Agreement between the ventilated capsule and the KuduSmart® device for measuring sweating responses to passive heat stress and exercise.

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/cm2/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.

Finnish sauna bathing and vascular health of adults with coronary artery disease: a randomized controlled trial.

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.

24-h movement behaviour, thermal perception, thirst, and heat management strategies of children and adults during heat alerts: a pilot study.

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.

Effect of Exercise Training on Blood Pressure in Healthy Postmenopausal Females: A Systematic Review with Meta-analysis.

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.

Impact of passive heat stress and passive heat acclimation on circulating extracellular vesicles: An exploratory analysis.

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.

The acute effect of heat exposure on forearm macro- and microvascular function: Impact of measurement timing, heating modality and biological sex.

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.

Extreme Heat and Adverse Cardiovascular Outcomes in Australia and New Zealand: What Do We Know?

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.

Comparison of Blood Pressure and Vascular Health in Physically Active Late Pre- and Early Postmenopausal Females.

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.

Acute effect of passive heat exposure on markers of cardiometabolic function in adults with type 2 diabetes mellitus.

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/m2] 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.

Revisiting the evaluation of central versus peripheral thermoregulatory control in humans.

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.

Thermoregulation During Pregnancy: a Controlled Trial Investigating the Risk of Maternal Hyperthermia During Exercise in the Heat.

OBJECTIVES: Despite the well-established benefits of exercise, pregnant women are discouraged from physical activity in hot/humid conditions to avoid hyperthermia (core temperature (Tcore) ≥ 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 Tcore 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.

A retrospective analysis to determine if exercise training-induced thermoregulatory adaptations are mediated by increased fitness or heat acclimation.

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 V̇O2max 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 V̇O2max 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 V̇O2max 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 V̇O2max , 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 V̇O2max independently influences thermoregulatory sweating, maximum skin wettedness (ωmax ) and the change in rectal temperature (ΔTre ) 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; V̇O2max : 41.7 ± 9.4 ml kg-1  min-1 ), aerobically fit (F; n = 7; V̇O2max : 55.6 ± 4.3 ml kg-1  min-1 ; P < 0.01) and aerobically unfit (n = 8) individuals, before (pre; V̇O2max : 45.8 ± 11.6 ml kg-1  min-1 ) and after (post; V̇O2max : 52.0 ± 11.1 ml kg-1  min-1 ; P < 0.001) an 8-week training intervention. ωmax was similar between UF (0.74 ± 0.09) and F (0.78 ± 0.08, P = 0.22). However, ωmax 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 ΔTre 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 V̇O2max per se, confers an increased ωmax , greater sweat rate, and smaller rise in core temperature during uncompensable heat stress in fit individuals.

Impact of passive heat acclimation on markers of kidney function during heat stress.

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.

Normobaric hypoxia does not alter the critical environmental limits for thermal balance during exercise-heat stress.

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, FIO2  = 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 (Pcrit ) 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 Pcrit 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.

The Change in Core Temperature and Sweating Response during Exercise Are Unaffected by Time of Day within the Wake Period.

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.

Heat risk exacerbation potential for neurology patients during the COVID-19 pandemic and related isolation.

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.

Steady-state sweating during exercise is determined by the evaporative requirement for heat balance independently of absolute core and skin temperatures.

KEY POINTS: When exercise was prescribed to elicit a fixed evaporative heat balance requirement (Ereq ), 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 (Hprod ), but a different Ereq (due to differences in air temperature), yielded higher steady-state sweat rates with a higher Ereq , 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 Ereq . Collectively, these data indicate that during exercise in a compensable environment, steady-state sudomotor responses are influenced by Ereq rather than absolute core and skin temperatures, or Hprod . ABSTRACT: The present study sought to determine whether absolute core temperature (modified via diurnal variation) and absolute skin temperature (modified by different air temperatures (Ta )) alters the steady-state sweating response to exercise at a fixed evaporative heat balance requirement (Ereq ). Ten males exercised for 60 min on six occasions. Three Ta /heat production (Hprod ) 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 Ereq (200 or 275 W·m-2 ) with different absolute core temperatures (AM vs. PM); (2) the same Ereq (200 W·m-2 ) with different skin temperatures (Ta : 23˚C vs. 33˚C); (3) the same heat production (525 W) with different Ereq (200 vs. 275 W·m-2 ). Oesophageal temperature (Toes ), local sweat rate (LSR) on the arm and upper-back, and whole-body sweat rate (WBSR) were measured. Steady-state Toes was always higher in PM versus AM at an Ereq 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 Ereq was matched (200 W·m-2 ) with different Ta (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 Hprod (525 W) but different Ereq (200 vs. 275 W·m-2 ), mean LSR (P < 0.001), and WBSR (P < 0.001) were higher with a greater Ereq . Collectively, steady-state sweating during exercise is altered by Ereq but not Toes , skin temperature, or Hprod .

Core Temperature and Sweating in Men and Women During a 15-km Race in Cool Conditions.

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.

Improved neural control of body temperature following heat acclimation in humans.

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.