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PubMed2000

Sweat testing following newborn screening for cystic fibrosis.

Sweat testing remains the "gold standard" for the diagnosis of cystic fibrosis (CF) and is a critical component of newborn screening programs. We retrospectively reviewed sweat test results reported to a neonatal screening program for CF with respect to completeness of reported results and the values recorded for sweat chloride (Cl(-)) and sodium (Na(+)) concentrations and the Cl(-):Na(+) ratio in screened infants. Thirty-nine of 85 DeltaF508 homozygous (DeltaF508/DeltaF508) and 270 of 274 DeltaF508 heterozygous (DeltaF508/-) infants had sweat tests reported to the screening program. Of those, 30 and 213 sweat test reports, respectively, were complete, i.e., sweat weight, sweat chloride, and sodium were reported. Three centers accounted for 37 of 68 (54%) incomplete results, and 4 centers performed 4 or less post-screening sweat tests in the study period. There were 6 DeltaF508 heterozygous infants with sweat Cl(-) concentrations of 40-60 mmol/L and 4 had CF confirmed by additional genotyping (n = 2) or clinical and repeat sweat Cl results (n = 2). Forty-one percent of DeltaF508/-infants with sweat Cl(-) <40 mmol/L had Cl:Na >1. We conclude that the reporting of incomplete sweat tests is common following newborn screening for CF. Infants with sweat Cl(-) levels of 40-60 mmol/L require further investigation and review, but they almost certainly have CF. The Cl(-):Na(+) ratio does not appear useful in establishing a diagnosis of CF in infants.

Chlorides↗

PubMed1988

Sweat iron loss of male and female runners during exercise.

Male (n = 9) and female (n = 8) collegiate cross-country runners were studied during a training session to determine the amount of iron lost in the sweat. Sweat samples were collected from the arm using polyethylene bags. Total sweat loss was determined by weighing subjects before and after the runs. Average time of sweat collection was 42 min for males and 39 min for females. Sweat rate for the males (717.5 +/- 145.9 g/m2/h) was significantly greater than for the females (460.1 +/- 142.9 g/m2/h); however, the sweat rate per km was not significantly different. Females had a significantly greater sweat iron concentration (0.417 +/- 0.024 mg/l) than males (0.179 +/- 0.011 mg/l). Rate of sweat iron loss was not significantly different for females (0.276 +/- 0.140 mg/h) and males (0.21 +/- 0.13 mg/h). Sweat iron concentration was inversely related with sweat rate (r = -0.64). Our data suggest that although males lose more total sweat than females, the higher sweat iron concentration of females leads to similar rates of iron loss. For female runners, sweat iron loss coupled with a low dietary iron intake may result in a negative iron balance.

Adolescent↗

PubMed2006

Selective sweat gland removal with minimal skin excision in the treatment of axillary hyperhidrosis: a retrospective clinical and histological review of 15 patients.

BACKGROUND: Limited axillary skin excision and selective sweat gland removal from adjacent skin (Shelley's procedure) is currently rarely used for hyperhidrosis. OBJECTIVES: To determine whether this technique is a good way of permanently reducing axillary sweating. METHODS: This was a prospective, open, nonrandomized trial of the therapy, conducted in a university dermatology department. A small skin ellipse, parallel to the skin crease lines, was excised from the centre of the area of maximal sweating. The wound edges were undermined to the extent of maximal sweating and the skin reflected. Large visible sweat glands attached to the undersurface of the adjacent skin could be readily identified and were snipped off using scissors. We treated 15 axillae in eight patients with axillary hyperhidrosis. Sweat reduction was assessed by the patients who estimated the percentage reduction in sweating postoperatively. The scar appearance was graded by the surgeon. Haematoxylin and eosin-stained transverse sections of eight axillary skin ellipses from five subjects were examined histologically to establish the size, position and depth of the sweat gland tissue. RESULTS: All of the patients responded to treatment: mean sweat reduction was 65% (range 40-90%). Mean follow up was 1.3 years (range 0.1-6) and sweat reduction was maintained over this period. Histological material was available from five patients: sweat glands lay slightly deeper than hair follicles; glandular tissue occupied an average thickness of 3.5 mm in the 5-mm thick piece of skin. Apocrine gland lobules were more numerous and larger than eccrine gland lobules. Both gland types were in close apposition and did not occupy distinctly different depths within the skin. CONCLUSIONS: Local surgery using limited axillary skin excision and selective sweat gland removal remains one of the safest ways of permanently reducing axillary sweating.

Adolescent↗

PubMed1995

Pilocarpine iontophoresis test: an index of physiological sweat secretion?

The pilocarpine iontophoresis test (P-test) is used as a predictor of the capacity to produce sweat. Therefore, we studied the reproducibility of this test in 12 normal subjects on 10 consecutive days. Furthermore, we determined whether the P-test reflects whole-body and regional sweat secretion during exercise in the heat. Finally, we determined whether the P-test stimulates the eccrine sweat glands to maximal sweat secretion. Six growth hormone-deficient (GHD) patients who are known to have decreased sweating, and 11 healthy control subjects were studied. To induce maximal sweat secretion, the patients exercised on a bicycle ergometer at a workload corresponding to 40% of their maximal aerobic power (VO2max). The 11 healthy subjects exercised at a workload of 150 W. All subjects exercised for 60 min in ambient air at 35 degrees C, with 50% relative humidity. The P-test showed a mean day-to-day variation of 20.8% between individual subjects. There was a significant positive correlation between the P-test and regional sweat secretion (r2 = 0.74). The correlation coefficient (r2) was 0.50 for the correlation between the P-test and whole-body sweat secretion, and 0.52 for the correlation between regional sweat secretion and whole-body sweat secretion. We conclude that the pilocarpine iontophoresis test reflects heat- and exercise-induced sweating capacity. However, this test does not induce maximal sweating, and it cannot be used as a single reliable predictor of whole-body sweating, due to considerable day-to-day variation.

Adult↗

PubMed1999

Sweating and skin temperature responses of normal and anhidrotic horses to intravenous adrenaline.

Anhidrosis has been recognised for over half a century, but despite some excellent epidemiological studies, there has been little progress in understanding the aetiology of the condition. Using a modified ventilated capsule, we obtained dynamic, quantitative data on sweating responses in anhidrotic horses and normal sweating controls from the same environment. Ten horses with current seasonal anhidrosis and 10 matched normal sweating controls were selected. Each horse was given two 10 min infusions of 1 and 2 micrograms/kg/min adrenaline, separated by at least 6 h. Sweating responses and skin temperatures on the neck and gluteal region were measured. Plasma and sweat for analysis of total protein and electrolytes and plasma for analysis of adrenaline were collected. Anhidrotic horses produced significantly less sweat, had lower initial and peak sweat rates and a greater neck:gluteal ratio for sweat production. Plasma adrenaline at rest or at the time of peak sweating rate was not different between groups. In nearly three-quarters of the anhidrotic horses, the shape of the sweat rate against time curve was different compared to controls. Volume of sweat produced was significantly correlated with skin temperature on the neck of controls and anhidrotic horses and on the gluteal region of controls, but not anhidrotic horses. Plasma total protein and electrolyte concentrations were not different between groups. There were significant differences in sweat electrolyte concentrations between controls and anhidrotic horses. These differences were reduced when sweat electrolytes were expressed per g of total protein, and no differences existed when expressed as g/m2. This study has provided insight into the response of anhidrotic horses to beta 2 adrenergic stimulation and may be a useful technique to investigate this condition.

Animals↗

PubMed2001

Relationship of osmotic inhibition in thermoregulatory responses and sweat sodium concentration in humans.

Heat acclimatization improves thermoregulatory responses to heat stress and decreases sweat sodium concentration ([Na(+)](sweat)). The reduced [Na(+)](sweat) results in a larger increase in plasma osmolality (P(osmol)) at a given amount of sweat output. The increase in P(osmol) inhibits thermoregulatory responses to increased body core temperature. Therefore, we hypothesized that the inhibitory effect of plasma hyperosmolality on the thermoregulatory responses to heat stress should be attenuated with the reduction of [Na(+)](sweat) due to heat acclimatization. Eleven subjects (9 male and 2 female) were passively heated by immersing their lower legs into water at 42 degrees C (room temperature 28 degrees C and relative humidity 30%) for 50 min following isotonic or hypertonic saline infusion. We determined the increase in the esophageal temperature (T(es)) required to elicit sweating and cutaneous vasodilation (CVD) (DeltaT(es) thresholds for sweating and CVD, respectively) in each condition and calculated the elevation of the T(es) thresholds per unit increase in P(osmol) as the osmotic inhibition of sweating and CVD. The osmotic shift in the DeltaT(es) thresholds for both sweating and CVD correlated linearly with [Na(+)](sweat) (r = 0.858 and r = 0.628, respectively). Thus subjects with a lower [Na(+)](sweat) showed a smaller osmotic elevation of the DeltaT(es) thresholds for sweating and CVD. These results suggest the possibility that heat acclimatization attenuates osmotic inhibition of thermoregulatory responses as well as reducing [Na(+)](sweat).

Adult↗

PubMed2005

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.

Adult↗

PubMed2007

Effect of age and gender on sweat lactate and ammonia concentrations during exercise in the heat.

The dependence of sweat composition and acidity on sweating rate (SR) suggests that the lower SR in children compared to adults may be accompanied by a higher level of sweat lactate (Lac-) and ammonia (NH3) and a lower sweat pH. Four groups (15 girls, 18 boys, 8 women, 8 men) cycled in the heat (42 degrees C, 20% relative humidity) at 50% VO2max for two 20-min bouts with a 10-min rest before bout 1 and between bouts. Sweat was collected into plastic bags attached to the subject's lower back. During bout 1, sweat from girls and boys had higher Lac- concentrations (23.6 +/- 1.2 and 21.2 +/- 1.7 mM; P < 0.05) than sweat from women and men (18.2 +/- 1.9 and 14.8 +/- 1.6 mM, respectively), but Lac- was weakly associated with SR (P > 0.05; r = -0.27). Sweat Lac- concentration dropped during exercise bout 2, reaching similar levels among all groups (overall mean = 13.7 +/- 0.4 mM). Children had a higher sweat NH3 than adults during bout 1 (girls = 4.2 +/- 0.4, boys = 4.6 +/- 0.6, women = 2.7 +/- 0.2, and men = 3.0 +/- 0.2 mM; P < 0.05). This difference persisted through bout 2 only in females. On average, children's sweat pH was lower than that of adults (mean +/- SEM, girls = 5.4 +/- 0.2, boys = 5.0 +/- 0.1, women = 6.2 +/- 0.5, and men = 6.2 +/- 0.4 for bout 1, and girls = 5.4 +/- 0.2, boys = 6.5 +/- 0.5, women = 5.2 +/- 0.2, and men = 6.9 +/- 0.4 for bout 2). This may have favored NH3 transport from plasma to sweat as accounted for by a significant correlation between sweat NH3 and H+ (r = 0.56). Blood pH increased from rest (mean +/- SEM; 7.3 +/- 0.02) to the end of exercise (7.4 +/- 0.01) without differences among groups. These results, however, are representative of sweat induced by moderate exercise in the absence of acidosis.

Adult↗

PubMed1978

Secretion of a potassium-rich fluid by the secretory coil of the rat paw eccrine sweat gland.

1. It is already known that the rat paw eccrine sweat contains high K(+) (greater than 150 mM) and low Na(+) concentrations (less than 70 mM). The present study was intended to clarify the site of K(+) secretion within the sweat gland, namely, the duct or the secretory coil. In vivo paw sweat was first induced by systemic pilocarpine injection or nerve stimulation. Both K(+) and Na(+) concentrations were studied in relation to the sweat rate to determine indirectly whether there is ductal secretion or reabsorption.2. Both Na(+) and K(+) concentrations in paw sweat agreed with the previous studies but did not show any saturation-type flow dependence at the high sweat rate range.3. A method has been developed to isolate a single segment of the secretory coil and induce sweat secretion directly from it in an in vitro condition.4. In the presence of fresh serum (30%, preincubated for 30 min at 56 degrees C) in the incubation medium, stable secretory activity due to 10(-6)M-Mecholyl could be maintained for 40 min or longer. The primary sweat thus induced contained low Na(+) (30 mM) and high K(+) (160 mM) concentrations.5. In the secretory coil sweat in vitro, K(+) concentration decreased and Na(+) concentration increased as the secretory rate fell either spontaneously or after addition of atropine or cyanide.6. It remains to be studied whether auxiliary ductal secretion or reabsorption is present at low rates of sweating in the rat sweat gland.7. It was concluded that the secretory coil of the rat paw sweat gland is the major, if not the sole, site of K(+) secretion.

Animals↗

PubMed1982

Effects of sweat gland training by repeated local heating.

Effects of sweat gland training by daily local heating were examined and its significance in heat acclimatization was evaluated. Training by 2-hr immersion of an arm in hot water of 43 degrees C caused distinct augmentation of sweat gland activity in the trained area, with reduction in the degree of hidromeiosis, when tested by an arm bag collection of sweat. Concentrations of sweat electrolytes also showed definite decreases. The general tendency that Na and Cl concentrations in sweat rise in the course of hidromeiosis was attenuated or even reversed after the training. The sweat test using resistance hygrometry failed to show a marked or consistent increase in sweat rate of the trained area, although an increase was the common case on the dorsum of the hand and the extensor aspect of the forearm. The effect of training appeared in a few days of training, developed progressively with training days and showed a tendency to develop even after 3 weeks of training. The same training in midsummer failed to exert significant effects on sweat gland activity, suggesting that the sweat gland had been naturally trained to a considerable degree by then. On the other hand, training by repeated radiant heating of a local area caused only obscure changes in the activity of sweat glands. The present results reveal that sweat glands can be trained to be resistant to hidromeiosis in a hot-humid environment and that such peripheral changes appear to play a predominant role in augmentation of sweating capacity in the early stage of heat acclimatization.

Adult↗

PubMed1990

Identification of sudomotor activity in cutaneous sympathetic nerves using sweat expulsion as the effector response.

In a warm environment at ambient temperatures between 25 degrees and 38 degrees C (relative humidity 50%-60%) the relationship between sympathetic activity in cutaneous nerves (SSA) and pulses of sweat expulsion was investigated in five young male subjects. The SSA was recorded from the peroneal nerve using a micro-electrode. Sweat expulsion was identified on the sweat rate records obtained from skin areas on the dorsal side of the foot, for spontaneous sweating and drug-induced sweating, using capacitance hygrometry. Sweat expulsion was always preceded by bursts of SSA with latencies of 2.4-3.0 s. This temporal relationship between bursts of SSA and sweat expulsion was noted not only in various degrees of thermal sweating but also in the sweating evoked by arousal stimuli, or by painful electric stimulation. The amplitude of the sudomotor burst was linearly related to the maximal rate of increase of the corresponding sweat expulsion, the amplitude of the expulsion and the integrated amount of sweat produced for the duration of the expulsion. The results provide direct evidence that sweat expulsion reflects directly centrally-derived sudomotor activity.

Adult↗

PubMed2004

The reproducibility of closed-pouch sweat collection and thermoregulatory responses to exercise-heat stress.

Seven active male subjects cycled for 60 min at 29.5 (0.8)% peak work rate on three separate occasions in a hot environmental condition [36.0 (0.1) degrees C, 60 (1)% relative humidity] in order to determine the reproducibility of a closed-pouch sweat collection technique for sweat composition at the scapula, forearm and thigh. To confirm that sweat composition was not influenced by between-trial variations in sudomotor drive, local sweat rate, whole-body sweat rate, heart rate (HR), rectal temperature (T(re)) and mean skin temperature (T(sk)) responses were also measured, consequently reproducibility was also established for these variables. Sweat composition did not differ among trials, with the mean coefficients of variation (CVs) for sweat [Na(+)], [K(+)] and pH being 10.4 (7.4)%, 8.1 (6.5)% and 1.3 (1.1)%, respectively. Local sweat rates did not differ among the three trials (P>0.05) although whole-body sweat rate was reduced in the third trial (P<0.05). The mean CVs were 11.0 (7.8)% and 4.7 (1.6)% for local and whole-body sweat rates, respectively. Between-trial differences were not evident for T(re), T(sk) or HR with mean CVs of 0.3 (0.2)%, 0.7 (0.6)% and 3.9 (1.7)%, respectively, although HR tended to be greater in the first trial ( P=0.08). It is proposed that moderate variations in sweat composition were influenced by variations in the local sweat rate, which were induced by application of the pouch.

Adult↗

PubMed2006

Prolonged residence of temperate natives in the tropics produces a suppression of sweating.

Tropical natives possess heat tolerance due to the ability to off-load endogenous and exogenous heat efficiently using a minimum amount of sweat. On the other hand, exposure of temperate natives to heat results in exaggerated production of sweat, of which part is lost by dripping and, thus, not available for evaporation. How sweating is modified in natives of temperate climate zones by prolonged residence in the tropics is not well-understood. The aim of this study was to investigate possible changes in the peripheral sweating mechanisms. Sweating responses to iontophoretically applied acetylcholine (ACh) were compared between Japanese subjects having either permanently resided in Japan (Japan resident Japanese, JRJ) or having stayed in the tropics for 2 years or longer (Tropics resident Japanese, TRJ). Quantitative sudomotor axon reflex tests by iontophoresis of ACh (10%, 2 mA for 5 min) were applied to determine directly activated (DIR) and axon reflex-mediated sweating during [AXR(1)] and after [AXR(2)] ACh iontophoresis. The sweat onset time of AXR(1) was 0.6 min shorter in JRJ than in TRJ (P<0.0001), and AXR(1) (P<0.0004), AXR(2) (P<0.0001), and DIR (P<0.0001) sweating responses were larger in JRJ than in TRJ. AXR and DIR sweating volumes (P<0.0001) were negatively correlated, and sweat onset times (P<0.0001) were positively correlated with the duration of residence in the tropics (2 to 13 years). The observed attenuation of sweating in TRJ suggests that temperate natives may acquire heat tolerance with improved sweating economy similar to tropical natives after prolonged residence in the tropics.

Acclimatization↗

PubMed1998

Sweating. Fluid and ion losses and replacement.

In the horse, sweat is produced by apocrine glands which are present over most haired and nonhaired skin. Although sweat secretion is initiated under a number of circumstances, the central drive for sweating in response to a thermal stimulus is the primary mechanism for its production. Sweating is an essential and primary mechanism for heat dissipation during exercise or exposure to hot ambient conditions. The rate of sweat production will reflect the interaction of numerous factors, including exercise intensity, ambient conditions, state of hydration, and the training or heat acclimation status of the individual horse. Thus, the sweating rates produced in response to an exercise-induced thermal load can be further increased by high ambient temperature or humidity which reduces evaporative efficiency, thereby contributing to the rate of rise in core body temperature. Equine sweat is an isotonic to slightly hypertonic secretion with sodium, chloride, and potassium contributing the major ionic components. The ionic composition of equine sweat is largely rate dependent and therefore is affected by factors such as ambient conditions and exercise intensity which result in elevations in sodium concentration in response to increases in sweating rate. Large sweat fluid losses associated with prolonged exercise will incur significant ion deficits, leading to alterations in skeletal muscle ion content and the potential for muscular dysfunction. With respect to exercise performance, however, the more important consequence of sweat fluid losses is the impairment of temperature regulation that accompanies severe dehydration. Although it is advantageous to restore a proportion of the fluid and ion losses incurred during prolonged exercise, few strategies will fully and safely replace the electrolyte losses incurred. Nevertheless, daily electrolyte supplementation of a good-quality diet will provide an effective method of replacing sweat ion losses during training and competition under most ambient conditions.

Animals↗

PubMed2002

Impaired sweating function in adult atopic dermatitis: results of the quantitative sudomotor axon reflex test.

BACKGROUND: Impaired sweating is thought to be a cause of barrier dysfunction in atopic dermatitis (AD). OBJECTIVES: To examine the sweating function in AD in a quantitative manner. METHODS: We investigated the sweating response of lesional and non-lesional skin of adult patients with AD by a quantitative sudomotor axon reflex test in which the axon reflex is stimulated by acetylcholine iontophoresis. Sweat volume on the volar aspect of the forearm was measured in 18 adult patients with AD and in 40 non-atopic controls; five patients with Sjögren's syndrome were also studied as disease comparators. We also evaluated the sweating function in four AD patients after topical corticosteroid therapy. Latency time, direct (DIR) sweat volume and axon reflex-mediated indirect (AXR) sweat volume were the variables studied. RESULTS: The latency time in AD patients was significantly prolonged and AXR sweat volume significantly reduced compared with those in non-atopic control subjects. The latency time and AXR sweat volume of lesional AD skin were significantly more prolonged and reduced, respectively, than those of non-lesional skin. In contrast, the DIR sweat volume of lesional or non-lesional AD skin induced by direct stimulation with acetylcholine was only slightly reduced when compared with that in non-atopic controls. Latency time and sweat volumes of lesional and non-lesional AD skin improved after topical corticosteroid therapy. CONCLUSIONS: These results suggest that the impaired sweat response in AD is attributable to an abnormal sudomotor axon reflex, which is reversed by topical corticosteroid administration.

Acetylcholine↗

PubMed2002

Effect of acute normobaric hypoxia on peripheral sweat rate.

Peripheral sweat rate was measured to determine if acute normobaric hypoxia exerted a local inhibition on sweat gland function. It was hypothesized that peripheral sweat rate would be reduced during hypoxia, following cholinergic stimulation. Nineteen subjects (24 +/- 3 yr; 177 +/- 9 cm; 75.5 +/- 20.1 kg), 8 females and 11 males, were tested once during normobaric hypoxia, simulating an altitude of approximately 3050 m (P(O2) = 13.9%; P(B) approximately 730 mmHg), and once at sea level (200 m; P(O2) = 20.9%; P(B) approximately 730 mmHg). While seated at rest, a approximately 7-cm(2) area of the anterior forearm was stimulated using pilocarpine iontophoresis to produce localized sweating at the site. Following stimulation, sweat was collected from the area for 15 min using a Macroduct Sweat Collection System. One-way repeated measures ANOVA indicated a significantly lower sweat rate during normobaric hypoxia (4.6 +/- 2.6 g x m(-2) x min(-1)) compared to sea level (5.5 +/- 3.0 g x m(-2) x min(-1); p = 0.006). Because sweating was initiated directly at the sweat gland, thus bypassing central nervous system input, changes in sweat rate were likely due to peripheral alterations. Although these peripheral mechanisms warrant further investigation, the results of this study suggest a direct hypoxic influence on sweat gland function as evidenced by a decrease in sweat rate.

Adult↗

PubMed1996

Sweat fluid and ion losses in horses during training and competition in cool vs. hot ambient conditions: implications for ion supplementation.

The objectives of this study were to: 1) determine incremental and total sweat fluid and ion losses during and following (a) exercise training and (b) a treadmill Speed and Endurance exercise test (SEET) which simulated running speeds and distances required for each phase of an Olympic level (CCI****) 3-day-event in cool and hot ambient conditions and 2) determine the requirement for ion supplementation based on the calculated ion losses associated with these activities. Six exercise-trained Thoroughbred horses completed 2 weeks of exercise training in each of 2 ambient conditions: cool, dry (CD, room temperature [T] = 20-22 degrees C, relative humidity [RH] = 45-55%), or hot and humid (HH, T = 33-35 degrees C, RH = 80-85%). Following the 2 week period of training in either CD or HH conditions, horses completed a SEET under similar conditions (either CD, or hot and dry (HD, T = 33-35 degrees C, RH = 45-55%). Sweating rate and sweat ion composition for each 5 min interval was determined from sweat samples collected from a sealed pouch attached to the lateral thorax. Total sweat fluid losses during training in the heat were 2- or 3-fold greater when compared to CD. Similarly, sweat fluid losses associated with the SEET in HD were almost double (19.2 litres) the losses in CD (11.7 litres). Total calculated ion losses associated with 2 h of training in HH (3724 mmol; 115.2 g) were significantly greater when compared to CD (1413 mmol; 43.5 g). Following the SEET and a 30 min recovery period, total ion losses in CD were 3636 mmol (112.2 g) compared with 6519 mmol (200.6 g) in HD. The differences in ion losses represent the increased sweating rates stimulated by higher core temperatures during moderate to high intensity exercise in warmer ambient conditions and increases in sweat ion concentrations associated with higher sweating rates. Extracellular fluid (ECF) ion losses during daily exercise training and the SEET were also calculated from changes in plasma ion concentrations and ECF volume. Calculated ECF ion losses were significantly higher in hot ambient conditions but were approximately 50% less than calculated sweat ion losses. The calculated sweat ion losses incurred during daily exercise training in hot and humid ambient conditions are > 3-fold higher than losses measured following exercise training in cooler conditions. Whereas fluid regulating hormones may have reduced urinary and faecal losses of ions during 2 weeks of training in HH, the quantity of sodium, potassium and chloride calculated to have been lost in sweat during the SEET in HD exceeded the daily dietary intake of these ions and suggests the need for appropriate ion supplementation during training and competition in hot ambient conditions.

Animals↗

PubMed1971

Studies on the nature of sweat gland 'fatigue' in the goat.

1. The nature of the ;fatigue' of sweating that occurs in the goat upon exposure to environmental conditions of 40 degrees C/26 degrees C (dry bulb/wet bulb) has been examined.2. Heat exposure activated all the sweat glands and the decrement in sweating which occurred was due to a decline in the amount of sweat produced by each gland.3. The decline in sweating activity was associated with a decrease in sweat gland volume and a thickening of the glandular wall. The restoration of sweat gland function took approximately 5-6 hr after removing the animal from the hot environment but the restoration of sweat gland volume took longer.4. The volume of sweat produced was greater than the decrease in sweat gland volume and it is concluded that ;fatigue' is due to the rate of expulsion exceeding the rate of sweat production.5. Repeated intravenous injections of adrenaline at 40 degrees C resulted in a decline in sweat output and reduced the normal glandular response to heat exposure.

Animals↗