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A woman with a history of parotidectomy on the left side presented with a 2-year history of facial sweating while eating. On examination, the left side of the face became erythematous and sweaty as she ate (shown in a video).

PurposeTo determine the effect of taurine supplementation on sweating and core temperature responses, including the transition from compensable to uncompensable heat stress, during prolonged low-intensity exercise of a fixed-heat production (~ 200W/m2) in hot conditions (37.5 °C), at both fixed and incremental vapour-pressure.MethodsFifteen females (n = 3) and males (n = 12; 27 ± 5 years, 78 ± 9 kg, V˙O2max 50.3 ± 7.8 mL/kg/min), completed a treadmill walking protocol (~ 200W/m2 heat production [Ḣprod]) in the heat (37.5 ± 0.1 °C) at fixed-(16-mmHg) and ramped-humidity (∆1.5-mmHg/5-min) following 1 week of oral taurine supplementation (50 mg/kg/bm) or placebo, in a double-blind, randomised, cross-over design. Participants were assessed for whole-body sweat loss (WBSL), local sweat rate (LSR), sweat gland activation (SGA), core temperature (Tcore), breakpoint of compensability (Pcrit) and calorimetric heat transfer components. Plasma volume and plasma taurine concentrations were established through pre- and post-trial blood samples.ResultsTaurine supplementation increased WBSL by 26.6% and 5.1% (p = 0.035), LSR by 15.5% and 7.8% (p = 0.013), SGA (1 × 1 cm) by 32.2% and 29.9% (p < 0.001) and SGA (3 × 3 cm) by 22.1% and 17.1% (p = 0.015) during the fixed- and ramped-humidity exercise periods, respectively. Evaporative heat loss was enhanced by 27% (p = 0.010), heat-storage reduced by 72% (p = 0.024) and Pcrit was greater in taurine vs placebo (25.0-mmHg vs 21.7-mmHg; p = 0.002).ConclusionTaurine supplementation increased sweating responses during fixed Ḣprod in hot conditions, prior to substantial heat strain and before the breakpoint of compensability, demonstrating improved thermoregulatory capacity. The enhanced evaporative cooling and reduced heat-storage delayed the subsequent upward inflection in Tcore—represented by a greater Pcrit—and offers a potential dietary supplementation strategy to support thermoregulation.

PurposeCaffeine is a commonly used ergogenic aid for endurance events; however, its efficacy and safety have been questioned in hot environmental conditions. The aim of this study was to investigate the effects of acute caffeine supplementation on cycling time to exhaustion and thermoregulation in the heat.MethodsIn a double-blind, randomised, cross-over trial, 12 healthy caffeine-habituated and unacclimatised males cycled to exhaustion in the heat (35 °C, 40% RH) at an intensity associated with the thermoneutral gas exchange threshold, on two separate occasions, 60 min after ingesting caffeine (5 mg/kg) or placebo (5 mg/kg).ResultsThere was no effect of caffeine supplementation on cycling time to exhaustion (TTE) (caffeine; 28.5 ± 8.3 min vs. placebo; 29.9 ± 8.8 min, P = 0.251). Caffeine increased pulmonary oxygen uptake by 7.4% (P = 0.003), heat production by 7.9% (P = 0.004), whole-body sweat rate (WBSR) by 21% (P = 0.008), evaporative heat transfer by 16.5% (P = 0.006) and decreased estimated skin blood flow by 14.1% (P < 0.001) compared to placebo. Core temperature was higher by 0.6% (P = 0.013) but thermal comfort decreased by − 18.3% (P = 0.040), in the caffeine condition, with no changes in rate of perceived exertion (P > 0.05).ConclusionThe greater heat production and storage, as indicated by a sustained increase in core temperature, corroborate previous research showing a thermogenic effect of caffeine ingestion. When exercising at the pre-determined gas exchange threshold in the heat, 5 mg/kg of caffeine did not provide a performance benefit and increased the thermal strain of participants.

BackgroundAcquired idiopathic generalised anhidrosis (AIGA) is characterised by the sudden onset of reduced or absent sweating across the body. It is suspected to be an autoimmune process.CaseA 25-year-old African male presented to an outpatient clinic with two years of intermittent generalised parasthesiae and heat intolerance. He reported an unpredictable, migratory prickling sensation affecting his face, scalp, torso, arms or legs, which was triggered with heat or exercise and was more noticeable in the winter. He also reported longstanding reduction in his sweating, particularly in the axillae. His neurological examination was normal. He had an elevated IgE (173 IU/L), moderate neutropenia, and mildly elevated LFTs. His ANA was 1:80 with normal ENA and negative anti-dsDNA; he had borderline anti-TPO antibodies. Large fibre nerve conduction studies were unremarkable, but there were impaired sympathetic skin responses in the palms and feet. Autonomic testing showed normal cardiovagal and adrenergic responses, while thermal sweat testing demonstrated sparse sweating on the trunk and extremities, and reduced sweating in the interdigital spaces of the feet. The test was aborted at 40 minutes after a 1 degC elevation in body temperature to 37.5 degC. He had no symptomatic response to antihistamines or gabapentin. Suspecting AIGA, three days of pulse methylprednisolone was arranged. He had complete resolution of symptoms after six weeks, and serial thermal sweat testing at six months showed substantial improvement in the sweating response.ConclusionWe report a rare case of AIGA which has demonstrated a promising response to high-dose pulse corticosteroid therapy.

Patients who undergo salivary gland, neck, or facelift surgery or suffer from diabetes mellitus often develop Frey syndrome (also known as auriculotemporal syndrome or gustatory sweating). Frey syndrome has been occasionally reported to occur in subjects without history of surgery or diabetes but this variant of Frey syndrome has not been systematically investigated. We searched for original articles of Frey syndrome unrelated to surgery or diabetes without date and language restriction. Article selection and data extraction were performed in duplicate. Our systematic review included 76 reports describing 121 individual cases (67 males and 54 females) of Frey syndrome not associated with surgery or diabetes. The age at onset of symptoms was ≤ 18 years in 113 (93%) cases. The time to diagnosis was 12 months or more in 55 (45%) cases. On the other hand, an allergy evaluation was performed in half of the cases. A possible cause for Frey syndrome was detected in 85 (70%) cases, most frequently history of forceps birth (N = 63; 52%). The majority of the remaining 22 cases occurred after a blunt face trauma, following an auriculotemporal nerve neuritis or in association with a neurocutaneous syndrome. The cause underlying Frey syndrome was unknown in 36 cases. Conclusion: Frey syndrome not associated with surgery or diabetes almost exclusively affects subjects in pediatric age and is uncommon and underrecognized. Most cases occur after forceps birth. There is a need to expand awareness of this pseudo-allergic reaction among pediatricians and allergists. What is Known:• Pre-auricular reddening, sweating, and warmth in response to mastication or a salivary stimulus characterize Frey syndrome.• It usually occurs after salivary gland surgery and in diabetes.What is New:• In children, Frey syndrome is rare, and most cases occur after a forceps-assisted birth.• In childhood, this condition is often erroneously attributed to food allergy.

PurposeTo quantify total sweat electrolyte losses at two relative exercise intensities and determine the effect of workload on the relation between regional (REG) and whole body (WB) sweat electrolyte concentrations.MethodsEleven recreational athletes (7 men, 4 women; 71.5 ± 8.4 kg) completed two randomized trials cycling (30 °C, 44% rh) for 90 min at 45% (LOW) and 65% (MOD) of VO2max in a plastic isolation chamber to determine WB sweat [Na+] and [Cl−] using the washdown technique. REG sweat [Na+] and [Cl−] were measured at 11 REG sites using absorbent patches. Total sweat electrolyte losses were the product of WB sweat loss (WBSL) and WB sweat electrolyte concentrations.ResultsWBSL (0.86 ± 0.15 vs. 1.27 ± 0.24 L), WB sweat [Na+] (32.6 ± 14.3 vs. 52.7 ± 14.6 mmol/L), WB sweat [Cl−] (29.8 ± 13.6 vs. 52.5 ± 15.6 mmol/L), total sweat Na+ loss (659 ± 340 vs. 1565 ± 590 mg), and total sweat Cl− loss (931 ± 494 vs. 2378 ± 853 mg) increased significantly (p < 0.05) from LOW to MOD. REG sweat [Na+] and [Cl−] increased from LOW to MOD at all sites except thigh and calf. Intensity had a significant effect on the regression model predicting WB from REG at the ventral wrist, lower back, thigh, and calf for sweat [Na+] and [Cl−].ConclusionTotal sweat Na+ and Cl− losses increased by ~ 150% with increased exercise intensity. Regression equations can be used to predict WB sweat [Na+] and [Cl−] from some REG sites (e.g., dorsal forearm) irrespective of intensity (between 45 and 65% VO2max), but other sites (especially ventral wrist, lower back, thigh, and calf) require separate prediction equations accounting for workload.

Athletes lose water and electrolytes as a consequence of thermoregulatory sweating during exercise and it is well known that the rate and composition of sweat loss can vary considerably within and among individuals. Many scientists and practitioners conduct sweat tests to determine sweat water and electrolyte losses of athletes during practice and competition. The information gleaned from sweat testing is often used to guide personalized fluid and electrolyte replacement recommendations for athletes; however, unstandardized methodological practices and challenging field conditions can produce inconsistent/inaccurate results. The primary objective of this paper is to provide a review of the literature regarding the effect of laboratory and field sweat-testing methodological variations on sweating rate (SR) and sweat composition (primarily sodium concentration [Na + ]). The simplest and most accurate method to assess whole-body SR is via changes in body mass during exercise; however, potential confounding factors to consider are non-sweat sources of mass change and trapped sweat in clothing. In addition, variability in sweat [Na + ] can result from differences in the type of collection system used (whole body or localized), the timing/duration of sweat collection, skin cleaning procedure, sample storage/handling, and analytical technique. Another aim of this paper is to briefly review factors that may impact intra/interindividual variability in SR and sweat [Na + ] during exercise, including exercise intensity, environmental conditions, heat acclimation, aerobic capacity, body size/composition, wearing of protective equipment, sex, maturation, aging, diet, and/or hydration status. In summary, sweat testing can be a useful tool to estimate athletes’ SR and sweat Na + loss to help guide fluid/electrolyte replacement strategies, provided that data are collected, analyzed, and interpreted appropriately.

The body naturally and continuously secretes sweat for thermoregulation during sedentary and routine activities at rates that can reflect underlying health conditions, including nerve damage, autonomic and metabolic disorders, and chronic stress. However, low secretion rates and evaporation pose challenges for collecting resting thermoregulatory sweat for non-invasive analysis of body physiology. Here we present wearable patches for continuous sweat monitoring at rest, using microfluidics to combat evaporation and enable selective monitoring of secretion rate. We integrate hydrophilic fillers for rapid sweat uptake into the sensing channel, reducing required sweat accumulation time towards real-time measurement. Along with sweat rate sensors, we integrate electrochemical sensors for pH, Cl − , and levodopa monitoring. We demonstrate patch functionality for dynamic sweat analysis related to routine activities, stress events, hypoglycemia-induced sweating, and Parkinson’s disease. By enabling sweat analysis compatible with sedentary, routine, and daily activities, these patches enable continuous, autonomous monitoring of body physiology at rest. Low secretion rates and evaporation pose challenges for collecting resting thermoregulatory sweat for non-invasive analysis of body physiology. Here the authors present wearable microfluidics-based patches for continuous sweat monitoring at rest that enable detection of pH, Cl − , and levodopa for dynamic sweat analysis related to routine activities, stress events, hypoglycemia-induced sweating, and Parkinson’s disease.

ObjectiveTo compare hyperthermia and physiological dehydration risk during exercise heat stress between children of different ages and adults and evaluate an existing adult sweat rate calculator in children.Methods68 fit and recreationally active children aged 10–16 years (31 girls), and 24 adults aged 18–40 years (11 females) completed three separate 45 min treadmill walking/running trials at different intensities on different days at 30°C, 40% relative humidity (RH) (WARM) or 40°C, 30% RH (HOT). Exposures were randomised to elicit intensities scaled to (1) fitness, (2) mass and (3) surface area. Core (gastrointestinal (Tgi)) temperature was measured continuously and dehydration determined using body mass changes.ResultsExcept for 60% V̇O2peak in WARM, in which adults exhibited a greater Tgi rise compared with 10–13 years, there was no effect of age on Tgi during exercise (p≥0.176). Physiological rates of dehydration were not affected by age in WARM (p≥0.08) or HOT (p≥0.08). Mean predicted sweat rate error was +0.08 kg/hour (95% CIs: −0.10, +0.25) across WARM and HOT, and 80.5% of variability in sweating was explained by the adult sweat rate calculator.ConclusionsUsing the most comprehensive paediatric exercise heat stress dataset from a single study to date, we show that children aged 10–16 years are at a similar risk of hyperthermia and dehydration as adults during exercise up to 40°C. This supports recent changes to paediatric sport heat policies that were based on limited data. Practitioners can potentially reduce behavioural dehydration risks from inadequate fluid consumption using an existing adult sweat rate calculator for children.