Explore the vast range of titles available.

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.

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.

Regional variation in sweating over the body is widely recognised. However, most studies only measured a limited number of regions, with the use of differing thermal states across studies making a good meta-analysis to obtain a whole body map problematic. A study was therefore conducted to investigate regional sweat rates (RSR) and distributions over the whole body in male athletes. A modified absorbent technique was used to collect sweat at two exercise intensities [55% (I1) and 75% (I2) ] in moderately warm conditions (25°C, 50% rh, 2 m s −1 air velocity). At I1 and I2, highest sweat rates were observed on the central (upper and mid) and lower back, with values as high as 1,197, 1,148, and 856 g m −2  h −1 , respectively, at I2. Lowest values were observed on the fingers, thumbs, and palms, with values of 144, 254, and 119 g m −2  h −1 , respectively at I2. Sweat mapping of the head demonstrated high sweat rates on the forehead (1,710 g m −2  h −1 at I2) compared with low values on the chin (302 g m −2  h −1 at I2) and cheeks (279 g m −2  h −1 at I2). Sweat rate increased significantly in all regions from the low to high exercise intensity, with exception of the feet and ankles. No significant correlation was present between RSR and regional skin temperature ( T sk ), nor did RSR correspond to known patterns of regional sweat gland density. The present study has provided detailed regional sweat data over the whole body and has demonstrated large intra- and inter-segmental variation and the presence of consistent patterns of regional high versus low sweat rate areas in Caucasians male athletes. This data may have important applications for clothing design, thermophysiological modelling and thermal manikin design.

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.

We investigated the thermoregulatory responses to ice slurry ingestion during low- and moderate-intensity exercises with restrictive heat loss. Randomised, counterbalanced, cross-over design. Following a familiarisation trial, ten physically active males exercised on a motorised treadmill at low-intensity (L; 40% VO2max) or moderate-intensity (M; 70% VO2max) for 75-min, in four randomised, counterbalanced trials. Throughout the exercise bout, participants donned a raincoat to restrict heat loss. Participants ingested 2gkg−1 body mass of ambient water (L+AMB and M+AMB trials) or ice slurry (L+ICE and M+ICE trials) at 15-min intervals during exercise in environmental conditions of Tdb, 25.1±0.6°C and RH, 63±5%. Heart rate (HR), gastrointestinal temperature (Tgi), mean weighted skin temperature (Tsk), estimated sweat loss, ratings of perceived exertion (RPE) and thermal sensation (RTS) were recorded. Compared to L+AMB, participants completed L+ICE trials with lower ΔTgi (0.8±0.3°C vs 0.6±0.2°C; p=0.03), mean RPE (10±1 vs 9±1; p=0.03) and estimated sweat loss (0.91±0.2L vs 0.78±0.27L; p=0.04). Contrastingly, Tgi (p=0.22), Tsk (p=0.37), HR (p=0.31), RPE (p=0.38) and sweat loss (p=0.17) were similar between M+AMB and M+ICE trials. RTS was similar during both low-intensity (4.9±0.5 vs 4.7±0.3; p=0.10) and moderate-intensity exercise (5.3±0.47 vs 5.0±0.4; p=0.09). Per-cooling using ice slurry ingestion marginally reduced thermal strain during low-intensity but not during moderate-intensity exercise. Ice slurry may be an effective and practical heat mitigation strategy during low-intensity exercise such as in occupational and military settings, but a greater volume should be considered to ensure its efficacy.

Sweat rate and electrolyte losses have a large inter-individual variability. A personalized approach to hydration can overcome this issue to meet an individual’s needs. This study aimed to investigate the effects of a personalized hydration strategy (PHS) on fluid balance and intermittent exercise performance. Twelve participants conducted 11 laboratory visits including a VO2max test and two 5-day trial arms under normothermic (NOR) or hyperthermic (HYP) environmental conditions. Each arm began with three days of familiarization exercise followed by two random exercise trials with either a PHS or a control (CON). Then, participants crossed over to the second arm for: NOR+PHS, NOR+CON, HYP+PHS, or HYP+CON. The PHS was prescribed according to the participants’ fluid and sweat sodium losses. CON drank ad libitum of commercially-available electrolyte solution. Exercise trials consisted of two phases: (1) 45 min constant workload; (2) high-intensity intermittent exercise (HIIT) until exhaustion. Fluids were only provided in phase 1. PHS had a significantly greater fluid intake (HYP+PHS: 831.7 ± 166.4 g; NOR+PHS: 734.2 ± 144.9 g) compared to CON (HYP+CON: 369.8 ± 221.7 g; NOR+CON: 272.3 ± 143.0 g), regardless of environmental conditions (p < 0.001). HYP+CON produced the lowest sweat sodium concentration (56.2 ± 9.0 mmol/L) compared to other trials (p < 0.001). HYP+PHS had a slower elevated thirst perception and a longer HIIT (765 ± 452 s) compared to HYP+CON (548 ± 283 s, p = 0.04). Thus, PHS reinforces fluid intake and successfully optimizes hydration status, regardless of environmental conditions. PHS may be or is an important factor in preventing negative physiological consequences during high-intensity exercise in the heat.

PurposeTo determine the impact of altering dietary sodium intake for 3 days preceding exercise on sweat sodium concentration [Na+], and cardiovascular and thermoregulatory variables.MethodsFifteen male endurance athletes (runners n = 8, cyclists n = 7) consumed a low (LNa, 15 mg kg−1 day−1) or high (HNa, 100 mg kg−1 day−1) sodium diet, or their usual free-living diet [UDiet, 46 (37–56) mg kg−1 day−1] for 3 days in a double-blind, randomized cross-over design, collecting excreted urine (UNa) and refraining from exercise. On day 4, they completed 2 h running at 55% \\[\\dot{V}\\]O2max or cycling at 55% maximum aerobic power in Tamb 35 °C. Pre- and post-exercise blood samples were collected, and sweat from five sites using absorbent patches along the exercise protocol.ResultsUNa on days 2–3 pre-exercise [mean (95% CI) LNa 16 (12–19) mg kg−1 day−1, UDiet 46 (37–56) mg kg−1 day−1, HNa 79 (72–85) mg kg−1 day−1; p < 0.001] and pre-exercise aldosterone [LNa 240 (193–286) mg kg−1 day−1, UDiet 170 (116–224) mg kg−1 day−1, HNa 141 (111–171) mg kg−1 day−1; p = 0.001] reflected sodium intake as expected. Pre-exercise total body water was greater following HNa compared to LNa (p < 0.05), but not UDiet. Estimated whole-body sweat [Na+] following UDiet was 10–11% higher than LNa and 10–12% lower than HNa (p < 0.001), and correlated with pre-exercise aldosterone (1st h r =  − 0.568, 2nd h r =  − 0.675; p < 0.01). Rectal temperature rose more quickly in LNa vs HNa (40–70 min; p < 0.05), but was similar at the conclusion of exercise, and no significant differences in heart rate or perceived exertion were observed.ConclusionsThree day altered sodium intake influenced urinary sodium excretion and sweat [Na+], and the rise in rectal temperature, but had no effect on perceived exertion during moderate-intensity exercise in hot ambient conditions.

PurposeHypoxic acclimation enhances convective oxygen delivery to the muscles. Heat acclimation-elicited thermoregulatory benefits have been suggested not to be negated by adding daily exposure to hypoxia. Whether concomitant acclimation to both heat and hypoxia offers a synergistic enhancement of aerobic performance in thermoneutral or hot conditions remains unresolved.MethodsEight young males (\\[\\dot{V}{\\text{O}}_{2\\max }\\]: 51.6 ± 4.6 mL min−1 kg−1) underwent a 10-day normobaric hypoxic confinement (FiO2 = 0.14) interspersed with daily 90-min normoxic controlled hyperthermia (target rectal temperature: 38.5 °C) exercise sessions. Prior to, and following the confinement, the participants conducted a 30-min steady-state exercise followed by incremental exercise to exhaustion on a cycle ergometer in thermoneutral normoxic (NOR), thermoneutral hypoxic (FiO2 = 0.14; HYP) and hot (35 °C, 50% relative humidity; HE) conditions in a randomized and counterbalanced order. The steady-state exercise was performed at 40% NOR peak power output (Wpeak) to evaluate thermoregulatory function. Blood samples were obtained from an antecubital vein before, on days 1 and 10, and the first day post-acclimation.Results\\[\\dot{V}{\\text{O}}_{2\\max }\\] and ventilatory thresholds were not modified in any environment following acclimation. Wpeak increased by 6.3 ± 3.4% in NOR and 4.0 ± 4.9% in HE, respectively. The magnitude and gain of the forehead sweating response were augmented in HE post-acclimation. EPO increased from baseline (17.8 ± 7.0 mIU mL−1) by 10.7 ± 8.8 mIU mL−1 on day 1 but returned to baseline levels by day 10 (15.7 ± 5.9 mIU mL−1).DiscussionA 10-day combined heat and hypoxic acclimation conferred only minor benefits in aerobic performance and thermoregulation in thermoneutral or hot conditions. Thus, adoption of such a protocol does not seem warranted.

Cycling is recognised as a sport in which there is a high incidence of poor bone health. Sweat calcium losses may contribute to this. To examine whether a calcium-rich pre-exercise meal attenuates exercise-induced perturbations of bone calcium homeostasis caused by maintenance of sweat calcium losses. Using a randomized, counterbalanced crossover design, 32 well-trained female cyclists completed two 90 min cycling trials separated by 1 day. Exercise trials were preceded 2 hours by either a calcium-rich (1352 ± 53 mg calcium) dairy based meal (CAL) or a control meal (CON; 46 ± 7 mg calcium). Blood was sampled pre-trial; pre-exercise; and immediately, 40 min, 100 min and 190 min post-exercise. Blood was analysed for ionized calcium and biomarkers of bone resorption (Cross Linked C-Telopeptide of Type I Collagen (CTX-I), Cross Linked C-Telopeptide of Type II Collagen (CTX-II), Parathyroid Hormone (PTH), and bone formation (Procollagen I N-Terminal Propeptide (PINP)) using the established enzyme-linked immunosorbent assay technique. PTH and CTX-I increased from pre-exercise to post-exercise in both conditions but was attenuated in CAL (p < 0.001). PTH was 1.55 [1.20, 2.01] times lower in CAL immediately post-exercise and 1.45 [1.12, 1.88] times lower at 40 min post-exercise. CTX-I was 1.40 [1.15, 1.70] times lower in CAL at immediately post-exercise, 1.30 [1.07, 1.57] times lower at 40 min post-exercise and 1.22 [1.00, 1.48] times lower at 190 min post-exercise (p < 0.05). There was no significant interaction between pre-exercise meal condition and time point for CTX-II (p = 0.732) or PINP (p = 0.819). This study showed that a calcium-rich pre-exercise breakfast meal containing ~1350 mg of calcium consumed ~90 min before a prolonged and high intensity bout of stationary cycling attenuates the exercise induced rise in markers of bone resorption--PTH and CTX-I. Australian New Zealand Clinical Trials Registry ACTRN12614000675628.