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Acute acetaminophen ( ACT) ingestion has been reported to reduce thermal strain during cycling in the heat. In this study, nine active participants ingested 20 mg of ACT per kg of total body mass ( ACT) or a placebo ( PLA), 60 min prior to cycling at a fixed rate of metabolic heat production ( ACT: 8.3 ± 0.3 W/kg; PLA: 8.5 ± 0.5 W/kg), which was equivalent to 55 ± 6% VO2max, for 60 min at 34.5 ± 0.1 ° C, 52 ± 1% relative humidity. Resting rectal temperature ( Tre; ACT: 36.70 ± 0.17 ° C; PLA: 36.80 ± 0.16 ° C, P = 0.24), esophageal temperature ( Tes; ACT: 36.54 ± 0.22 ° C; PLA: 36.61 ± 0.17 ° C, P = 0.50) and mean skin temperature ( Tsk; ACT: 34.00 ± 0.14 ° C; PLA: 33.96 ± 0.20 ° C, P = 0.70) were all similar among conditions. At end-exercise, no differences in Δ Tre ( ACT: 1.12 ± 0.15 ° C; PLA: 1.11 ± 0.21 ° C, P = 0.92), Δ Tes ( ACT: 0.90 ± 0.28 ° C; PLA: 0.88 ± 0.23 ° C, P = 0.84), Δ Tsk ( ACT: 0.80 ± 0.39 ° C; PLA: 0.70 ± 0.46 ° C, P = 0.63), mean local sweat rate ( ACT: 1.02 ± 0.15 mg/cm2/min; PLA: 1.02 ± 0.13 mg/cm2/min, P = 0.98) and whole-body sweat loss ( ACT: 663 ± 83 g; PLA: 663 ± 77 g, P = 0.995) were evident. Furthermore, ratings of perceived exertion and thermal sensation and thermal comfort were not different between ACT and PLA conditions. In conclusion, ACT ingested 60 min prior to moderate intensity exercise in hot-humid conditions does not alter physiologic thermoregulatory control nor perceived strain. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study? How does passive heat stress and subsequent heat acclimation affect the circulating concentration of extracellular vesicles? What is the main finding and its importance? Passive heat stress increased the circulating concentration of total and platelet extracellular vesicles. Seven days of hot water immersion did not modify the change in circulating concentrations of extracellular vesicles during passive heat stress., Abstract: This retrospective exploratory analysis aimed to improve our understanding of the effect of passive heat stress and subsequent heat acclimation on the circulating concentration of extracellular vesicles (EVs). Healthy young adults (four females and six males, 25 ± 4 years of age, 1.72 ± 0.08 m in height and weighing 71.6 ± 9.0 kg) were heated with a water-perfused suit before and after seven consecutive days of hot water immersion. Pre-acclimation, participants were heated until oesophageal temperature increased to ∼1.4°C above baseline values. Post-acclimation, participants were heated until oesophageal temperature reached the same absolute value as the pre-acclimation visit (∼38.2°C). Venous blood samples were obtained before and at the end of passive heating to quantify plasma concentrations of EVs from all cell types (CSFE + ), all cell types except erythrocytes (CSFE + MHCI + ), platelets (CSFE + MHCI + CD41 + ), endothelial cells (CSFE + MHCI + CD62e + ), red blood cells (CSFE + CD235a + ) and leucocytes (CSFE + MHCI + CD45 + ) via flow cytometry. Passive heat stress increased the concentration of CFSE + EVs (46,150,000/ml [3,620,784, 88,679,216], P = 0.036), CFSE + MHCI + EVs (28,787,500/ml [9,851,127, 47,723,873], P = 0.021) and CSFE + MHCI + CD41 + EVs (28,343,500/ml [9,637,432, 47,049,568], P = 0.008). The concentration of CSFE + MHCI + CD62e + EVs (94,230/ml [-55,099, 243,559], P = 0.187), CSFE + CD235a + EVs (-1,414/ml [-15,709, 12,882], P = 0.403) or CSFE + MHCI + CD45 + EVs (-192,915/ml [-690,166, 304,336], P = 0.828) did not differ during heat stress. The change in circulating EVs during passive heat stress did not differ after heat acclimation (thermal state × acclimation interactions, all P ≥ 0.180). These results demonstrate that passive heat stress increases the circulating concentration of total and platelet EVs and that passive heat acclimation does not alter this increase., (© 2022 The Authors. Experimental Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society.)

New Findings: What is the central question of this study? Do measurement timing, heating modality and biological sex modulate the acute effect of heat exposure on brachial artery flow-mediated dilatation and postocclusion reactive hyperaemia? What is the main finding and its importance? The acute effect of heat exposure on brachial artery flow-mediated dilatation and postocclusion reactive hyperaemia is: (1) transient and short lasting; (2) different between forearm and whole-body heating; (3) unaffected by forearm heating during whole-body heating; and (4) not different but not always equivalent between males and females. These findings provide a useful basis for future studies to investigate the acute effect of heat exposure on vascular function., Abstract: The aim of this study was to gain a better understanding of the acute effect of heat exposure on brachial artery flow-mediated dilatation (FMD) and postocclusion reactive hyperaemia (PORH) by: characterizing the time course of changes post-heating; comparing forearm and whole-body heating; determining the impact of forearm heating during whole-body heating; and comparing males and females. Twenty adults (11 males and nine females; 28 ± 6 years of age) underwent two forearm [10 min electric blanket (EB) or 30 min hot water immersion (WI)] and two whole-body [60 min water-perfused suit with forearm covered (WBH-C) or uncovered (WBH-U)] heating modalities. The FMD and PORH were measured before and after (≤5, 30, 60, 90 and 120 min) heating. The FMD increased from baseline 30 min after EB, and 30 and 90 min after WI. In contrast, FMD decreased from baseline immediately after both WBH modalities. Peak PORH increased immediately after WI and both WBH modalities. Total PORH did not differ after WI, whereas it decreased immediately after both WBH modalities. Covering the forearm during WBH did not alter acute changes in FMD or PORH. Changes in FMD and PORH did not differ statistically between males and females during each heating modality, although the observed differences could not always be considered equivalent. These results demonstrate that the acute effect of heat exposure on brachial artery FMD and PORH is: (1) transient and short lasting; (2) different between forearm heating and WBH; (3) unaffected by direct forearm heating during WBH; and (4) not different but not always equivalent between males and females., (© 2022 The Authors. Experimental Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society.)

New Findings: What is the central question of this study? Are fitness-related improvements in thermoregulatory responses during uncompensable heat stress mediated by aerobic capacity V ̇ O 2 max or is it the partial heat acclimation associated with training? What is the main finding and its importance? During uncompensable heat stress, individuals with high and low V ̇ O 2 max displayed similar sweating and core temperature responses whereas exercise training in previously untrained individuals resulted in a greater sweat rate and a smaller rise in core temperature. These observations suggest that it is training, not V ̇ O 2 max per se, that mediates thermoregulatory improvements during uncompensable heat stress., Abstract: It remains unclear whether aerobic fitness, as defined by the maximum rate of oxygen consumption V ̇ O 2 max , independently improves heat dissipation in uncompensable environments, or whether the thermoregulatory adaptations associated with heat acclimation are due to repeated bouts of exercise-induced heat stress during regular aerobic training. The present analysis sought to determine if V ̇ O 2 max independently influences thermoregulatory sweating, maximum skin wettedness (ω max ) and the change in rectal temperature (ΔT re ) during 60 min of exercise in an uncompensable environment (37.0 ± 0.8°C, 4.0 ± 0.2 kPa, 64 ± 3% relative humidity) at a fixed rate of heat production per unit mass (6 W kg -1 ). Retrospective analyses were performed on 22 participants (3 groups), aerobically unfit (UF; n = 7; V ̇ O 2 max : 41.7 ± 9.4 ml kg -1  min -1 ), aerobically fit (F; n = 7; V ̇ O 2 max : 55.6 ± 4.3 ml kg -1  min -1 ; P < 0.01) and aerobically unfit (n = 8) individuals, before (pre; V ̇ O 2 max : 45.8 ± 11.6 ml kg -1  min -1 ) and after (post; V ̇ O 2 max : 52.0 ± 11.1 ml kg -1  min -1 ; P < 0.001) an 8-week training intervention. ω max was similar between UF (0.74 ± 0.09) and F (0.78 ± 0.08, P = 0.22). However, ω max was greater post- (0.84 ± 0.08) compared to pre- (0.72 ± 0.06, P = 0.02) training. During exercise, mean local sweat rate (forearm and upper-back) was greater post- (1.24 ± 0.20 mg cm -2  min -1 ) compared to pre- (1.04 ± 0.25 mg cm -2  min -1 , P < 0.01) training, but similar between UF (0.94 ± 0.31 mg cm -2  min -1 , P = 0.90) and F (1.02 ± 0.30 mg cm -2  min -1 ). The ΔT re at 60 min of exercise was greater pre- (1.13 ± 0.16°C, P < 0.01) compared to post- (0.96 ± 0.14°C) training, but similar between UF (0.85 ± 0.29°C, P = 0.22) and F (0.95 ± 0.22°C). Taken together, aerobic training, not V ̇ O 2 max per se, confers an increased ω max , greater sweat rate, and smaller rise in core temperature during uncompensable heat stress in fit individuals., (© 2020 The Authors. Experimental Physiology © 2020 The Physiological Society.)

New Findings: What is the central question of this study? Hypoxia reportedly does not impair thermoregulation during exercise in compensable heat stress conditions: does it have an impact on maximal heat dissipation and therefore the critical environmental limit for the physiological compensability of core temperature? What is the main finding and its importance? Although skin blood flow was higher in hypoxia, no differences in sweat rates or the critical environmental limit for the physiological compensability of core temperature - an indicator of maximal heat loss - were found compared to exercise in normoxia, indicating no influence of normobaric hypoxia on thermoregulatory capacity in warm conditions., Abstract: Altered control of skin blood flow (SkBF) in hypoxia does not impair thermoregulation during exercise in compensable conditions, but its impact on maximal heat dissipation is unknown. This study therefore sought to determine whether maximum heat loss is altered by hypoxia during exercise in warm conditions. On separate days, eight males exercised for 90 min at a fixed heat production of ∼500 W in normoxia (NORM) or normobaric hypoxia (HYP, F I O 2  = 0.13) in a 34°C environment. Ambient vapour pressure was maintained at 2.13 kPa for 45 min, after which it was raised 0.11 kPa every 7.5 min. The critical ambient vapour pressure at which oesophageal temperature inflected upward (P crit ) indicated that maximum heat dissipation had been reached. Neither local sweat rates on the upper arm, back and forehead (average NORM: 1.46 (0.15) vs. HYP: 1.41 (0.16) mg cm -2  min -1 ; P = 0.59) nor whole-body sweat losses (NORM: 1029 (137) g vs. HYP: 1025 (150) g; P = 0.95) were different between trials. Laser-Doppler flux values (LDF; arbitrary units), an index of SkBF, were not different between NORM and HYP on the forearm (P = 0.23) or back (P = 0.73); however, when normalized as a percentage of maximum, LDF values tended to be higher in HYP compared to NORM at the forearm (condition effect, P = 0.05) but not back (P = 0.19). Despite potentially greater SkBF in hypoxia, there was no difference in P crit between conditions (NORM: 3.67 (0.35) kPa; HYP: 3.46 (0.39) kPa; P = 0.22). These findings suggest that hypoxia does not independently alter thermoregulatory capacity during exercise in warm conditions., (© 2020 The Authors. Experimental Physiology © 2020 The Physiological Society.)

New Findings: What is the central question of this study? Does passive heat acclimation alter glomerular filtration rate and urine-concentrating ability in response to passive heat stress? What is the main finding and its importance? Glomerular filtration rate remained unchanged after passive heat stress, and heat acclimation did not alter this response. However, heat acclimation mitigated the reduction in urine-concentrating ability and reduced the incidence of albuminuria in young healthy adults after passive heat stress. Collectively, these results suggest that passive heat acclimation might improve structural integrity and reduce glomerular permeability during passive heat stress., Abstract: Little is known about the effect of heat acclimation on kidney function during heat stress. The purpose of this study was to determine the impact of passive heat stress and subsequent passive heat acclimation on markers of kidney function. Twelve healthy adults (seven men and five women; 26 ± 5 years of age; 72.7 ± 8.6 kg; 172.4 ± 7.5 cm) underwent passive heat stress before and after a 7 day controlled hyperthermia heat acclimation protocol. The impact of passive heat exposure on urine and serum markers of kidney function was evaluated before and after heat acclimation. Glomerular filtration rate, determined from creatinine clearance, was unchanged with passive heat stress before (pre, 133 ± 41 ml min -1 ; post, 127 ± 51 ml min -1 ; P = 0.99) and after (pre, 129 ± 46 ml min -1 ; post, 130 ± 36 ml min -1 ; P = 0.99) heat acclimation. The urine-to-serum osmolality ratio was reduced after passive heating (P < 0.01), but heat acclimation did not alter this response. In comparison to baseline, free water clearance was greater after passive heating before (pre, -0.86 ± 0.67 ml min -1 ; post, 0.40 ± 1.01 ml min -1 ; P < 0.01) but not after (pre, -0.16 ± 0.57 ml min -1 ; post, 0.76 ± 1.2 ml min -1 ; P = 0.11) heat acclimation. Furthermore, passive heating increased the fractional excretion rate of potassium (P < 0.03) but not sodium (P = 0.13) or chloride (P = 0.20). Lastly, heat acclimation reduced the fractional incidence of albuminuria after passive heating (before, 58 ± 51%; after, 8 ± 29%; P = 0.03). Collectively, these results demonstrate that passive heat stress does not alter the glomerular filtration rate. However, heat acclimation might improve urine-concentrating ability and filtration within the glomerulus., (© 2020 The Authors. Experimental Physiology © 2020 The Physiological Society.)