Work-rest regimens for work in hot environments: A scoping review.

BACKGROUND: To limit exposures to occupational heat stress, leading occupational health and safety organizations recommend work-rest regimens to prevent core temperature from exceeding 38°C or increasing by ≥1°C. This scoping review aims to map existing knowledge of the effects of work-rest regimens in hot environments and to propose recommendations for future research based on identified gaps. METHODS: We performed a search of 10 databases to retrieve studies focused on work-rest regimens under hot conditions. RESULTS: Forty-nine articles were included, of which 35 were experimental studies. Most studies were conducted in laboratory settings, in North America (71%), on healthy young adults, with 94% of the 642 participants being males. Most studies (66%) employed a protocol duration ≤240 min (222 ± 162 min, range: 37-660) and the time-weighted average wet-bulb globe temperature was 27 ± 4°C (range: 18-34). The work-rest regimens implemented were those proposed by the American Conference of Governmental and Industrial Hygiene (20%), National Institute of Occupational Safety and Health (11%), or the Australian Army (3%). The remaining studies (66%) did not mention how the work-rest regimens were derived. Most studies (89%) focused on physical tasks only. Most studies (94%) reported core temperature, whereas only 22% reported physical and/or mental performance outcomes, respectively. Of the 35 experimental studies included, 77% indicated that core temperature exceeded 38°C. CONCLUSIONS: Although work-rest regimens are widely used, few studies have investigated their physiological effectiveness. These studies were mainly short in duration, involved mostly healthy young males, and rarely considered the effect of work-rest regimens beyond heat strain during physical exertion.

Passive heat therapy: a promising preventive measure for people at risk of adverse health outcomes during heat extremes.

The world is experiencing increased frequency, duration, and severity of life-threatening heat extremes. Most hospitalizations and excess deaths during extreme heat events are associated with preexisting diseases in older adults. As climate change persists, the global population ages and the number of individuals with chronic diseases expands, more people are at risk of adverse health outcomes during extreme heat events. Therefore, proactive preventive measures are urgently needed to mitigate heat-related health risks within these populations. In this context, passive heat therapy (e.g., hot baths, saunas, and water-perfused suits) emerges as a promising countermeasure to improve physiological resilience to a warming planet. Passive heating improves cardiovascular function and overall health in older adults and individuals living with chronic diseases, offering the prospect of reducing cardiovascular strain during hotter days. Moreover, some studies suggest that passive heat therapy can be an effective strategy for heat acclimation (i.e., improved thermoregulation). This review describes the existing literature on the effects of passive heat therapy on cardiovascular and thermoregulatory responses in individuals with higher heat-related health risks and explores the use of passive heating as a strategy for heat acclimation to mitigate health risks during extreme heat events.NEW & NOTEWORTHY Passive heat therapy improves cardiovascular function and health in middle-aged and older adults living with or without chronic diseases. In addition, preliminary studies indicate that passive heat interventions can induce heat acclimation, improving thermoregulatory responses. Thus, passive heat therapy could serve as a preventive measure for people at risk of adverse health outcomes during extreme heat events, improving resilience to ongoing climate change.

Shifting focus: Time to look beyond the classic physiological adaptations associated with human heat acclimation.

Planet Earth is warming at an unprecedented rate and our future is now assured to be shaped by the consequences of more frequent hot days and extreme heat. Humans will need to adapt both behaviorally and physiologically to thrive in a hotter climate. From a physiological perspective, countless studies have shown that human heat acclimation increases thermoeffector output (i.e., sweating and skin blood flow) and lowers cardiovascular strain (i.e., heart rate) during heat stress. However, the mechanisms mediating these adaptations remain understudied. Furthermore, several possible benefits of heat acclimation for other systems and functions involved in maintaining health and performance during heat stress remain to be elucidated. This review summarizes recent advances in human heat acclimation, with emphasis on recent studies that (1) advanced our understanding of the mechanisms mediating improved thermoeffector output and (2) investigated adaptations that go beyond those classically associated with heat acclimation. We highlight that these studies have contributed to a better understanding of the integrated physiological responses underlying human heat acclimation while leaving key unanswered questions that will need to be addressed in the future.

A dataset of proteomic changes during human heat stress and heat acclimation.

Hotter climates have important impacts on human health and performance. Yet, the cellular and molecular responses involved in human heat stress and acclimation remain understudied. This dataset includes physiological measurements and the plasma concentration of 2,938 proteins collected from 10 healthy adults, before and during passive heat stress that was performed both prior to and after a 7-day heat acclimation protocol. Physiological measurements included body temperatures, sweat rate, cutaneous vascular conductance, blood pressure, and skin sympathetic nerve activity. The proteomic dataset was generated using the Olink Explore 3072 assay, enabling a high-multiplex antibody-based assessment of protein changes based on proximity extension assay technology. The data need to be interpreted in the context of the moderate level of body hyperthermia attained and the specific demographic of young, healthy adults. We have made this dataset publicly available to facilitate research into the cellular and molecular mechanisms involved in human heat stress and acclimation, crucial for addressing the health and performance challenges posed by rising temperatures.

Mediterranean diet and time-restricted eating as a cardiac rehabilitation approach for patients with coronary heart disease and pre-diabetes: the DIABEPIC-1 protocol of a feasibility trial.

INTRODUCTION: Despite proven programmes, implementing lifestyle interventions for pre-diabetes and type 2 diabetes is challenging. Cardiac rehabilitation, provide a valuable opportunity to promote the adoption of healthy lifestyle behaviours for patients with atherosclerotic cardiovascular disease (ASCVD). However, only a limited number of studies have explored the potential for reversing the underlying causes of ASCVD in this setting. OBJECTIVES: The DIABEPIC1 study is an ongoing single-arm lifestyle clinical trial to assess the feasibility of an upgraded 6-month intensive cardiac rehabilitation programme combining an innovative diet assignment with exercise training to reverse newly onset pre-diabetes (glycated haemoglobin 5.7%-6.4%) to normal glucose concentrations in patients with coronary heart disease. METHODS AND ANALYSIS: 36 patients referred from the Montreal Heart Institute for cardiac rehabilitation, aged ≥40 years with a recent diagnosis of pre-diabetes in the last 6 months, will be offered to participate in the upgraded programme. Interventions will include four sessions of nutritional counselling on ultra-processed foods intake reduction and a moderate-carbohydrate (<40%) ad libitum Mediterranean diet coupled with 36 1-hour sessions of supervised exercise training (continuous and interval aerobic training, and resistance training) and educational intervention. Phase 2 will continue the same interventions adding 8:16 hour time-restricting eating (TRE) at least 5 days per week. During this second phase, exercise training will be performed with autonomy. The primary objectives will be to evaluate the recruitment rate, the completion rates at 3 and 6 months, and the compliance of participants. The secondary objectives will be to assess the proportion of prediabetic participants in remission of pre-diabetes at the programme's end and to characterise the factors associated with remission. ETHICS AND DISSEMINATION: The DIABEPIC1 feasibility study is approved by the Research Ethics Board of the Montreal Heart Institute (Project Number ICM 2022-3005). Written informed consent will be obtained from each participant prior to inclusion. Results will be available through research articles and conferences. CONCLUSIONS: The DIABEPIC1 trial will examine the feasibility and effectiveness of an enhanced cardiac rehabilitation programme combining exercise training with an ultra-processed food reduction intervention, a Mediterranean diet, and TRE counselling to remit pre-diabetes to normal glucose concentrations. TRIAL REGISTRATION NUMBER: NCT05459987.

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.

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.

The Presence of Wind Worsens the Effect of Cold Temperature on Time to Ischemia in Patients with Stable Angina.

PURPOSE: This study tested the hypothesis that the combination of cold temperature and wind further reduces time to ischemia during treadmill stress testing compared with cold temperature alone. METHODS: Eighteen participants (56 ± 9 yr) with stable angina performed four treadmill stress tests in a randomized crossover design at +20°C and -8°C, with and without a 24-km·h -1 headwind. Time to ischemia (≥1-mm ST-segment depression) and angina, rate pressure product, and total exercise duration were determined. RESULTS: At -8°C, time to ischemia was reduced by 22% (-58 s (-85 to -31 s), P < 0.01) compared with +20°C. The addition of wind at -8°C reduced time to ischemia by a further 15% (-31 s (-58 to -4 s) vs -8°C without wind, P = 0.02). The addition of wind did not affect time to ischemia at +20°C ( P = 0.38). Cold temperature and wind did not affect time to angina ( P = 0.46 and P = 0.61) or rate pressure product ( P = 0.46 and P = 0.09). Total exercise time was reduced in the presence of wind at -8°C (-29 s (-51 to -7 s), P = 0.01), but not at +20°C ( P = 0.09). CONCLUSIONS: The presence of wind reduces time to ischemia when exercise stress testing is performed in a cold environment. These results suggest that wind should be considered when evaluating the risks posed by cold weather in patients with coronary artery disease and exercise-induced ischemia.

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.

Control of blood pressure in the cold: differentiation of skin and skeletal muscle vascular resistance.

NEW FINDINGS: What is the central question of this study? Why does blood pressure increases during cold air exposure? Specifically, what is the contribution of skin and skeletal muscle vascular resistance during whole body versus isolated face cooling? What is the main finding and its importance? Whole-body cooling caused an increase in blood pressure through an increase in skeletal muscle and cutaneous vascular resistance. However, isolated mild face cooling caused an increase in blood pressure predominately via an increase in cutaneous vasoconstriction. ABSTRACT: The primary aim of this investigation was to determine the individual contribution of the cutaneous and skeletal muscle circulations to the cold-induced pressor response. To address this, we examined local vascular resistances in the cutaneous and skeletal muscle of the arm and leg. Thirty-four healthy individuals underwent three different protocols, whereby cold air to clamp skin temperature (27°C) was passed over (1) the whole-body, (2) the whole-body, but with the forearm pre-cooled to clamp cutaneous vascular resistance, and (3) the face. Cold exposure applied to the whole body or isolated to the face increased mean arterial pressure (all, P < 0.001) and total peripheral resistance (all, P < 0.047) compared to thermal neutral baseline. Whole-body cooling increased femoral (P < 0.005) and brachial artery resistance (P < 0.003) compared to thermoneutral baseline. Moreover, when the forearm was pre-cooled to remove the contribution of cutaneous resistance (P = 0.991), there was a further increase in lower arm vasoconstriction (P = 0.036) when whole-body cooling was superimposed. Face cooling also caused a reflex increase in lower arm cutaneous (P = 0.009) and brachial resistance (P = 0.050), yet there was no change in femoral resistance (P = 0.815) despite a reflex increase in leg cutaneous resistance (P = 0.010). Cold stress causes an increase in blood pressure through a change in total peripheral resistance that is largely due to cutaneous vasoconstriction with face cooling, but there is additional vasoconstriction in the skeletal muscle vasculature with whole-body cooling.

A Cross-Sectional Comparison of Arterial Stiffness and Cognitive Performances in Physically Active Late Pre- and Early Post-Menopausal Females.

Menopause accelerates increases in arterial stiffness and decreases cognitive performances. The objective of this study was to compare cognitive performances in physically active pre- and post-menopausal females and their relationship with arterial stiffness. We performed a cross-sectional comparison of blood pressure, carotid−femoral pulse wave velocity (cf-PWV) and cognitive performances between physically active late pre- and early post-menopausal females. Systolic (post-menopause­pre-menopause: +6 mmHg [95% CI −1; +13], p = 0.27; ŋ2 = 0.04) and diastolic (+6 mmHg [95% CI +2; +11], p = 0.06; ŋ2 = 0.12) blood pressures, and cf-PWV (+0.29 m/s [95% CI −1.03; 1.62], p = 0.48; ŋ2 = 0.02) did not differ between groups. Post-menopausal females performed as well as pre-menopausal females on tests evaluating executive functions, episodic memory and processing speed. Group differences were observed on the computerized working memory task. Post-menopausal females had lower accuracy (p = 0.02; ŋ2 = 0.25) but similar reaction time (p = 0.70; ŋ2 < 0.01). Moreover, this performance was inversely associated with the severity of menopausal symptoms (r = −0.38; p = 0.05). These results suggest that arterial stiffness and performance on tests assessing episodic memory and processing speed and executive functions assessing inhibition and switching abilities did not differ between physically active pre- and post-menopausal females. However, post-menopausal females had lower performance on a challenging condition of a working memory task, and this difference in working memory between groups cannot be explained by increased arterial stiffness.

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.

Human temperature regulation under heat stress in health, disease, and injury.

The human body constantly exchanges heat with the environment. Temperature regulation is a homeostatic feedback control system that ensures deep body temperature is maintained within narrow limits despite wide variations in environmental conditions and activity-related elevations in metabolic heat production. Extensive research has been performed to study the physiological regulation of deep body temperature. This review focuses on healthy and disordered human temperature regulation during heat stress. Central to this discussion is the notion that various morphological features, intrinsic factors, diseases, and injuries independently and interactively influence deep body temperature during exercise and/or exposure to hot ambient temperatures. The first sections review fundamental aspects of the human heat stress response, including the biophysical principles governing heat balance and the autonomic control of heat loss thermoeffectors. Next, we discuss the effects of different intrinsic factors (morphology, heat adaptation, biological sex, and age), diseases (neurological, cardiovascular, metabolic, and genetic), and injuries (spinal cord injury, deep burns, and heat stroke), with emphasis on the mechanisms by which these factors enhance or disturb the regulation of deep body temperature during heat stress. We conclude with key unanswered questions in this field of research.

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.

Passive heat acclimation does not modulate processing speed and executive functions during cognitive tasks performed at fixed levels of thermal strain.

This study evaluated if passive controlled hyperthermia heat acclimation modulates cognitive performance during passive heat stress. Eight healthy adults (25 ± 4 years) underwent 7 consecutive days of hot water immersion (core temperature ≥38.6 °C) and a 7-day time-control period. On days 1 and 7 of heat acclimation, participants performed a digital Stroop test at baseline, when core temperature reached 38.6 °C, and after 60 minutes at a core temperature ≥38.6 °C to evaluate reaction time during tasks targeting processing speed (reading and counting) and executive functions (inhibition and switching). On days 1 and 7 of the time-control intervention, participants performed the Stroop test with equivalent amounts of time separating each task as for heat acclimation. During day 1 of heat acclimation, reaction time was quicker during the reading (-44 ms [-71 to -17], P < 0.01) and counting (-39 ms [-76 to -2], P = 0.04) tasks when the rectal temperature reached 38.6 °C, but after a further 60 minutes of heat exposure, reaction time only remained quicker during the reading task (-56 ms [-83 to -29], P < 0.01). Changes in reaction time during heat exposure were unaffected by subsequent heat acclimation (interaction, all P ≥ 0.09). In conclusion, 7 days of heat acclimation does not modulate processing speed and executive functions during passive heat exposure. Novelty: Whether heat acclimation improves cognitive performance during heat exposure remains unclear. We tested the hypothesis that heat acclimation modulates reaction time during cognitive tasks performed at matched levels of thermal strain. Despite the classical signs of heat acclimation, reaction time during heat exposure is unaffected by heat acclimation.

Extreme Heat and Cardiovascular Health: What a Cardiovascular Health Professional Should Know.

As global temperatures continue to rise, extreme heat events are becoming more frequent and intense. Extreme heat affects cardiovascular health as it is associated with a greater risk of adverse cardiovascular events, especially for adults with preexisting cardiovascular diseases. Nonetheless, the pathophysiology underlying the association between extreme heat and cardiovascular risk remains understudied. Furthermore, specific recommendations to mitigate the effects of extreme heat on cardiovascular health remain limited to guide clinical practice within the context of a warming climate. The overall objective of this review article is to raise awareness that extreme heat poses a risk for cardiovascular health. Specifically, the review discusses why cardiovascular healthcare professionals should care about extreme heat, how extreme heat affects cardiovascular health, and recommendations to minimise the cardiovascular consequences of extreme heat. Future research directions are also provided to further our understating of the cardiovascular health consequences of extreme heat. A better awareness and understanding of the cardiovascular consequences of extreme heat will help cardiovascular health professionals assess the risk and optimise the care of their patients exposed to an increasingly warm climate.