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PubMed1996

Responses of sweating and body temperature to sinusoidal exercise in physically trained men.

The effect of physical training on the dynamic responses of sweating to transient exercise is still controversial. We determined the phase response and amplitude response (delta) of sweating rate and body temperature to sinusoidal exercise in physically trained and untrained subjects. Eight trained and seven untrained male subjects exercised on a cycle ergometer with a constant load for 30 min; for the next 28 min, they exercised with a sinusoidal load. The sinusoidal load variation ranged from approximately 10 to 60% of peak O2 uptake with a 4-min period. The ambient temperature and the relative humidity during exercise were 25 degrees C and 35%, respectively. There was no difference between the groups in the phase lags of esophageal temperature (Tes) and mean skin temperature (Tsk), whereas the phase lags of sweating rates for the chest and forearm were significantly shorter in the trained group (P < 0.05). The delta of Tes and Tsk per 1 W of exercise load in the trained group was significantly smaller than that in the untrained group (both, P < 0.05), whereas there was no difference between the groups in the delta of sweating rate for the chest and forearm. We conclude that subjects who have undergone long-term physical training show prompter dynamic characteristics of sweating response compared with untrained subjects and have a higher capacity to maintain constant body temperature during exercise at transient load.

Adult↗

PubMed2003

Active recovery attenuates the fall in sweat rate but not cutaneous vascular conductance after supine exercise.

The purpose of this study was to identify whether baroreceptor unloading was responsible for less efficient heat loss responses (i.e., skin blood flow and sweat rate) previously reported during inactive compared with active recovery after upright cycle exercise (Carter R III, Wilson TE, Watenpaugh DE, Smith ML, and Crandall CG. J Appl Physiol 93: 1918-1929, 2002). Eight healthy adults performed two 15-min bouts of supine cycle exercise followed by inactive or active (no-load pedaling) supine recovery. Core temperature (T(core)), mean skin temperature (T(sk)), heart rate, mean arterial blood pressure (MAP), thoracic impedance, central venous pressure (n = 4), cutaneous vascular conductance (CVC; laser-Doppler flux/MAP expressed as percentage of maximal vasodilation), and sweat rate were measured throughout exercise and during 5 min of recovery. Exercise bouts were similar in power output, heart rate, T(core), and T(sk). Baroreceptor loading and thermal status were similar during trials because MAP (90 +/- 4, 88 +/- 4 mmHg), thoracic impedance (29 +/- 1, 28 +/- 2 Omega), central venous pressure (5 +/- 1, 4 +/- 1 mmHg), T(core) (37.5 +/- 0.1, 37.5 +/- 0.1 degrees C), and T(sk) (34.1 +/- 0.3, 34.2 +/- 0.2 degrees C) were not significantly different at 3 min of recovery between active and inactive recoveries, respectively; all P > 0.05. At 3 min of recovery, chest CVC was not significantly different between active (25 +/- 6% of maximum) and inactive (28 +/- 6% of maximum; P > 0.05) recovery. In contrast, at this time point, chest sweat rate was higher during active (0.45 +/- 0.16 mg.cm(-2).min(-1)) compared with inactive (0.34 +/- 0.19 mg.cm(-2).min(-1); P < 0.05) recovery. After exercise CVC and sweat rate are differentially controlled, with CVC being primarily influenced by baroreceptor loading status while sweat rate is influenced by other factors.

Adult↗

PubMed2003

Effect of exercise intensity on the postexercise sweating threshold.

The hypothesis that the magnitude of the postexercise onset threshold for sweating is increased by the intensity of exercise was tested in eight subjects. Esophageal temperature was monitored as an index of core temperature while sweat rate was measured by using a ventilated capsule placed on the upper back. Subjects remained seated resting for 15 min (no exercise) or performed 15 min of treadmill running at either 55, 70, or 85% of peak oxygen consumption (V(o2 peak)) followed by a 20-min seated recovery. Subjects then donned a liquid-conditioned suit used to regulate mean skin temperature. The suit was first perfused with 20 degrees C water to control and stabilize skin and core temperature before whole body heating. Subsequently, the skin was heated ( approximately 4.0 degrees C/h) until sweating occurred. Exercise resulted in an increase in the onset threshold for sweating of 0.11 +/- 0.02, 0.23 +/- 0.01, and 0.33 +/- 0.02 degrees C above that measured for the no-exercise resting values (P < 0.05) for the 55, 70, and 85% of V(o2 peak) exercise conditions, respectively. We did note that there was a greater postexercise hypotension as a function of exercise intensity as measured at the end of the 20-min exercise recovery. Thus it is plausible that the increase in postexercise threshold may be related to postexercise hypotension. It is concluded that the sweating response during upright recovery is significantly modified by exercise intensity and may likely be influenced by the nonthermal baroreceptor reflex adjustments postexercise.

Anaerobic Threshold↗

PubMed1990

A neuropathic deficit, decreased sweating, is prevented and ameliorated by euglycemia in streptozocin diabetes in rats.

Decreased sweating, especially of feet and legs, occurs in human diabetic neuropathy. It might be studied in experimental diabetes to characterize it, elucidate its mechanisms, and determine whether it can be prevented or treated. The pilocarpine-induced sweat responses (SR) in the hind foot pads of groups of control and streptozocin diabetic rats, in good (GC) and in poor (PC) glycemic control and with a crossover design after 20 wk of diabetes, were evaluated with the silicone mold sweat test to determine the number of sweat droplets per group of foot pads. The SR was dose dependent and reproducible. The SR disappeared with denervation and reappeared with reinnervation; denervation hypersensitivity did not develop. In the GC group, euglycemia was achieved by regulating the caloric intake and using multiple daily injections of Ultralente insulin. The SR was not different from that of the control group for up to 136 d. In the PC group, the SR became abnormal (P less than 0.005) at 16 d and progressively worsened: 40% of baseline values at 14 wk (P less than 0.001). After restoring euglycemia in the PC group, a normal SR occurred at 12 d. These results show that one human neuropathic deficit, failure of sweating, can be prevented or ameliorated by good glycemic control.

Animals↗

PubMed1990

Sweat sodium and chloride concentrations--essential criteria for the diagnosis of cystic fibrosis in adults.

Criteria for a positive sweat test in children (sweat sodium greater than 60 mmol/L and sweat chloride greater than 70 mmol/L) were investigated in a series of adults aged between 18 and 40 years using the standard Gibson and Cooke technique of pilocarpine iontophoresis. A significant number of non-cystic fibrosis adults had sweat sodium values greater than 60 mmol/L whereas a concentration of chloride greater than 70 mmol/L always discriminated adults with cystic fibrosis from normal adults and those with chest disease not due to cystic fibrosis. In all cases of adult cystic fibrosis the sweat sodium concentration was greater than 80 mmol/L. The Na:Cl ratio and sum of Na and Cl provided additional helpful criteria in distinguishing between adults with and without cystic fibrosis.

Adolescent↗

PubMed1993

Demonstration of anionic sites in human eccrine and apocrine sweat glands in post-embedded ultra-thin sections with cationic colloidal gold: effect of enzyme digestion on these anionic sites.

We localized anionic sites ultrastructurally in human eccrine and apocrine sweat glands with a poly-L-lysine-gold complex (cationic colloidal gold). Anionic sites were labeled by incubating Lowicryl K4M-embedded sections on droplets of cationic colloidal gold. In eccrine sweat glands, colloidal gold particles were restricted to the basolateral membrane of the secretory cells at low pH, whereas the luminal membrane did not react with the gold particles. Chondroitinase ABC digested these anionic sites. This indicates that chondroitin sulfate and/or dermatan sulfate constitutes anionic sites in the basal labyrinth of eccrine sweat glands. In apocrine sweat glands, the luminal membrane of the secretory cells showed strong reaction at low pH, whereas the contraluminal membrane did not show any reaction. Neuraminidase completely digested these anionic sites, which indicated that the anionic charge of the apocrine lumen was due to sialic acid. Differences in distribution and susceptibility to enzymes of anionic sites in cell membranes between eccrine and apocrine sweat glands may reflect functional differences between these glands. Dark cell granules in eccrine secretory cells were negative for the anionic sites when sections were labeled without any pre-treatment. However, pre-incubation of the grids on EGTA or deionized water unmasked the anionic sites on the dark cell granules. The positive staining after EGTA treatment was greatly decreased by reincubation with CaCl2. These results suggested that Ca blocked anionic sites in dark cell granules. Exposed anionic sites were digested with chondroitinase ABC. This indicated that chondroitinase ABC and/or dermatan sulfate composed the anionic sites in dark cell granules.

Anions↗

PubMed2006

Gender differences in the sweat response during spinning exercise.

The purpose of this field study was to examine gender differences in the sweat response reported in the literature in trained men and women during indoor cycling. In the present study, 14 men and 12 women took part in a 90-minute spinning class in preparation for a 108-km road race. Delta body mass, corrected for the volume of water consumed, was used to estimate sweat loss during the exercise period. Men had a significantly higher sweat rate (1.12 L.h(-1)) compared to women (0.57 L.h(-1)), despite the fact that there were no significant gender differences in ad libitum fluid intake. Future research should focus on determining whether women may be more efficient in sweat production and evaporation and whether men may have a greater reserve capacity for increased sweating.

Adult↗

PubMed1975

Eccrine sweat gland sensitivity to catecholamines in patients with pheochromocytoma and primary aldosteronism.

The sensitivity of the eccrine sweat glands to adrenaline and noradrenaline was examined in 9 patients with pheochromocytoma and 12 patients with primary aldosteronism by Wada's method for determining threshold concentrations of local sweat response to intradermal injection. In pheochromocytoma most of the patients characteristically showed considerably reduced sensitivity to catecholamines in the sweat glands. Sensitivity was rapidly restored after the extirpation of the tumor in all cases. In primary aldosteronism the sweat gland sensitivity varied over a very wide range from subnormal to supernormal levels. These were restored to normal range after extirpation of the adrenocortical adenoma. In both diseases it was found that the sensitivity of the sweat glands to catecholamines and the vascular system to noradrenaline altered almost in parallel.

Adenoma↗

PubMed1998

Seasonal variation of sweating responses under identical heat stress.

The seasonal variation of sweating responses under identical heat stress was investigated to make clear the seasonal acclimatization in daily human life on the experiments. The heat stress of 33 degrees C air temperature, 50% relative humidity laid in the experiments was chosen as a usual daytime condition in summer in metropolitan cities such as Tokyo and Osaka. Five subjects were exposed under the identical heat stress in the climate chamber every two months through the year. Results were discussed on the mean values for five subjects. Although the relation of skin temperature to daily mean air temperature showed a variation of high in summer and low in winter before the heat stress, it rose and showed almost constant value during the heat stress. The seasonal variation of tympanic temperature appeared a little before the heat stress, but disappeared during the heat stress. The seasonal variation of sweating responses was evident, that was high in summer and low in winter. The concluding remarks are as follows: 1) It could be considered that there is a seasonal acclimatization on the threshold temperature for sweat onset. 2) The seasonal acclimatization on sweating is supposed to be caused by the seasonal acclimatization of the threshold temperature. 3) The seasonal acclimatization on sweating could be comprehended in four stages corresponding closely to the daily mean air temperature (Ta). The 1st stage is December-April when Ta < 15 degrees C, the 2nd stage is April-August when 15 degrees C < Ta < 25 degrees C, the 3rd stage is the term centering on August when Ta > 25 degrees C and the 4th stage is August-December when 15 degrees C < Ta < 25 degrees C.

Adult↗

PubMed2006

Possible biphasic sweating response during short-term heat acclimation protocol for tropical natives.

The aim of the present study was to evaluate the sweat loss response during short-term heat acclimation in tropical natives. Six healthy young male subjects, inhabitants of a tropical region, were heat acclimated by means of nine days of one-hour heat-exercise treatments (40+/-0 degrees C and 32+/-1% relative humidity; 50% (.)VO(2peak) on a cycle ergometer). On days 1 to 9 of heat acclimation whole-body sweat loss was calculated by body weight variation corrected for body surface area. On days 1 and 9 rectal temperature (T(re)) and heart rate (HR) were measured continuously, and rating of perceived exertion (RPE) every 4 minutes. Heat acclimation was confirmed by reduced HR (day 1 rest: 77+/-5 b.min(-1); day 9 rest: 68+/-3 b.min(-1); day 1 final exercise: 161+/-15 b.min(-1); day 9 final exercise: 145+/-11 b.min(-1), p<0.05), RPE (13 vs. 11, p<0.05) and T(re) (day 1 rest: 37.2+/-0.2 degrees C; day 9 rest: 37.0+/-0.2 degrees C; day 1 final exercise: 38.2+/-0.2 degrees C; day 9 final exercise: 37.9+/-0.1 degrees C, p<0.05). The main finding was that whole-body sweat loss increased in days 5 and 7 (9.49+/-1.84 and 9.56+/-1.86 g.m(-2).min(-1), respectively) compared to day 1 (8.31+/-1.31 g.m(-2).min(-1), p<0.05) and was not different in day 9 (8.48+/-1.02 g.m(-2).min(-1)) compared to day 1 (p>0.05) of the protocol. These findings are consistent with the heat acclimation induced adaptations and suggest a biphasic sweat response (an increase in the sweat rate in the middle of the protocol followed by return to initial values by the end of it) during short-term heat acclimation in tropical natives.

Acclimatization↗

PubMed1996

The influence of work loads on regional differences in sweating rates.

The influence of work loads (20, 40 and 60% VO2max) on regional differences in sweating rates was investigated in six healthy male students. The ratios of local sweating rate (msw) on the chest and back to estimated total sweating rate (mean msw of four sites examined x body surface area) at 20% work load were significantly greater than those on the forearm and forehead, whereas the ratio on the forehead at 60% work load was greater than at the other sites. The ratios on the forearm at 40 and 60% work loads were significantly greater than at 20% work load. The regional differences in sweating rates change with the increase in work load as seen by the greater variation in the ratios of msw on each site at 20% work load compared with 40 and 60% work loads. The results indicate that redistribution of this sweat activity to whole body or head with the rise in work load induces favorable conditions for evaporation and controlling brain temperature.

Adult↗

PubMed1989

IgE antibody to sweat in atopic dermatitis.

Of 45 patients with atopic dermatitis skin-tested with their own sweat, 43 showed positive immediate-type skin reactions to titres between 1 and 256. Of 22 non-atopic patients 18 showed negative reactions. Skin reactivity of the atopic patients to the sweat and house dust did not run parallel. Radioallergosorbent test (RAST) using the sweat collected from a healthy subject detected IgE antibody in 24 atopic patients with a score from 0.5 to 3.5, whereas all the control subjects showed the score 0. This IgE antibody to sweat did not cross-react with the mite extract (Dermatophagoides farinae) or Staphylococcus aureus. These results indicate that atopic patients have specific IgE antibody to sweat.

Adolescent↗

PubMedDate not supplied

A 5-month-old boy with recurrent respiratory infections, failure to thrive, and borderline elevated sweat chloride levels.

Both severe combined immunodeficiency (SCID) and cystic fibrosis (CF) may present in infancy with a history of respiratory infections and failure to thrive. Elevated sweat chloride levels on multiple sweat tests is diagnostic of CF; transient elevation of sweat chloride has been reported in patients with hypogammaglobulinemia and antibody deficiency without CF. This article presents a case report of a 5-month-old boy with recurrent respiratory infections, failure to thrive, and two borderline elevated sweat test levels. Laboratory evaluation including testing for CF as well as immune deficiency was performed in this patient. Two borderline abnormal sweat chloride tests together with isolation of Pseudomonas from the airway caused clinicians initially to suspect CF; however, mutation in gene coding for the gamma-chain of the IL-2 receptor and a negative CF genetic mutation analysis ultimately led to the final diagnosis of SCID. It is essential to make the diagnosis of SCID as early as possible because infants with SCID who do not undergo reconstitution of their immune system universally die in infancy because of infection. Early diagnosis and intervention can lead to an excellent prognosis in a previously fatal disease.

Chlorides↗

PubMed1992

[Assessment of autonomic nervous function in impotence using sweat response induced by intradermal injection of acetylcholine].

It is important to evaluate the autonomic nervous function which controls penile erection. One method utilizes intradermal injection of acetylcholine to produce localized sweat response. The sweat response depends on the peripheral autonomic nervous supply. Therefore, the response can be used to detect peripheral autonomic nervous dysfunction. We tried to evaluate the peripheral autonomic dysfunction in 29 impotence using a sweat spots test. We classified the 29 impotence into 6 groups with standard tests such as the papaverine test, nocturnal penile tumescence monitoring, recordings of bulbocavernous reflex, etc. The results were as follows: psychogenic IMP; 8, neurogenic IMP; 8, arterial insufficiency; 5, corporeal veno-occlusive insufficiency; 6 neurogenic with arterial insufficiency; 1, and neurogenic with corporeal veno-occlusive insufficiency; 1. The score of sweat spots test was 25.3 +/- 10.9, being in normal, nineteen severe in 3 and slightly abnormal in 7. Many cases of severe and slightly abnormal patients were DM patients classified into neurogenic IMP. We found 2 cases that were not detected by bulbocavernous reflex but found to be abnormal by sweat spots test. Therefore we conclude that this test effective to detect the autonomic nervous dysfunction in impotence.

Acetylcholine↗

PubMed1992

Cholinergic and adrenergic sweating in atopic dermatitis.

Sweating responses to methacholine and adrenaline were compared with an evaporimeter in normal-looking back and forearm skin from patients with atopic dermatitis (AD) and from non-atopic controls (NA). With both stimulants, the sweat rates were higher in forearm than in back skin in both groups, and between the two sites the rates showed positive correlations which were statistically significant in both groups. With methacholine the responses were slightly depressed in both areas in AD. With a low suprathreshold adrenaline concentration (5 x 10(-6) mol/l) the responses were equal in both groups but a tenfold higher adrenaline concentration elicited an increase of 55% in sweating rates in the back skin of NA and a 15% depression in the back skin of AD subjects (p less than 0.05). On arm skin there was a similar trend, but less marked. Between the cholinergic and adrenergic sweating responses a positive correlation was found on arm skin in AD, suggesting that the unknown mechanism of sweat depression in AD might be the same for both drugs.

Adrenergic Fibers↗

PubMed1975

[Secretion of pepsinogen, amylase and alkaline phosphatase by human sweat glands].

Human sweat contains pepsinogen, amylase, and alkaline phosphatase excretion of which depends on functional state of the digestive and sweat glands and on the topography of latter. Pepsinogen excreted with sweat has the gastric origin. Different food irritants activate amylase and alkaline phosphatase excretion with sweat. A high positive correlation exists between amylase and pepsinogen excretion by kidneys and sweat glands in healthy subjects.

Alkaline Phosphatase↗

PubMed2002

An indigenously developed method for sweat collection and estimation of chloride for diagnosis of cystic fibrosis.

An indigenously developed method for sweat collection and titration method for estimation of chloride was validated. The mean difference in estimated chloride value from the known strength of saline in 50 samples was -1.04 +/- 4.13 mEq/L (95% CI: -0.07 to 2.28). The mean difference in the estimated chloride values between two observers when the test was performed on known strengths of saline solution was -2.5 +/- 4.24 mEq/L (95% CI: -3.67 to 1.33). The inter observer variability between two observers when the test was performed on sweat samples obtained from 50 individuals was -1.12 +/- 4.34 mEq/L (95% CI: -2.23 to 0.8 ). Sweat weight of more than 100 mg could be collected in first attempt in 602 of 757 (80%) patient with an average sweat weight of 230 mg. This inexpensive method of sweat collection and chloride estimation has acceptable accuracy and repeatability and can be used in resource poor setting for making a diagnosis of cystic fibrosis.

Cystic Fibrosis↗

PubMed1976

Sweating responses of normal, paraplegic and anhidrotic subjects.

Dynamic sudomotor response to changing ambient temperatures (30 C to 45 C) was measured on eight unacclimatized subjects including five normals, two paraplegics and one anhidrotic patient. Mean sweating rates, computed from five simultaneously observed local rates, were used to compare the overall sudomotor response to heat exposure of the three groups. In the normal subjects, an average rise of 0.34 C in oral temperature and 2.5 C in mean skin temperature was found in a period of 65 minutes. The paraplegics developed a higher rise in both oral and skin temperatures due to a lower sweating rate in the insentinent region. (Insentient describes the sensory state of the skin below the level of the lesion where the subject has no awareness of surface stimulation). A relatively higher sweating rate was observed on the forehead and the cyclic sweating behavior of the insentient skin was not synchronous with that in the sentient. (Sentient describes the state where partial or total awareness is elicited by stimulation). The anhidrotic patient showed a twofold increase of moisture loss from the skin but no cyclic pattern of sweat gland activity on exposure to heat. In this case, hyperthermia developed with a rise in oral temperature of 1.1 C in 52 minutes versus 0.4 C rise in the controls in a period of 63 minutes.

Body Temperature↗