitro. Removal of Ca2+ from the incubation medium promptly abolished sweat secretion induced by methacholine or phenylephrine. In contrast, isoproterenol-induced sweat secretion lasted from 40 to 220 min in a Ca2+-free medium. The methacholine-induced maximal sweat rate was a hyperbolic function of the Ca2+ concentration in the bath and reached a plateau at 1 mM Ca2+. Higher Ca2+ concentrations rather suppressed the secretory rate. The Ca2+ ionophore A23187, but not X537A, at 3 X 10(-6) M induced copious prolonged sweat secretion after a latent period of 10 min. A23187-induced sweat secretion was not inhibited by either atropine or propranolol. D 600 (methoxyverapamil) at 10(-3) M inhibited sweat secretion induced by methacholine or by isoproterenol, although the latter lasted longer than methacholine sweating (20 vs. 5 min) in the presence of D 600. The data support the notion that Ca2+ influx into the cell plays a crucial role in cholinergic and alpha-adrenergic sweating, whereas a partial supply of Ca2+ for isoproterenol-induced sweating is derived from an intracellular store.

Animals↗

PubMed1993

Generation and transit pathway of H+ is critical for inhibition of palmar sweating by iontophoresis in water.

Passing galvanic current across the skin (known as "tap water iontophoresis" or TWI) inhibits sweating; however, its mechanism of action is unclear. Using improved methods, we confirmed that anodal current has more of an inhibitory effect than cathodal current, water is superior to saline, and the inhibitory effect is a function of the amperage used. To address the importance of current flowing through the pores, a layer of silicone grease was placed on the skin to reduce the shunt pathway across the epidermis. With silicone, total skin conductance decreased 60% without the sweat pores being occluded, swelling of the stratum corneum and collapse of the poral lumen was prevented, and current-induced inhibition of sweating was enhanced, most likely because of an increase in current density in the pores. The pH of anodal water, but not of saline, dropped to 3, whereas that of cathodal water increased to 10 during passage of current through the skin. Acidified anodal water was superior to alkaline water. Sweat glands isolated from TWI-induced anhidrotic palmar skin responded to methacholine in vitro, but the sweat rate and pharmacological sensitivity were slightly lowered. Thus the strong acidity generated by hydrolysis of water in the anodal bath and the further accumulation of H+ in the sweat duct by anodal current may be responsible for TWI-induced inhibition of sweating due to an unknown lesion(s) in the duct or sweat pore. The secretory coil function may also be altered because of exposure to intense acidity during TWI. The importance of H+ movement into the sweat pore for inhibition of sweating could be further exploited to develop new strategies for the control of sweating.

Adolescent↗

PubMed2000

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.

Animals↗