False negative sweat tests with apparently adequate sweat collections.
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Child↗
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Results for “Sweating”
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Improved correlation of sweat chloride quantification by the CF Indicator System and the Gibson-Cooke Sweat Test.
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Chlorides↗
Na+, K+, H+, Cl-, and Ca2+ concentrations in cystic fibrosis eccrine sweat in vivo and in vitro.
Sweat Na+, K+, H+, Cl-, Ca2+, and protein concentrations were reexamined with the use of three methods; namely, in vitro sweat induction from isolated single sweat glands, intradermal methacholine-induced sweating, and thermally induced sweating. [Na+] and [K+] in the primary sweat induced in vitro were nearly isotonic to the bath in both cystic fibrosis (CF) and control. In CF the [Na+] in both proximal ductal and skin surface sweat was always higher than 100 mmol/L. However, [Na+] never reached the isotonic level of 151 mmol/L, even at the highest sweat rate. Thus Na+ absorption never saturates, suggesting that the net NaCl absorption may increase with increasing sweat rate. pH of the primary sweat was 7.13 for CF and 7.29 for control, which corresponds to a [HCO3-] of 7.3 and 10.5 mmol/L, respectively. [Cl-] in the primary sweat was hypertonic (134 mmol/L for CF and 129 mmol/L for control) to the bath (118.4 mmol/L). In CF, ductal acidification of sweat occurred normally during intradermal methacholine-induced sweating, whereas ductal acidification of sweat was much higher in control than in CF in thermally induced sweating. [K+] in CF was higher in the skin surface sweat but not in the proximal duct sweat, suggesting that the predominant site of K+ secretion in CF may be in the distal duct. [K+] in the intradermal methacholine-induced sweat was much higher than that of thermally induced sweat in both CF and control samples. Free but not total [Ca2+] was also increased in CF skin surface sweat. The sweat protein concentration was the same in both CF and control samples. The mechanisms of the different electrolyte concentrations in CF sweat remain to be studied. However, the present observations will provide the basis for future studies on normal and abnormal regulation of membrane transport in CF sweat glands.
Adolescent↗
Recurrent gustatory sweating (Frey syndrome) after intracutaneous injection of botulinum toxin type A: incidence, management, and outcome.
OBJECTIVE: To evaluate the duration of effectiveness of intracutaneous injection of botulinum toxin type A for gustatory sweating as well as the incidence, severity, management, and outcome of recurrent gustatory sweating. DESIGN: An inception cohort with a minimum of 18 months of follow-up. SETTING: A tertiary care center and university teaching hospital. PATIENTS: Thirty-three patients with severe gustatory sweating. INTERVENTION: Intracutaneous injection of 25 to 175 IU (mean, 86 IU) of botulinum toxin type A. MAIN OUTCOME MEASURES: Analysis of the effectiveness of the intracutaneous injection of botulinum toxin type A using the Kaplan-Meier actuarial life-table method; completion of the Minor starch-iodine test in patients without symptomatic recurrent gustatory sweating; and the patients' self-assessment of the severity of the recurrent gustatory sweating. RESULTS: The 1-, 2-, and 3-year actuarial estimate for symptomatic recurrent gustatory sweating was 27%, 63%, and 92%, respectively. In the 7 patients without symptomatic recurrent gustatory sweating, the Minor starch-iodine test revealed persistent gustatory sweating in 6, resulting in an overall 97% rate (32 of 33 patients) for recurrent gustatory sweating. No statistical relationship could be demonstrated between the duration of effectiveness, the incidence of recurrent gustatory sweating, the severity of recurrent gustatory sweating, and the following variables: age, sex, cause of gustatory sweating, skin surface involved, and dose of botulinum toxin type A injection. Within the group of 26 patients with symptomatic recurrent gustatory sweating, (1) the severity of the recurrent gustatory sweating was always reduced when compared with the severity of the initial gustatory sweating, and (2) the recurrent gustatory sweating always remained amenable to reinjection of botulinum toxin type A. CONCLUSIONS: The present series demonstrated a linear regression in the effectiveness of the intracutaneous injection of botulinum toxin type A in patients with gustatory sweating, while no factors appeared to be statistically related to the duration of effectiveness and/or the incidence of recurrent gustatory sweating. However, because the severity of recurrent gustatory sweating is reduced when compared with the severity of the initial gustatory sweating and because recurrent gustatory sweating remains amenable to reinjection of botulinum toxin type A, we believe that the intracutaneous injection of botulinum toxin type A should become the first-line treatment option in patients with gustatory sweating.
Adolescent↗
Monitoring opiate use in substance abuse treatment patients with sweat and urine drug testing.
Although urine testing remains the standard for drug use monitoring, sweat testing for drugs of abuse is increasing, especially in criminal justice programs. One reason for this increase is sweat testing may widen the detection window compared to urine testing. Drug metabolites are rapidly excreted in urine limiting the window of detection of a single use to a few days. In contrast, sweat collection devices can be worn for longer periods of time. This study was designed to compare the efficacy of sweat testing versus urine testing for detecting drug use. Paired sweat patches that were applied and removed weekly on Tuesdays were compared to 3-5 consecutive urine specimens collected Mondays, Wednesdays, and Fridays (355 matched sweat and urine specimen sets) from 44 patients in a methadone-maintenance outpatient treatment program. All patches (N = 925) were extracted in 2.5 mL of solvent and analyzed by ELISA immunoassay for opiates (cutoff concentration 10 ng/mL). A subset (N = 389) of patches was analyzed by gas chromatography-mass spectrometry (GC-MS). Urine specimens (N = 1886) were subjected to qualitative analysis by EMIT (cutoff 300 ng/mL). Results were evaluated to (1) determine the identity and relative amounts of opiates in sweat; (2) assess replicability in duplicate patches; (3) compare ELISA and GC-MS results for opiates in sweat; and (4) compare the detection of opiate use by sweat and urine testing. Opiates were detected in 38.5% of the sweat patches with the ELISA screen. GC-MS analysis confirmed 83.4% of the screen-positive sweat patches for heroin, 6-acetylmorphine, morphine, and/or codeine (cutoff concentration 5 ng/mL) and 90.2% of the screen-negative patches. The sensitivity, specificity, and efficiency of ELISA opiate results as compared to GC-MS results in sweat were 96.7%, 72.2%, and 89.5%, respectively. Heroin and/or 6-acetylmorphine were detected in 78.1% of the GC-MS-positive sweat patches. Median concentrations of heroin, 6-acetylmorphine, morphine, and codeine in the positive sweat samples were 10.5, 13.6, 15.9, and 13.0 ng/mL, respectively. Agreement in paired sweat patch test results was 90.6% by ELISA analysis. For the purposes of this comparison of ELISA sweat patch to EMIT urine screening for opiates, the more commonly used urine test was considered to be the reference method. The sensitivity, specificity, and efficiency of sweat patch results to urine results for opiates were 68.6%, 86.1%, and 78.6%, respectively. There were 13.5% false-negative and 7.9% false-positive sweat results as compared to urine tests. Analysis of sweat patches provides an alternate method for objectively monitoring drug use and provides an advantage over urine drug testing by extending drug detection times to one week or longer. In addition, identification of heroin and/or 6-acetylmorphine in sweat patches confirmed the use of heroin in 78.1% of the positive cases and differentiated illicit heroin use from possible ingestion of codeine or opiate-containing foods. However, the percentage of false-negative results, at least in this treatment population, indicates that weekly sweat testing may be less sensitive than thrice weekly urine testing in detecting opiate use.
Adolescent↗
Localization of aquaporin-5 in sweat glands and functional analysis using knockout mice.
Sweat secretion involves the transport of salt and water into the lumen of the secretory coil of the sweat gland. By analogy to salivary and submucosal glands, where fluid secretion is aquaporin-5 (AQP5) dependent, we postulated that aquaporin water channels might facilitate sweat secretion. Immunolocalization with specific antibodies revealed strong expression of AQP5 at the luminal membrane of secretory epithelial cells in sweat glands in mouse paw skin. Novel quantitative methods were developed to compare sweat secretion in wild-type mice and mice lacking AQP5. Total hindpaw sweat secretion was measured by proton nuclear magnetic resonance of sweat-derived (1)H(2)O in (2)H(2)O solvent, and sweat secretion from individual glands was measured by real-time video imaging of sweat droplet formation under oil. Sweat secretion rates after pilocarpine stimulation did not differ in wild-type mice (0.21 +/- 0.03 nl min(-1) gland(-1)) vs. mice lacking AQP5 (0.19 +/- 0.04 nl min(-1) gland(-1)). The lack of effect of AQP5 on sweat secretion rate was confirmed by microcapillary collections of sweat from defined regions of mouse paws. Also, as by direct counting of droplets, the number of functional sweat glands was not affected by AQP5 deletion. Sweat gland morphology was similar in wild-type and AQP5 null mice. From sweat coil geometry and gland secretion rate, the rate of fluid secretion was estimated to be 130 nl min(-1) cm(-2) of secretory epithelium, substantially lower than that of > 500 nl min(-1) cm(-2) in kidney proximal tubules and salivary glands, where active fluid absorption or secretion is aquaporin dependent. These results indicate the expression of AQP5 in sweat gland secretory epithelium, but provide direct evidence against its physiological involvement in sweat fluid secretion in mice.
Animals↗
Evaluation of pilocarpine effects on sweat proteome.
BACKGROUND: Sweat is increasingly recognized as a valuable, non-invasive biofluid for biomarker discovery, yet its composition depends on the stimulation method. This study aimed to determine how pharmacological induction with pilocarpine compares to physiologically induced sweat through exercise in shaping the sweat proteome. RESULTS: We analyzed thermoregulatory sweat from exercise, pilocarpine-induced sweat, and combined pilocarpine plus exercise sweat. Total protein concentrations were similar across conditions, but pilocarpine markedly increased proteomic diversity, with combined pilocarpine plus exercise sweat showing the highest number of identifications. The core sweat proteome remained stable, while pilocarpine selectively enriched low-abundance proteins involved in vesicular trafficking, cytoskeletal remodelling, and metabolism. Proteins linked to the canonical M3-Gq-PLC-Ca2+ pathway, including AQP5, CALML5, and CLIC1, were consistently enriched, confirming cholinergic activation. Pilocarpine-induced sweat also contained plasma-derived and immune-related proteins, reflecting enhanced secretion and reduced ductal reabsorption. CONCLUSIONS: Exercise yields a physiologically relevant but less complex proteome, pilocarpine-induced sweat produces a pharmacologically enriched yet biased profile, and combined pilocarpine plus exercise sweat maximizes protein detection at the expense of interpretability. These findings highlight the critical impact of stimulation paradigm on sweat proteomics and provide a reference framework for biomarker research. SIGNIFICANCE: This study employed LC-MS/MS to systematically characterize eccrine sweat and delineate how stimulation paradigms-exercise, pilocarpine, and their combination-shape its proteomic landscape. By demonstrating that pharmacological induction profoundly alters protein diversity and composition compared to physiologically induced sweat, these findings establish a critical benchmark for sweat-based biomarker research and highlight the need for paradigm-aware sampling strategies in clinical and translational contexts. Nonetheless, several methodological constraints warrant consideration: the limited sample size (five individuals per group), the exclusive inclusion of women under combined oral contraceptive treatment (21 active pills followed by 7 pill-free days), which restricts extrapolation to naturally cycling women, and the focus on healthy young adults (18-25 years), limiting generalizability to older or clinically heterogeneous populations. Despite these limitations, this work provides a foundational framework for optimizing sweat collection protocols and advancing precision approaches in non-invasive diagnostics.
Pilocarpine↗
Effects of essential hypertension and antihypertensive medications on sweat formation.
OBJECTIVE: Sweat volume and ionic composition depend to a large extent upon the cytosolic free calcium level in secretory sweat cells and sodium and potassium transport in the reabsorptive sweat duct. Since essential hypertension and its treatment with antihypertensive drugs is likely to be associated with altered cellular ionic regulation, the objective of this research was to explore sweat formation and sweat parameters in hypertensive and normotensive subjects. DESIGN: Black and white hypertensive and normotensive subjects of both genders were studied. Essential hypertensives were on or off antihypertensive medication. METHODS: Pilocarpine iontophoresis was used to induce sweat in a 5-cm2 area of the middle forearm. Sweat was analyzed for volume, sodium and potassium concentrations. RESULTS: Females demonstrated lower sweat volumes after pilocarpine stimulation than males. Untreated hypertensive white males exhibited a higher pilocarpine-induced sweat volume and sweat sodium excretion than normotensive white males, whilst hypertensive white males on antihypertensive medication showed a lower sweat volume and sweat sodium excretion than both normotensive white males and untreated essential hypertensive white males. Although untreated hypertensive white females did not show significant alterations in sweat parameters, treated hypertensive white females exhibited lower sweat volume and sweat sodium excretion than both the normotensive and untreated essential hypertensive white females. These hypertension and drug related alterations were not present in hypertensive black males and females. CONCLUSIONS: The results are consistent with the heterogeneous nature of essential hypertension and the diversity of the response to antihypertensive therapy. They suggest that the effect of antihypertensive medication on sweat formation is mediated through cytosolic free calcium.
Adult↗
Sweat testing for cocaine, codeine and metabolites by gas chromatography-mass spectrometry.
Sweat testing for drugs of abuse provides a convenient and considerably less invasive method for monitoring drug exposure than blood or urine. Numerous devices have been developed for collection of sweat specimens. The most common device in current use is the PharmChek Sweat Patch, which usually is worn by an individual for five to ten days. This device has been utilized in several field trials comparing sweat test results to conventional urinalysis and the results have been favorable. Two new Fast Patch devices have been developed and tested that allow rapid collection of sweat specimens. The Hand-held Fast Patch was applied to the palm of the hand and the Torso Fast Patch was applied to the abdomen or the sides of the trunk (flanks) of volunteer subjects participating in a research study. Both patches employed heat-induced sweat stimulation and a larger cellulose pad for increased drug collection. Sweat specimens were collected for 30 min at various times following administration of cocaine or codeine in controlled dosing studies. After patch removal, the cellulose pad was extracted with sodium acetate buffer, followed by solid-phase extraction. Extracts were derivatized and analyzed by gas chromatography mass spectrometry (GC-MS) simultaneously for cocaine, codeine and metabolites. Cocaine and codeine were the primary analytes detected in sweat. Peak cocaine and codeine concentrations ranged from 33 to 3579 ng/patch and 11 to 1123 ng/patch, respectively, across all doses for the Hand-held Patch compared to 22-1463 ng/patch and 12-360 ng/patch, respectively, for the Torso Fast Patch. Peak concentrations generally occurred 4.5-24 h after dosing. Both drugs could be detected for at least 48 h after dosing. Considerably smaller concentrations of metabolites of cocaine and codeine were also present in some patches. Generally, concentrations of cocaine and codeine were higher in sweat specimens collected with the Hand-held Fast Patch than for the Torso Fast Patch. Drug concentrations were also considerably higher than those reported for the PharmChek Sweat Patch. The predominance of cocaine and codeine in sweat over metabolites is consistent with earlier studies of cocaine and codeine secretion in sweat. Multiple mechanisms appear to be operative in determining the amount of drug and metabolite secreted in sweat including passive diffusion from blood into sweat glands and outward transdermal migration of the drug. Additional important factors are the physico-chemical properties of the drug analyte, specific characteristics of the sweat collection device, site of sweat collection and, in this study, the application of heat to increase the amount of drug secreted.
Adult↗
Irregular activation of individual sweat glands in human sole observed by a videomicroscopy.
Sweat secretion from individual sweat glands on the human sole was observed in four male subjects by using a videomicroscope and correlated with sudomotor neural activity recorded from the tibial nerve by means of microneurography. Individual sweat glands could be distinguished as active, less active and inactive according to the incidence of sweat secretion during spontaneous sweating. The threshold amplitude of the sudomotor burst necessary for sweat secretion varied from gland to gland. The number of sweat secretion was significantly related to the threshold amplitude. Sweat glands often failed to produce sweat secretion even when a suprathreshold burst occurred: only 46.1+/-3.8% (mean +/- S.E.M.) of the suprathreshold bursts elicited sweat secretion. Failure of the sweat secretion tended to appear after several bursts occurred consecutively with short intervals. In spite of the variability in sweat gland activity, the number of sweat glands recruited was linearly related to the amplitude of the sudomotor burst (P < 0.001). Thus, although sweat secretion from each sweat gland depends primarily on the intensity of sudomotor neural activity. the activity of each sweat gland may fluctuate temporally as the result of irregular activation of sudomotor fibers and possibly some intrinsic factors of the gland.
Adult↗
Comparison of sweat rate during graded exercise and the local rate induced by pilocarpine.
Centrally stimulated sweat rate produced by graded exercise until exhaustion was compared to the local sweat rate induced by pilocarpine, often used as a sweating index for healthy individuals. Nine young male volunteers (22 +/- 4 years) were studied in temperate environment in two situations: at rest and during progressive exercise with 25 W increases every 2 min until exhaustion, on a cycle ergometer. In both situations, sweating was induced on the right forearm with 5 ml 0.5% pilocarpine hydrochloride applied by iontophoresis (1.5 mA, 5 min), with left forearm used as control. Local sweat rate was measured for 15 min at rest. During exercise, whole-body sweat rate was calculated from the body weight variation. Local sweat rate was measured from the time when heart rate reached 150 bpm until exhaustion and was collected using absorbent filter paper. Pharmacologically induced local sweat rate at rest (0.4 +/- 0.2 mg cm-2 min-1) and mean exercise-induced whole-body sweat rate (0.4 +/- 0.1 mg cm-2 min-1) were the same (P > 0.05) but were about five times smaller than local exercise-induced sweat rate (control = 2.1 +/- 1.4; pilocarpine = 2.7 +/- 1.2 mg cm-2 min-1), indicating different sudorific mechanisms. Both exercise-induced whole-body sweat rate (P < 0.05) and local sweat rate (P < 0.05) on control forearm correlated positively with pilocarpine-induced local sweat rate at rest. Assuming that exercise-induced sweating was a result of integrated physiological mechanisms, we suggest that local and whole-body sweat rate measured during graded exercise could be a better sweating index than pilocarpine.
Adult↗
Defective beta adrenergic response of cystic fibrosis sweat glands in vivo and in vitro.
Abnormal ductal NaCl absorption has been known as the only defect in cystic fibrosis (CF) sweat glands. We have fortuitously found that the secretory portion of CF sweat glands is also abnormal in that it failed to show a sweating response to beta adrenergic stimulation (isoproterenol, [ISO]) both in vivo and in vitro. For the in vitro sweat test, eccrine sweat glands were isolated from skin biopsy specimens of the forearm, cannulated, and stimulated to secrete sweat. All 14 isolated CF sweat glands failed to respond to ISO + theophylline (TH, as aminophylline), but 17 of 18 control glands responded with a mean rate (SR) of 1.1 nl/min per gland. Cholinergic responsiveness of isolated CF sweat glands was comparable with that of control glands. The in vivo sweat test was performed by intradermal injection in the forearm of 0.2 ml of 2.4 or 8 X 10(-5) M ISO with or without 10(-2) M TH (and 1.4 X 10(-4) M atropine as a necessary anticholinergic agent). The beads of sweat secreted into the oil-filled sweat collection ring glued to the skin were then collected with a glass capillary under a stereomicroscope. Of 28 CF patients, 26 failed to show a secretory response to intradermal injection of ISO + TH, and 2 CF patients gave SR of less than 0.007 nl/min per gland in the first test but no response in the repeat test performed later. In contrast, all 35 age- and sex-matched control subjects responded with the mean SR of 0.72 nl/min per gland. Response of CF patients to epinephrine and phenylephrine was comparable with control, indicating that the alpha adrenergic responsiveness of CF sweat glands is not defective. A preliminary attempt was made to determine tissue cyclic AMP accumulation by radioimmunoassay in isolated sweat glands. No significant difference was observed between CF and control glands in their maximal accumulation of tissue cAMP in response to ISO or ISO + TH, except that the rise time of ISO + TH-induced cAMP accumulation in CF glands was significantly slower during the first 5 min of incubation. The data suggest that beta adrenergic regulation is abnormal in CF sweat glands and justifies further investigations into the mechanism of beta adrenergic regulation of the eccrine sweat gland in both normal and CF subjects.
Atropine↗
Prevalence of night sweats in primary care patients: an OKPRN and TAFP-Net collaborative study.
OBJECTIVE: To estimate the prevalence and factors associated with night sweats among adult primary care patients. STUDY DESIGN: This was a cross-sectional study. POPULATION: Adult patients in 2 primary care practice-based research networks (PBRNs) during 1 week in the summer and 1 week in the winter in the years 2000 and 2001. OUTCOME MEASURES: We measured the prevalence of pure night sweats and night and day sweats in all patients and subgroups defined by age and sex, clinical variables associated with night sweats, and the frequency, severity, and rate of reporting. RESULTS: Of the 2267 patients who participated, 41% reported experiencing night sweats within the last month, including 23% with pure night sweats and an additional 18% with day and night sweats. The prevalence of night sweats in both men and women was highest in the group aged 41 years to 55 years. In multivariate analyses, factors associated with pure night sweats in women were hot flashes and panic attacks; in men, sleep problems. Variables associated with night and day sweats in women were increased weight, hot flashes, sleep disturbances, use of antihistamines, selective serotonin reuptake inhibitors (SSRIs), and other (non-SSRI, non-tricyclic) antidepressants; in men, increased weight, hot flashes, and greater alcohol use. A majority of patients had not reported their night sweats to their physicians, even when frequent and severe. CONCLUSIONS: Night sweats are common and under-reported. Pure night sweats and night and day sweats may have different causes. With regard to the etiologies of pure night sweats, panic attacks and sleep disorders need further investigation.
Adult↗
Human eccrine sweat contains tissue kallikrein and kininase II.
We attempted to determine the level of sweat kallikrein (kininogenase) and to purify and characterize it using sweat collected over a white petrolatum barrier. Thermally induced eccrine sweat obtained from 24 healthy subjects showed kallikrein activity of 24.4 ng kinins generated/1 mg of sweat protein when heated plasma was used as the substrate and 16.1 ng kinin when purified low molecular weight bovine kininogen was used as the substrate. Sweat was sequentially purified by Sephacryl S-200, diethyaminoethyl Sephacel, and fast flow liquid chromatography Mono Q chromatography. Sweat kallikrein had a M(r) of 40,000 and was inhibited by aprotinin but not by soybean trypsin inhibitor. The peptide generated by sweat kallikrein was identified as lys-bradykinin using reverse phase high-performance liquid chromatography and by its amino acid sequence. Anti-human urinary kallikrein immunoglobulin G neutralized the sweat kallikrein activity completely, indicating that the sweat kallikrein is the glandular type. Purified sweat and salivary kallikrein showed similar M(r) and responses to inhibitors and antibodies. Using immunohistochemistry, kallikrein activity was localized in luminal ductal cells and in the peripheral rim of secretory coil segments, presumably the outer membrane of the myoepithelium. We also observed kininase activity in sweat at M(r) 160,000, which was inhibited by ethylenediamine tetraacetic acid, captopril, and angiotensin converting enzyme inhibitor peptide, indicating that it is kininase II (or angiotensin converting enzyme). Sweat also contains abundant non-kallikrein hydrolases for S-2266 and S-2302. The demonstration of glandular kallikrein, its tissue localization, and the presence of kininase II in sweat provide the basis for future studies on the physiologic role of the kallikrein/kinin system in the eccrine sweat gland.
Angiotensin-Converting Enzyme Inhibitors↗
A modified anaerobic method of sweat collection.
In an attempt to devise a method for collecting large volumes of thermally induced sweat with less epidermal contamination and evaporative water loss, we developed an anaerobic sweat collector by using a sheet of polyethylene film placed over a thin layer of Vaseline and paraffin oil on the skin. To test the validity of the new method, sweat samples collected every 5 min from the new collector (sweat A) were compared with those obtained from a second collector using no oil (sweat B) and scraped sweat for concentrations of adenosine 3',5'-cyclic monophosphate (cAMP), protein, glucose, urea, lactic acid, calcium, sodium, potassium, and cholesterol. The concentration of sweat ingredients in scraped sweat was often far greater than could be expected from evaporative water loss alone. When compared with sweat A, sweat B also had higher concentrations of these ingredients in the initial samples, indicating epidermal contamination, which was especially marked in cAMP, protein, urea, cholesterol, and calcium. Concomitant with a rise in plasma glucose following the administration of a glucose bolus, the sweat glucose significantly increased, indicating the plasma as a major source of sweat glucose. We conclude that the new sweat collector is instrumental in collecting large volumes of the cleanest possible human sweat.
Adult↗
Feasibility of sweat collection by whole body washdown in moderate to high humidity environments.
When sweat rates are sufficiently elevated, i.e., in high ambient temperatures or during exercise, due to potential losses of sweat by runoff, the whole body washdown technique of sweat collection is considered invalid in all but low humidity environments. This paper describes a modification of this technique that makes its use possible in moderate to high humidity environments. During exercise, sweat loss by runoff was minimized by maximizing evaporation of sweat (subjects wore little clothing and electric fans were utilized) and by drying the surface of the body when sweat became excessive (with small hand towels). Sweat rate was calculated from weight changes with appropriate corrections. Total sweat content and concentration of urea N were determined from the rinsings of the body, hand towels, and clothing. To validate this procedure, runoff sweat that was not collected was estimated from the weight change of collecting towels positioned under a bicycle ergometer. Eight subjects exercised at approximately 60% VO2max for 30 min in 22.6 degrees +/- 0.46 degrees C (means +/- SD) and 66.1% +/- 2.34% RH. Volume of sweat secreted was 581 +/- 31 ml (1.162 +/- .062 l X h-1; means +/- SE). Sweat content of the collecting towels (corrected for evaporation loss) was 4.675 ml (0.8%) of total sweat rate), indicating that it is possible to prevent significant sweat loss with this procedure. Moreover, we have found that this procedure can be employed with little difficulty at exercise intensities up to approximately 75% VO2max, in RH of approximately 70%, and with sweat rates as high as 1.65 l X h-1.(ABSTRACT TRUNCATED AT 250 WORDS)
Exercise Test↗
The sweating apparatus in growth hormone deficiency, following treatment with r-hGH and in acromegaly.
Adult growth hormone deficient patients are known to exhibit reduced sweating and their ability to thermoregulate is diminished. Treatment of these patients with recombinant human growth hormone (r-hGH) is claimed to reverse these abnormalities. We have investigated this claim, as well as the mechanism underlying these altered sweating responses in GH-deficient patients as part of a placebo-controlled study on the effects of 6-12 months r-hGH therapy. Skin biopsies were obtained from these subjects and changes in morphology and innervation parameters for the eccrine sweat glands were examined. These included histochemistry for acetylcholinesterase (AChE) and immunohistochemistry for the neuropeptide vasoactive intestinal polypeptide (VIP) and for PGP9.5, a general neuronal marker. Sweat gland acinar size and periacinar innervation were measured by computerised image analysis. The patients underwent pilocarpine iontophoresis sweat rate tests and their serum insulin-like growth factor 1 (IGF-1) levels were assessed. Since active acromegaly involves excess GH secretion and hyperhidrosis, skin biopsies and sweat tests were also carried out on a group of these patients, as well as on control subjects. We have demonstrated a sweating defect in adult GH-deficiency which is accompanied by a reduction in AChE and VIP levels in the nerve supply to sweat glands. Following r-hGH therapy, an increase in AChE and VIP staining is seen in the sudomotor nerves accompanied by restoration of sweat rates and serum IGF-1 levels. Hence, normalization of sweat gland function includes recovery of sudomotor synapse constituents. A trophic effect of GH on sweat gland epithelium and/or on the associated nerves is proposed, supported by the observation that in acromegaly the size of sweat gland acini and the density of innervation to the sweat glands was greater than in controls.
Acetylcholinesterase↗
Sweat gland function in isolated perfused skin.
1. A technique for perfusion of skin has been used to investigate a possible neurochemical basis for the different patterns of sweating in domestic animals. Evaporative water loss was measured from excised trunk skin, ears or tails perfused with a nutrient Krebs solution, to which drugs were added as required. Perfused skin was observed to sweat in response to administration of sudorific drugs, and some features of the patterns of sweating were similar to those which could be induced by heating or by drugs in conscious animals. 2. In sheep and goat skin, injections of adrenaline, and to a lesser extent of noradrenaline, elicited brief sweat discharges but these were not sustained when the drugs were infused during 10-20 min. Injections of isoprenaline, carbachol, 5-HT, bradykinin, oxytocin and histamine were all ineffective. 3. Injections of adrenaline into cattle skin evoked longer-lasting sweat discharges, and infusions of adrenaline elicited continuous discharges. Injections of noradrenaline and sometimes of bradykinin caused only brief sweat discharges; other drugs were ineffective. 4. In horse and donkey skin, injections or infusions of noradrenaline, oxytocin and bradykinin elicited brief discharges of sweat. Infusions of isoprenaline caused a continuous and profuse outflow of sweat. Infusions of adrenaline also caused a continuous discharge which was usually biphasic in its onset. Other drugs were ineffective. 5. Assuming that the brief sweat discharges are due to myoepithelial contractions and the continuous discharges to sustained increases in secretion, equine sweat glands seem to have a alpha-adrenergically controlled myoepithelium and a beta-adrenergically controlled secretory mechanism. Sheep and goats may have a similar alpha-adrenergic control of the sweat gland myoepithelium but only a feeble sweat secretory mechanism. In cattle, an alpha-adrenergic mechanism appears to control sweat secretion, but the control of the myoepithelium is uncertain.
Animals↗