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Background: Ethyl alcohol (ethanol) consumption is ostensibly known to increase the risk of morbidity and mortality during hot weather and heatwaves. However, how alcohol independently alters physiological, perceptual, and behavioral responses to heat stress remains poorly understood. Therefore, we conducted a systematic scoping review to understand how alcohol consumption affects thermoregulatory responses to the heat., Methods: We searched five databases employing the following eligibility criteria, studies must have: 1) involved the oral consumption of ethanol, 2) employed a randomized or crossover-control study design with a control trial consisting of a volume-matched, non-alcoholic beverage, 3) been conducted in healthy adult humans, 4) reported thermophysiological, perceptual, hydration status markers, and/or behavioral outcomes, 5) been published in English, 6) been conducted in air or water at temperatures of > 28°C, 7) involved passive rest or exercise, and 8) been published before October 4th, 2023., Results: After removing duplicates, 7256 titles were screened, 29 papers were assessed for eligibility and 8 papers were included in the final review. Across the 8 studies, there were a total of 93 participants (93 male/0 female), the average time of heat exposure was 70 min and average alcohol dose was 0.68 g·kg 1 . There were 23 unique outcome variables analyzed from the studies. The physiological marker most influenced by alcohol was core temperature (lowered with alcohol consumption in 3/4 studies). Additionally, skin blood flow was increased with alcohol consumption in the one study that measured it. Typical markers of dehydration, such as increased urine volume (1/3 studies), mass loss (1/3 studies) and decreased plasma volume (0/2 studies) were not consistently observed in these studies, except for in the study with the highest alcohol dose., Conclusion: The effect of alcohol consumption on thermoregulatory responses is understudied, and is limited by moderate doses of alcohol consumption, short durations of heat exposure, and only conducted in young-healthy males. Contrary to current heat-health advice, the available literature suggests that alcohol consumption does not seem to impair physiological responses to heat in young healthy males., (© 2024. The Author(s).)

Introduction: Despite sparse systematic evidence, current exercise heat safety recommendations suggest that antihistamines blunt sweating and increase the risk for heat-related injury during exertional heat stress. The primary purpose of the present study was to examine whether diphenhydramine hydrochloride (DPH), a first-generation antihistamine, effects the sweating, core temperature, and heart rate response during exertional heat stress using a double-blind randomized crossover design., Methods: On two occasions separated by >48 h, 20 healthy adults (10 females, 23 ± 3 y, BSA: 1.9 ± 0.2 m2, BMI: 23.7 ± 2.2 kg·m-2) orally consumed either 50 mg of DPH or placebo (PLA), and then rested for 2 h in a climate-controlled room maintained at 30 °C and 35%RH (Heat Index of ~29 °C), followed by a 60-minute fixed-heat production treadmill walk (6.3 ± 1.0 W·kg-1). Whole-body sweat loss (WBSL), local sweat rate (LSR), rectal temperature (Trec), and heart rate (HR) were measured., Results: WBSL was not different between conditions (PLA: 406 ± 78 g; DPH: 396 ± 75 g, P = 0.26, treatment effect: -10 g 95%CI [-28, 8]). No differences were observed for the onset for sweating (PLA: 13.5 ± 2.4 min; DPH: 13.3 ± 2.7 mins, P = 0.79), and steady-state LSR (PLA: 0.83 ± 0.26 mg·cm-2·min-1; DPH: 0.82 ± 0.27 mg·cm-2·min-1, P = 0.99). No difference in baseline Trec was observed (PLA: 37.09 ± 0.35 °C, DPH: 37.13 ± 0.33 °C, P = 0.68), and the 60-min ΔTrec was not different (P = 0.99) between PLA (0.83 ± 0.29 °C) and DPH (0.81 ± 0.30 °C). HR was similar at baseline (PLA: 86 ± 13 BPM, DPH: 84 ± 11 BPM, P = 0.30) and end-exercise (PLA: 134 ± 28 BPM, DPH: 132 ± 26BPM, P = 0.90)., Conclusions: 50 mg of DPH does not modify the sweating, core temperature, and heart rate response during exertional heat stress in young healthy adults., Competing Interests: Conflict of Interest and Funding Source: This research was supported by Dr. Ravanelli’s Research Seed Grant from the Centre for Research in Occupational Safety & Health, and by Dr. Ravanelli’s Natural Sciences and Engineering Research Council of Canada Discovery Grant (PIN#2022-05096). Dr. Nicholas Ravanelli is an executive faculty member at the Centre for Research in Occupational Safety & Health. All other authors have no conflicts of interest that are directly relevant to the content of this article., (Copyright © 2024 by the American College of Sports Medicine.)

The present study assessed agreement between a wireless sweat rate monitor (KuduSmart® device) and the ventilated capsule (VC) technique for measuring: (i) minute-averaged local sweat rate (LSR), (ii) sweating onset, (iii) sudomotor thermosensitivity, and (iv) steady-state LSR, during passive heat stress and exercise. It was hypothesized that acceptable agreement with no bias would be observed between techniques for all assessed sweating characteristics. On two separate occasions for each intervention, participants were either passively heated by recirculating hot water (49 °C) through a tube-lined garment until rectal temperature increased 1 °C over baseline ( n  = 8), or a 60 min treadmill march at a fixed rate of heat production (∼500 W, n  = 9). LSR of the forearm was concurrently measured with a VC and the KuduSmart® device secured within ∼2 cm. Using a ratio scale Bland-Altman analysis with the VC as the reference, the KuduSmart® device demonstrated systematic bias and not acceptable agreement for minute-averaged LSR (1.17 [1.09, 1.27], CV = 44.5%), systematic bias and acceptable agreement for steady-state LSR (1.16 [1.09,1.23], CV = 19.5%), no bias and acceptable agreement for thermosensitivity (1.07 [0.99, 1.16], CV = 23.2%), and no bias and good agreement for sweating onset (1.00 [1.00, 1.00], CV = 11.1%). In total, ≥73% of all minute-averaged LSR observations with the KuduSmart ® device ( n  = 2743) were within an absolute error of <0.2 mg/cm 2 /min to the VC, the reference minimum detectable change in measurement error of a VC on the forearm. Collectively, the KuduSmart ® device may be a satisfactory solution for assessing the sweating response to heat stress where a VC is impractical., Competing Interests: The KuduSmart® device was provided at no cost to Dr. Nicholas Ravanelli from Crossbridge Scientific Ltd. Crossbridge Scientific Ltd was not involved in study design, data collection, analysis, interpretation of results, or manuscript preparation.

Regular Finnish sauna use is associated with a reduced risk of cardiovascular mortality. However, physiological mechanisms underlying this association remain unknown. This study determined if an 8-wk Finnish sauna intervention improves peripheral endothelial function, microvascular function, central arterial stiffness, and blood pressure in adults with coronary artery disease (CAD). Forty-one adults (62 ± 6 yr, 33 men/8 women) with stable CAD were randomized to 8 wk of Finnish sauna use ( n = 21, 4 sessions/wk, 20-30 min/session, 79°C, 13% relative humidity) or a control intervention ( n = 20, lifestyle maintenance). Brachial artery flow-mediated dilation (FMD), carotid-femoral pulse wave velocity (cf-PWV), total (area under the curve) and peak postocclusion forearm reactive hyperemia, and blood pressure (automated auscultation) were measured before and after the intervention. After the sauna intervention, resting core temperature was lower (-0.27°C [-0.54, -0.01], P = 0.046) and sweat rate during sauna exposure was greater (0.3 L/h [0.1, 0.5], P = 0.003). The change in brachial artery FMD did not differ between interventions (control: 0.07% [-0.99, +1.14] vs. sauna: 0.15% [-0.89, +1.19], interaction P = 0.909). The change in total ( P = 0.031) and peak ( P = 0.024) reactive hyperemia differed between interventions due to a nonsignificant decrease in response to the sauna intervention and an increase in response to control. The change in cf-PWV ( P = 0.816), systolic ( P = 0.951), and diastolic ( P = 0.292) blood pressure did not differ between interventions. These results demonstrate that four sessions of Finnish sauna bathing per week for 8 wk does not improve markers of vascular health in adults with stable CAD. NEW & NOTEWORTHY This study determined if unsupervised Finnish sauna bathing for 8 wk improves markers of vascular health in adults with coronary artery disease. Finnish sauna bathing reduced resting core temperature and improved sweating capacity, indicative of heat acclimation. Despite evidence of heat acclimation, Finnish sauna bathing did not improve markers of endothelial function, microvascular function, arterial stiffness, or blood pressure.

Introduction: The prevalence of hypertension is greater in postmenopausal females compared with males of similar age. Previous meta-analyses of normotensive and hypertensive adults have shown that aerobic exercise training reduces systolic blood pressure (SBP) and/or diastolic blood pressure (DBP). However, the effect of aerobic exercise training on blood pressure specifically within healthy postmenopausal females remains unclear. This systematic review with meta-analysis quantified the effect of aerobic exercise training on resting SBP and DBP in healthy postmenopausal females., Methods: The systematic review and meta-analysis followed the Preferred Reporting Items for Systematic Review and Meta-analyses guidelines and was registered in PROSPERO (CRD42020198171). The literature search was done in MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials, CINAHL Plus, and SPORTDiscus. Randomized controlled trials involving healthy postmenopausal females with normal or high normal blood pressure and undergoing ≥4 wk of aerobic exercise training were included. The total weighted mean change in SBP and DBP was compared between the exercise and the control interventions. A random-effects model was used to calculate the overall effect sizes of the weighted mean differences and the 95% confidence interval (CI)., Results: Twelve studies were included in the meta-analysis (exercise interventions: n = 357, age = 60 ± 4 yr, baseline SBP/DBP = 128 ± 13/79 ± 8 mm Hg; control interventions: n = 330, age = 60 ± 4 yr, baseline SBP/DBP = 126 ± 11/77 ± 6 mm Hg). Compared with the change observed in response to the control interventions, exercise training significantly reduced SBP (-0.43 mm Hg, 95% CI = -0.78 to -0.09, P = 0.02) and DBP (-0.39 mm Hg, 95% CI = -0.73 to -0.05, P = 0.05)., Conclusions: Aerobic exercise training significantly reduces resting SBP and DBP in healthy postmenopausal females with normal or high normal blood pressure. However, this reduction is small and of uncertain clinical significance., (Copyright © 2023 by the American College of Sports Medicine.)

Background: Heat waves caused by climate change are increasingly challenging the wellbeing of individuals across the lifespan. Current efforts to understand the thermal perceptions and behaviours of people throughout the lifespan during heat waves are limited. Methods: Since June 2021, the Active Heatwave project has been recruiting households to better understand how individuals perceive, cope, and behave during heat waves. Using our novel web platform, participants were prompted to answer our Heat Alert Survey on days when a participants geolocation corresponded to a broadcasted local heat alert. Participants provided 24-h movement behaviour, thirst, thermal perception, and cooling strategies via validated questionnaires. Results: A total of 285 participants (118 children) from 60 distinct weather station locations globally participated between June and September 2021 and 2022. At least 1 heat alert (834 total) were identified from 95% (57/60) of the weather stations. Children reported spending more time performing vigorous intensity exercise compared to adults ( p < 0.05), but no differences in thermal sensation, thermal comfort, or thirst sensation (all p > 0.31) were observed. For thirst management, 88% of respondents used water to relieve thirst, although notably, 15% of adults reported using alcohol. Regardless of age, staying indoors was the most common heat management strategy, whereas visiting cooling centres was the least. Conclusion: The present study presents a proof-of-concept combining local heat alert notifications with e-questionnaires for collecting near-real-time perceptual and behavioural data for both children and adults during heat waves. The observed patterns of behaviour suggest that present public heat-health guidelines are often ignored, children engage in fewer heat management strategies compared to adults, and these disparities highlight the need to improve public health communication and knowledge dissemination around promoting effective and accessible cooling solutions for children and adults., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Ravanelli, Morris and Morrison.)

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.)

Extreme heat events are a leading natural hazard risk to human health. Under all future climate change models, extreme heat events will continue to increase in frequency, duration, and intensity. Evidence from previous extreme heat events across the globe demonstrates that adverse cardiovascular events are the leading cause of morbidity and mortality, particularly amongst the elderly and those with pre-existing cardiovascular disease. However, less is understood about the adverse effects of extreme heat amongst specific cardiovascular diseases (i.e., heart failure, dysrhythmias) and demographics (sex, ethnicity, age) within Australia and New Zealand. Furthermore, although Australia has implemented regional and state heat warning systems, most personal heat-health protective advice available in public health policy documents is either insufficient, not grounded in scientific evidence, and/or does not consider clinical factors such as age or co-morbidities. Dissemination of evidence-based recommendations and enhancing community resilience to extreme heat disasters within Australia and New Zealand should be an area of critical focus to reduce the burden and negative health effects associated with extreme heat. This narrative review will focus on five key areas in relation to extreme heat events within Australia and New Zealand: 1) the potential physiological mechanisms that cause adverse cardiovascular outcomes during extreme heat events; 2) how big is the problem within Australia and New Zealand?; 3) what the heat-health response plans are; 4) research knowledge and translation; and, 5) knowledge gaps and areas for future research., (Copyright © 2022 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier B.V. All rights reserved.)

Purpose: The benefits of exercise on vascular health are inconsistent in postmenopausal females. We investigated if blood pressure and markers of vascular function differ between physically active early post- and late premenopausal females., Methods: We performed a cross-sectional comparison of 24-h blood pressure, brachial artery flow-mediated dilation, microvascular reactivity (reactive hyperemia), carotid-femoral pulse wave velocity, and cardiac baroreflex sensitivity between physically active late premenopausal (n = 16, 48 ± 2 yr) and early postmenopausal (n = 14, 53 ± 2 yr) females., Results: Physical activity level was similar between premenopausal (490 ± 214 min·wk-1) and postmenopausal (550 ± 303 min·wk-1) females (P = 0.868). Brachial artery flow-mediated dilation (pre, 4.6 ± 3.9, vs post, 4.7% ± 2.2%; P = 0.724), 24-h systolic (+5 mm Hg, 95% confidence interval [CI] = -1 to +10, P = 0.972) and diastolic (+4 mm Hg, 95% CI = -1 to +9, P = 0.655) blood pressures, total reactive hyperemia (pre, 1.2 ± 0.5, vs post, 1.0 ± 0.5 mL·mm Hg-1; P = 0.479), carotid-femoral pulse wave velocity (pre, 7.9 ± 1.7, vs post, 8.1 ± 1.8 m·s-1; P = 0.477), and cardiac baroreflex sensitivity (-8 ms·mm Hg-1, 95% CI = -20.55 to 4.62, P = 0.249) did not differ between groups. By contrast, peak reactive hyperemia (-0.36 mL·min-1⋅mm Hg-1, 95% CI = -0.87 to +0.15, P = 0.009) was lower in postmenopausal females., Conclusions: These results suggest that blood pressure and markers of vascular function do not differ between physically active late pre- and early postmenopausal females., (Copyright © 2022 by the American College of Sports Medicine.)

Heat therapy is a promising strategy to improve cardiometabolic health. This study evaluated the acute physiological responses to hot water immersion in adults with type 2 diabetes mellitus (T2DM). On separate days in randomized order, 13 adults with T2DM [8 males/5 females, 62 ± 12 yr, body mass index (BMI): 30.1 ± 4.6 kg/m 2 ] were immersed in thermoneutral (34°C, 90 min) or hot (41°C, core temperature ≥38.5°C for 60 min) water. Insulin sensitivity was quantified via the minimal oral model during an oral glucose tolerance test (OGTT) performed 60 min after immersion. Brachial artery flow-mediated dilation (FMD) and reactive hyperemia were evaluated before and 40 min after immersion. Blood samples were drawn to quantify protein concentrations and mRNA levels of HSP70 and HSP90, and circulating concentrations of cytokines. Relative to thermoneutral water immersion, hot water immersion increased core temperature (+1.66°C [+1.47, +1.87], P < 0.01), heart rate (+34 beats/min [+24, +44], P < 0.01), antegrade shear rate (+96 s -1 [+57, +134], P < 0.01), and IL-6 (+1.38 pg/mL [+0.31, +2.45], P = 0.01). Hot water immersion did not exert an acute change in insulin sensitivity (-0.3 dL/kg/min/μU/mL [-0.9, +0.2], P = 0.18), FMD (-1.0% [-3.6, +1.6], P = 0.56), peak (+0.36 mL/min/mmHg [-0.71, +1.43], P = 0.64), and total (+0.11 mL/min/mmHg × min [-0.46, +0.68], P = 0.87) reactive hyperemia. There was also no change in eHSP70 ( P = 0.64), iHSP70 ( P = 0.06), eHSP90 ( P = 0.80), iHSP90 ( P = 0.51), IL1-RA ( P = 0.11), GLP-1 ( P = 0.59), and NF-κB ( P = 0.56) after hot water immersion. The physiological responses elicited by hot water immersion do not acutely improve markers of cardiometabolic function in adults with T2DM. NEW & NOTEWORTHY Heat therapy has been shown to improve markers of cardiometabolic health in preclinical and clinical studies. However, the effects of heat therapy in individuals with type 2 diabetes mellitus (T2DM) remain understudied. We examined the acute effect of hot water immersion on glucose tolerance, flow-mediated dilation, reactive hyperemia, inflammatory markers, and heat shock proteins in adults with T2DM. Hot water immersion did not acutely improve the markers studied.

Objectives: Despite the well-established benefits of exercise, pregnant women are discouraged from physical activity in hot/humid conditions to avoid hyperthermia (core temperature (T core ) ≥ 39.0 °C). Recent epidemiological evidence also demonstrates greater risk of negative birth outcomes following heat exposure during pregnancy, possibly due to thermoregulatory impairments. We aimed to determine (1) the risk of pregnant women exceeding a T core of 39.0 °C during moderate-intensity exercise in the heat; and (2) if any thermoregulatory impairments are evident in pregnant (P) versus non-pregnant (NP) women., Methods: Thirty participants (15 pregnant in their second trimester or third trimester) completed two separate exercise-heat exposures in a climate chamber (32 °C, 45%RH). On separate occasions, each participant cycled on a semi-recumbent cycle ergometer for 45 min at a workload representative of a moderate-intensity (1) non-weight-bearing (NON-WB), or (2) weight-bearing (WB) activity. Thermoregulatory responses were monitored throughout., Results: The highest rectal temperature observed in a pregnant individual was 37.93 °C. Mean end-exercise rectal temperature did not differ between groups (P:37.53 ± 0.22 °C, NP:37.52 ± 0.34 °C, P = 0.954) in the WB trial, but was lower in the P group (P:37.48 ± 0.25 °C, vs NP:37.73 ± 0.38 °C, P = 0.041) in the NON-WB trial. Whole-body sweat loss was unaltered by pregnancy during WB (P:266 ± 62 g, NP:264 ± 77 g; P = 0.953) and NON-WB P:265 ± 51 g, NP:300 ± 75 g; P = 0.145) exercise. Pregnant participants reported higher ratings of thermal sensation (felt hotter) than their non-pregnant counterparts in the WB trial (P = 0.002) but not in the NON-WB trial, (P = 0.079)., Conclusion: Pregnant women can perform 45 min of moderate-intensity exercise at 32 °C, 45%RH with very low apparent risk of excessive maternal hyperthermia. No thermoregulatory impairments with pregnancy were observed., (© 2021. The Author(s), under exclusive licence to Springer Nature Switzerland AG.)

Human thermoregulatory control is often evaluated through the relationship between thermoeffector output and core or mean body temperature. In addition to providing a general indication of whether a variable of interest alters thermoregulatory control, this relationship is often used to determine how this alteration may occur. This latter interpretation relies upon two parameters of the thermoeffector output-body temperature relationship: the onset threshold and thermosensitivity. Traditionally, changes in the onset threshold and thermosensitivity are interpreted as "central" or "peripheral" modulation of thermoregulatory control, respectively. This mini-review revisits the origins of the thermoeffector output-body temperature relationship and its use to interpret "central" or "peripheral" modulation of thermoregulatory control. Against this background, we discuss the strengths and weaknesses of this approach and highlight that "central" thermoregulatory control reflects the neural control of body temperature whereas "peripheral" thermoregulatory control reflects properties specific to the thermoeffector organs. We highlight studies that employed more direct approaches to investigate the neural control of body temperature and peripheral properties of thermoeffector organs. We conclude by encouraging future investigations interested in studying thermoregulatory control to more directly investigate the component of the thermoeffector loop under investigation.heat; human; skin blood flow; sweat; thermoregulatory.

Introduction: Exercise thermoregulation studies typically control for time of day. The present study assessed whether circadian rhythm independently alters time-dependent changes in core temperature and sweating during exercise at a fixed rate of metabolic heat production (Hprod) during the wake period., Methods: Ten men (26 ± 2 yr, 76.6 ± 6.3 kg, 1.95 ± 0.10 m2) cycled for 60 min in three combinations of ambient temperature and Hprod (23°C-7.5 W·kg-1, 33°C-5.5 W·kg-1, and 33°C-7.5 W·kg-1) at two times of day (a.m.: 0800 h, p.m.: 1600 h). Rectal temperature (Tre), local sweat rate, and whole-body sweat losses were measured., Results: Absolute Tre was lower at baseline in a.m. versus p.m. for all three conditions (a.m.: 36.8°C ± 0.2°C, p.m.: 37.0°C ± 0.2°C, P < 0.01). The ΔTre was not altered by time of day (P > 0.22) and not different at 60 min between a.m. and p.m. for 23°C-7.5 W·kg-1 (a.m.: 0.83°C ± 0.14°C, p.m.: 0.75°C ± 0.20°C; P = 0.20), 33°C-5.5 W·kg-1 (a.m.: 0.51°C ± 0.14°C, p.m.: 0.47°C ± 0.14°C; P = 0.22), and 33°C-7.5 W·kg-1 (a.m.: 0.77°C ± 0.20°C, p.m.: 0.73°C ± 0.21°C; P = 0.80). The change in local sweat rate was unaffected by time of day (P > 0.16) and not different at 60 min in 23°C-7.5 W·kg-1 (a.m.: 0.67 ± 0.20 mg·cm-2·min-1, p.m.: 0.62 ± 0.21 mg·cm-2·min-1; P = 0.55), 33°C-5.5 W·kg-1 (a.m.: 0.59 ± 0.13 mg·cm-2·min-1, p.m.: 0.57 ± 0.12 mg·cm-2·min-1; P = 0.65), and 33°C-7.5 W·kg-1 (a.m.: 0.91 ± 0.19 mg·cm-2·min-1, p.m.: 0.84 ± 0.15 mg·cm-2·min-1; P = 0.33). Whole-body sweat loss was not different between a.m. and p.m. for 23°C-7.5 W·kg-1 (a.m.: 579 ± 72 g, p.m.: 579 ± 96 g; P = 0.99), 33°C-5.5 W·kg-1 (a.m.: 558 ± 48 g, p.m.: 555 ± 83 g; P = 0.89), and 33°C-7.5 W·kg-1 (a.m.: 796 ± 72 g, p.m.: 783 ± 75 g; P = 0.31)., Conclusions: The change in core temperature and sweating throughout a 60-min exercise bout in 23°C and 33°C were unaffected by circadian rhythm during the wake period when exercise intensity was prescribed to elicit comparable rates of Hprod, suggesting that scheduling thermoregulatory exercise trials for the same time of day is unnecessary., (Copyright © 2020 by the American College of Sports Medicine.)

COVID-19 may increase the risk of heat-related symptoms during hot weather since vulnerable populations, including the elderly and those with neurological disabilities, must continue to self-isolate, often indoors. Within the chronic neurological patient population, indoor conditions in summer months present a hazard because of impaired and/or altered thermoregulation, including poor hydration status due to both autonomic and behavioral dysfunction(s). To address this increased risk, telemedicine protocols should include an assessment of the patient's environmental parameters, and when combined with physiological data from wearable devices, identify those with neurological diseases who are at higher risk of heat illness. Personalized medicine during times of self-isolation must be encouraged, and using smart technology in ambient assisted living solutions, including e-health to monitor physiological parameters are highly recommended, not only during extreme weather conditions but also during times of increased isolation and vulnerability.

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.)

Key Points: When exercise was prescribed to elicit a fixed evaporative heat balance requirement (E req ), no differences in steady-state sweat rates were observed with different absolute oesophageal and/or skin temperatures, secondary to differences in time of the day (i.e. morning (AM) vs. afternoon (PM)) and ambient temperature (i.e. 23°C vs. 33°C). Exercise at a fixed metabolic heat production (H prod ), but a different E req (due to differences in air temperature), yielded higher steady-state sweat rates with a higher E req , irrespective of absolute oesophageal temperature. Circadian rhythm did not alter the change in core temperature prior to the onset for sudomotor activation, nor the thermosensitivity, resulting in similar cumulative whole-body sweat rates irrespective of time of day at a fixed E req . Collectively, these data indicate that during exercise in a compensable environment, steady-state sudomotor responses are influenced by E req rather than absolute core and skin temperatures, or H prod ., Abstract: The present study sought to determine whether absolute core temperature (modified via diurnal variation) and absolute skin temperature (modified by different air temperatures (T a )) alters the steady-state sweating response to exercise at a fixed evaporative heat balance requirement (E req ). Ten males exercised for 60 min on six occasions. Three T a /heat production (H prod ) combinations (23°C/525 W, 33°C/400 W, 33˚C/525 W) were completed in the morning (08.00 h, AM) and afternoon (16.00 h, PM), to yield: (1) the same E req (200 or 275 W·m -2 ) with different absolute core temperatures (AM vs. PM); (2) the same E req (200 W·m -2 ) with different skin temperatures (T a : 23˚C vs. 33˚C); (3) the same heat production (525 W) with different E req (200 vs. 275 W·m -2 ). Oesophageal temperature (T oes ), local sweat rate (LSR) on the arm and upper-back, and whole-body sweat rate (WBSR) were measured. Steady-state T oes was always higher in PM versus AM at an E req of 200 W·m -2 (23°C, P = 0.001; 33°C, P = 0.004) and 275 W·m -2 , (33°C, P = 0.001). However steady-state mean LSR (200 W·m -2 /23°C: P = 0.25; 200 W·m -2 /33°C: P = 0.86; 275 W·m -2 /33°C: P = 0.53) and WBSR (200 W·m -2 /23°C: P = 0.79; 200 W·m -2 /33°C: P = 0.48; 275W·m -2 /33°C: P = 0.32) were similar. When E req was matched (200 W·m -2 ) with different T a (23°C vs. 33°C), steady-state LSR (P > 0.17) and WBSR (P > 0.93) were similar despite different skin temperatures. For the same H prod (525 W) but different E req (200 vs. 275 W·m -2 ), mean LSR (P < 0.001), and WBSR (P < 0.001) were higher with a greater E req . Collectively, steady-state sweating during exercise is altered by E req but not T oes , skin temperature, or H prod ., (© 2020 The Authors. The Journal of Physiology © 2020 The Physiological Society.)

Purpose: Studies often assess the impact of sex on the relation between core body temperature (CBT), whole-body sweat rate (WBSR), and heat production during exercise in laboratory settings, but less is known in free-living conditions. Therefore, the authors compared the relation between CBT, WBSR, and heat production between sexes in a 15-km race under cool conditions., Methods: During 3 editions of the Seven Hills Run (Nijmegen, the Netherlands) with similar ambient conditions (8-12°C, 80-95% relative humidity), CBT and WBSR were measured among 375 participants (52% male) before and immediately after the 15-km race. Heat production was estimated using initial body mass and mean running speed, assuming negligible external work., Results: Men finished the race in 76 (12) minutes and women in 83 (13) minutes (P < .001, effect size [ES] = 0.55). Absolute heat production was higher in men than in women (1185 [163] W vs 867 [122] W, respectively, P < .001, ES = 1.47), even after normalizing to body mass (15.0 [2.2] W/kg vs 13.8 [1.9] W/kg, P < .001, ES = 0.56). Finish CBT did not differ between men and women (39.2°C [0.7°C] vs 39.2°C [0.7°C], P = .71, ES = 0.04). Men demonstrated a greater increase in CBT (1.5°C [0.8°C] vs 1.3°C [0.7°C], respectively, P = .013, ES = 0.31); the sex difference remains after correcting for heat production (P = .004). WBSR was larger in men (18.0 [6.9] g/min) than in women (11.4 [4.7] g/min; P < .001, ES = 0.97). A weak correlation between WBSR and heat production was found irrespective of sex (R2 = .395, P < .001)., Conclusions: WBSR was associated with heat production, irrespective of sex, during a self-paced 15-km running race in cool environmental conditions. Men had a higher ΔCBT than women.

Key Points: With the advent of more frequent extreme heat events, adaptability to hot environments will be crucial for the survival of many species, including humans. However, the mechanisms that mediate human heat adaptation have remained elusive. We tested the hypothesis that heat acclimation improves the neural control of body temperature. Skin sympathetic nerve activity, comprising the efferent neural signal that activates heat loss thermoeffectors, was measured in healthy adults exposed to passive heat stress before and after a 7 day heat acclimation protocol. Heat acclimation reduced the activation threshold for skin sympathetic nerve activity, leading to an earlier activation of cutaneous vasodilatation and sweat production. These findings demonstrate that heat acclimation improves the neural control of body temperature in humans., Abstract: Heat acclimation improves autonomic temperature regulation in humans. However, the mechanisms that mediate human heat adaptation remain poorly understood. The present study tested the hypothesis that heat acclimation improves the neural control of body temperature. Body temperatures, skin sympathetic nerve activity, cutaneous vasodilatation, and sweat production were measured in 14 healthy adults (nine men and five women, aged 27 ± 5 years) during passive heat stress performed before and after a 7 day heat acclimation protocol. Heat acclimation increased whole-body sweat rate [+0.54 L h -1 (0.32, 0.75), P < 0.01] and reduced resting core temperature [-0.29°C (-0.40, -0.18), P < 0.01]. During passive heat stress, the change in mean body temperature required to activate skin sympathetic nerve activity was reduced [-0.21°C (-0.34, -0.08), P < 0.01] following heat acclimation. The earlier activation of skin sympathetic nerve activity resulted in lower activation thresholds for cutaneous vasodilatation [-0.18°C (-0.35, -0.01), P = 0.04] and local sweat rate [-0.13°C (-0.24, -0.01), P = 0.03]. These results demonstrate that heat acclimation leads to an earlier activation of the neural efferent outflow that activates the heat loss thermoeffectors of cutaneous vasodilatation and sweating., (© 2020 The Authors. The Journal of Physiology © 2020 The Physiological Society.)

This study assessed whether, notwithstanding lower resting absolute core temperatures, alterations in time-dependent changes in thermoregulatory responses following partial and complete heat acclimation (HA) are only evident during uncompensable heat stress. Eight untrained individuals underwent 8 wk of aerobic training (i.e., partial HA) followed by 6 days of HA in 38°C/65% relative humidity (RH) (i.e., complete HA). On separate days, esophageal temperature (T es ), arm (LSR arm ), and back (LSR back ) sweat rate, and whole body sweat rate (WBSR) were measured during a 45-min compensable (37°C/30% RH) and 60-min uncompensable (37°C/60% RH) heat stress trial pre-training (PRE-TRN), post-training (POST-TRN), and post-heat acclimation (POST-HA). For compensable heat stress trials, resting T es was lower POST-TRN (36.74 ± 0.27°C, P = 0.05) and POST-HA (36.60 ± 0.27°C, P = 0.001) compared with PRE-TRN (36.99 ± 0.19°C); however, ΔT es was similar in all trials (PRE-TRN:0.40 ± 0.23°C; POST-TRN:0.42 ± 0.20°C; POST-HA:0.43 ± 0.12°C, P = 0.97). While LSR back was unaltered by HA ( P = 0.94), end-exercise LSR arm was higher POST-TRN (0.70 ± 0.14 mg·cm -2 ·min -1 , P < 0.001) and POST-HA (0.75 ± 0.16 mg·cm -2 ·min -1 , P < 0.001) compared with PRE-TRN (0.61 ± 0.15 mg·cm -2 ·min -1 ). Despite matched evaporative heat balance requirements, steady-state WBSR (31st-45th min) was greater POST-TRN (12.7 ± 1.0 g/min, P = 0.02) and POST-HA (12.9 ± 0.8 g/min, P = 0.004), compared with PRE-TRN (11.7 ± 0.9 g/min). For uncompensable heat stress trials, resting T es was lower POST-TRN (36.77 ± 0.22°C, P = 0.05) and POST-HA (36.62 ± 0.15°C, P = 0.03) compared with PRE-TRN (36.86 ± 0.24°C). But ΔT es was smaller POST-TRN (0.77 ± 0.19°C, P = 0.05) and POST-HA (0.75 ± 0.15°C, P = 0.04) compared with PRE-TRN (1.10 ± 0.32°C). LSR back and LSR arm increased with HA ( P < 0.007), supporting the greater WBSR with HA (POST-TRN:14.4 ± 2.4 g/min, P < 0.001; POST-HA:16.8 ± 2.8 g/min, P < 0.001) compared with PRE-TRN (12.7 ± 3.2 g/min). In conclusion, the thermal benefits of HA are primarily evident when conditions challenge the physiological capacity to dissipate heat. NEW & NOTEWORTHY We demonstrate that neither partial nor complete heat acclimation alters the change in core temperature during compensable heat stress compared with an unacclimated state, despite a marginally greater whole body sweat rate. However, the greater local and whole body sweat rate with partial and complete heat acclimation reduced the rise in core temperature during 60 min of uncompensable heat stress compared with an unacclimated state, suggesting the improvements in heat dissipation associated with heat acclimation are best observed when the upper physiological limits for evaporative heat loss are challenged.

Objective: Pregnant women are advised to avoid heat stress (eg, excessive exercise and/or heat exposure) due to the risk of teratogenicity associated with maternal hyperthermia; defined as a core temperature (T core ) ≥39.0°C. However, guidelines are ambiguous in terms of critical combinations of climate and activity to avoid and may therefore unnecessarily discourage physical activity during pregnancy. Thus, the primary aim was to assess T core elevations with different characteristics defining exercise and passive heat stress (intensity, mode, ambient conditions, duration) during pregnancy relative to the critical maternal T core of ≥39.0°C., Design: Systematic review with best evidence synthesis., Data Sources: EMBASE, MEDLINE, SCOPUS, CINAHL and Web of Science were searched from inception to 12 July 2017., Study Eligibility Criteria: Studies reporting the T core response of pregnant women, at any period of gestation, to exercise or passive heat stress, were included., Results: 12 studies satisfied our inclusion criteria (n=347). No woman exceeded a T core of 39.0°C. The highest T core was 38.9°C, reported during land-based exercise. The highest mean end-trial T core was 38.3°C (95% CI 37.7°C to 38.9°C) for land-based exercise, 37.5°C (95% CI 37.3°C to 37.7°C) for water immersion exercise, 36.9°C (95% CI 36.8°C to 37.0°C) for hot water bathing and 37.6°C (95% CI 37.5°C to 37.7°C) for sauna exposure., Conclusion: The highest individual core temperature reported was 38.9°C. Immediately after exercise (either land based or water immersion), the highest mean core temperature was 38.3°C; 0.7°C below the proposed teratogenic threshold. Pregnant women can safely engage in: (1) exercise for up to 35 min at 80%-90% of their maximum heart rate in 25°C and 45% relative humidity (RH); (2) water immersion (≤33.4°C) exercise for up to 45 min; and (3) sitting in hot baths (40°C) or hot/dry saunas (70°C; 15% RH) for up to 20 min, irrespective of pregnancy stage, without reaching a core temperature exceeding the teratogenic threshold., Competing Interests: Competing interests: None declared., (© Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2019. All rights reserved. No commercial use is permitted unless otherwise expressly granted.)

Purpose: To quantify how maximum skin wettedness (ωmax); that is, the determinant of the boundary between compensable and uncompensable heat stress, is altered by aerobic training in previously unfit individuals and further augmented by heat acclimation., Methods: Eight untrained individuals completed an 8-wk aerobic training program immediately followed by 8 d of hot/humid (38°C, 65%RH) heat acclimation. Participants completed a humidity ramp protocol pretraining (PRE-TRN), posttraining (POST-TRN), and after heat acclimation (POST-HA), involving treadmill marching at a heat production of 450 W for 105 min in 37.5°C, 2.0 kPa (35%RH). After attaining a steady-state esophageal temperature (Tes), humidity increased 0.04 kPa·min. An upward inflection in Tes indicated the upper limit of physiological compensability (Pcrit), which was then used to quantify ωmax. Local sweat rate, activated sweat gland density, and sweat gland output on the back and arm were simultaneously measured throughout., Results: Peak aerobic capacity increased POST-TRN by approximately 14% (PRE-TRN: 45.8 ± 11.8 mL·kg·min; POST-TRN: 52.0 ± 11.1 mL·kg·min, P < 0.001). ωmax values became progressively greater from PRE-TRN (0.72 ± 0.06) to POST-TRN (0.84 ± 0.08; P = 0.02), to POST-HA (0.95 ± 0.05; P = 0.03). These shifts in ωmax were facilitated by a progressively greater local sweat rate and activated sweat gland density from PRE-TRN (0.84 ± 0.21 mg·cm·min; 67 ± 20 glands per square centimeter) to POST-TRN (0.96 ± 0.21 mg·cm·min, P = 0.03; 86 ± 27 glands per square centimeter; P = 0.009), to POST-HA (1.15 ± 0.21 mg·cm·min; P < 0.001; 98 ± 35 glands per square centimeter; P < 0.001). No differences in sweat gland output were observed., Conclusions: A greater ωmax occurred after 8 wk of aerobic training, but ωmax was further augmented with heat acclimation, indicating only a partially increased heat loss capacity with training. These ωmax values may assist future predictions of heat stress risk in untrained/trained unacclimated individuals and trained heat-acclimated individuals.

Some studies have observed a functional relationship between sweating and skin blood flow. However, the implications of this relationship during physiologically relevant conditions remain unclear. We manipulated sudomotor activity through changes in sweating efficiency to determine if parallel changes in vasomotor activity are observed. Eight young men completed two trials at 36°C and two trials at 42°C. During these trials, air temperature remained constant while ambient vapor pressure increased from 1.6 to 5.6 kPa over 2 h. Forced airflow across the skin was used to create conditions of high (HiS eff ) or low (LoS eff ) sweating efficiency. Local sweat rate (LSR), local skin blood flow (SkBF), as well as mean skin and esophageal temperatures were measured continuously. It took longer for LSR to increase during HiS eff at 36°C (HiS eff : 99 ± 11 vs. LoS eff : 77 ± 11 min, P < 0.01) and 42°C (HiS eff : 72 ± 16 vs. LoS eff : 51 ± 15 min, P < 0.01). In general, an increase in LSR preceded the increase in SkBF when expressed as ambient vapor pressure and time for all conditions ( P < 0.05). However, both responses were activated at a similar change in mean body temperature (average across all trials, LSR: 0.26 ± 0.15 vs. SkBF: 0.30 ± 0.18°C, P = 0.26). These results demonstrate that altering the point at which LSR is initiated during heat exposure is paralleled by similar shifts for the increase in SkBF. However, local sweat production occurs before an increase in SkBF, suggesting that SkBF is not necessarily a prerequisite for sweating., (Copyright © 2017 the American Physiological Society.)

This study sought to assess the within-subject influence of acute hypoxia on exercise-induced changes in core temperature and sweating. Eight participants [1.75 (0.06) m, 70.2 (6.8) kg, 25 (4) yr, 54 (8) ml·kg -1 ·min -1 ] completed 45 min of cycling, once in normoxia (NORM; [Formula: see text] = 0.21) and twice in hypoxia (HYP1/HYP2; [Formula: see text]= 0.13) at 34.4(0.2)°C, 46(3)% RH. These trials were designed to elicit 1 ) two distinctly different %V̇o 2peak [NORM: 45 (8)% and HYP1: 62 (7)%] at the same heat production (H prod ) [NORM: 6.7 (0.6) W/kg and HYP1: 7.0 (0.5) W/kg]; and 2 ) the same %V̇o 2peak [NORM: 45 (8)% and HYP2: 48 (5)%] with different H prod [NORM: 6.7 (0.6) W/kg and HYP2: 5.5 (0.6) W/kg]. At a fixed %V̇o 2peak , changes in rectal temperature (ΔT re ) and changes in esophageal temperature (ΔT es ) were greater at end-exercise in NORM [ΔT re : 0.76 (0.19)°C; ΔT es : 0.64 (0.22)°C] compared with HYP2 [ΔT re : 0.56 (0.22)°C, P < 0.01; ΔT es : 0.42 (0.21)°C, P < 0.01]. As a result of a greater H prod ( P < 0.01) in normoxia, and therefore evaporative heat balance requirements, to maintain a similar %V̇o 2peak compared with hypoxia, mean local sweat rates (LSR) from the forearm, upper back, and forehead were greater (all P < 0.01) in NORM [1.10 (0.20) mg·cm -2 ·min -1 ] compared with HYP2 [0.71 (0.19) mg·cm -2 ·min -1 ]. However, at a fixed H prod , ΔT re [0.75 (0.24)°C; P = 0.77] and ΔT es [0.63 (0.29)°C; P = 0.69] were not different in HYP1, compared with NORM. Likewise, mean LSR [1.11 (0.20) mg·cm -2 ·min -1 ] was not different ( P = 0.84) in HYP1 compared with NORM. These data demonstrate, using a within-subjects design, that hypoxia does not independently influence thermoregulatory responses. Additionally, further evidence is provided to support that metabolic heat production, irrespective of %V̇o 2peak , determines changes in core temperature and sweating during exercise. NEW & NOTEWORTHY Using a within-subject design, hypoxia does not independently alter core temperature and sweating during exercise at a fixed rate of heat production. These findings also further contribute to the development of a methodological framework for assessing differences in thermoregulatory responses to exercise between various populations and individuals. Using the combined environmental stressors of heat and hypoxia we conclusively demonstrate that exercise intensity relative to aerobic capacity (i.e., %V̇o 2max ) does not influence changes in thermoregulatory responses., (Copyright © 2017 the American Physiological Society.)

We sought to identify the appropriate exercise intensity for unbiased comparisons of changes in rectal temperature (ΔT re ) and local sweat rates (LSR) between groups unmatched for body size during uncompensable heat stress. Sixteen males vastly different in body morphology were separated into two equal groups [small (SM): 65.8 ± 6.2 kg, 1.8 ± 0.1 m 2 ; large (LG): 100.0 ± 13.1 kg, 2.3 ± 0.1 m 2 ], but matched for sudomotor thermosensitivity (SM: 1.3 ± 0.6; LG: 1.1 ± 0.4 mg·cm -2 ·min -1 ·°C -1 ). The maximum potential for evaporation (E max ) for each participant was assessed using an incremental humidity protocol. On separate occasions, participants then completed 60 min of cycling in a 35°C and 70% RH environment at (1) 50% of VO 2max , (2) a heat production (H prod ) of 520 W, (3) H prod relative to mass (6 W·kg -1 ), and (4) H prod relative to mass above E max (3 W·kg -1 >E max ). E max was similar between LG (347 ± 39 W, 154 ± 15 W·m -2 ) and SM (313 ± 63 W, 176 ± 34 W·m -2 , P  >   0.12). ΔT re was greater in SM compared to LG at 520 W (SM: 1.5 ± 0.5; LG 0.8 ± 0.3°C, P  <   0.001) and at 50% of VO 2max (SM: 1.4 ± 0.5; LG 0.9 ± 0.3°C, P  <   0.001). However, ΔT re was similar between groups when H prod was either 6 W·kg -1 (SM: 0.9 ± 0.3; LG 0.9 ± 0.2°C, P  =   0.98) and 3 W·kg -1 >E max (SM: 1.4 ± 0.5; LG 1.3 ± 0.4°C, P  =   0.99). LSR was similar between LG and SM irrespective of condition, suggesting maximum LSR was attained (SM: 1.10 ± 0.23; LG: 1.07 ± 0.35 mg·cm -2 ·min -1 , P  =   0.50). In conclusion, systematic differences in ΔT re and LSR between groups unmatched for body size during uncompensable heat stress can be avoided by a fixed H prod in W·kg -1 or W·kg -1 >E max ., (© 2017 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.)

The systemic inflammatory response syndrome (SIRS) is triggered by lipopolysaccharide (LPS) from Gram-negative bacteria. Insulin was shown to have a protective role in SIRS related to sepsis. Lungs are particularly affected in this condition and provide a second wave of mediators/cytokines which amplifies SIRS. The aim of the present study was to investigate the effect of insulin on the signaling pathways elicited by LPS in alveolar macrophages (AMs) and its consequence in cellular response to LPS measured as production of tumor necrosis factor (TNF). To this purpose, resident AMs from male Wistar rats were obtained by lung lavage and stimulated by LPS (100 ng/mL). Insulin (1 mU/mL) was added 10 min before LPS. Activation (phosphorylation) of signaling molecules by LPS was analyzed by western blot, 30 min after LPS stimulation. TNF was measured in the AMs culture supernatants by bioassay using L-929 tumor cells. Relative to controls, LPS induced a significant increase in the activation of ERK (3.6-fold), p38 (4.4-fold), Tyr-326 Akt (4.7-fold), Ser-473 Akt (6.9-fold), PKCalpha (4.7-fold) and PKCdelta (2.3-fold). Treatment of AMs with insulin before LPS stimulation, significantly reduced the activation of ERK (54%), p38 (48%), Tyr-326 Akt (64%), Ser-473 Akt (41%), PKCalpha (62%) and PKCdelta (39%). LPS induced TNF production in AMs which was also inhibited by insulin (60%). These results show that insulin down-regulates MAPK, PI3K and PKCs and inhibits a downstream effect of LPS, TNF production, in rat AMs stimulated with LPS and suggest that the protective effect of insulin in sepsis could be through modulation of signal transduction pathways elicited by LPS in lung macrophages., ((c) 2008 S. Karger AG, Basel)

The development of septic shock is a common and frequently lethal consequence of gram-negative infection. Mediators released by lung macrophages activated by bacterial products such as lipopolysaccharide (LPS) contribute to shock symptoms. We have shown that insulin down-regulates LPS-induced TNF production by alveolar macrophages (AMs). In the present study, we investigated the effect of insulin on the LPS-induced production of nitric oxide (NO) and prostaglandin (PG)-E(2), on the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2, and on nuclear factor kappa B (NF-kappaB) activation in AMs. Resident AMs from male Wistar rats were stimulated with LPS (100 ng/mL) for 30 minutes. Insulin (1 mU/mL) was added 10 min before LPS. Enzymes expression, NF-kappaB p65 activation and inhibitor of kappa B (I-kappaB)alpha phosphorylation were assessed by immunobloting; NO by Griess reaction and PGE(2) by enzyme immunoassay (EIA). LPS induced in AMs the expression of iNOS and COX-2 proteins and production of NO and PGE(2), and, in parallel, NF-kappaB p65 activation and cytoplasmic I-kappaBalpha phosphorylation. Administration of insulin before LPS suppressed the expression of iNOS and COX-2, of NO and PGE(2) production and Nuclear NF-kappaB p65 activation. Insulin also prevented cytoplasmic I-kappaBalpha phosphorylation. These results show that in AMs stimulated by LPS, insulin prevents nuclear translocation of NF-kappaB, possibly by blocking I-kappaBalpha degradation, and supresses the production of NO and PGE(2), two molecules that contribute to septic shock., (Copyright 2008 S. Karger AG, Basel.)