A critical review of the effectiveness of electric fans as a personal cooling intervention in hot weather and heatwaves.

Health agencies worldwide have historically cautioned that electric fans accelerate body-heat gain during hot weather and heatwaves (typically in air temperatures ≥35°C). However, guidance published since 2021 has suggested that fans can still cool the body in air temperatures up to 40°C by facilitating sweat evaporation, and therefore are an inexpensive yet sustainable alternative to air conditioning. In a critical analysis of the reports cited to support this claim, we found that although fan use improves sweat evaporation, these benefits are of insufficient magnitude to exert meaningful reductions in body core temperature in air temperatures exceeding 35°C. Health agencies should continue to advise against fan use in air temperatures higher than 35°C, especially for people with compromised sweating capacity (eg, adults aged 65 years or older). Improving access to ambient cooling strategies (eg, air conditioning or evaporative coolers) and minimising their economic and environmental costs through policy initiatives, efficient cooling technology, and combined use of low-cost personal interventions (eg, skin wetting or fan use) are crucial for climate adaptation.

Exercise intensity- and body region-specific differences in sweating in middle-aged-to-older men with and without type 2 diabetes.

Type 2 diabetes is associated with reduced whole-body sweating during exercise-heat stress. However, it is unclear if this impairment is related to exercise intensity and whether it occurs uniformly across body regions. We evaluated whole-body (direct calorimetry) and local (ventilated-capsule technique; chest, back, forearm, thigh) sweat rates in physically active men with type 2 diabetes (T2D; aged 59 (7) years; V̇O2peak 32.3 (7.6) mL·kg-1·min-1; n=26; HbA1c 5.1-9.1%) and without diabetes (Control; aged 61 (5) years; V̇O2peak 37.5 (5.4) mL·kg-1·min-1; n=26) during light (~40%V̇O2peak), moderate (~50%V̇O2peak), and vigorous (~65%V̇O2peak) intensity exercise (elicited by fixing metabolic heat production at ~150, 200, 250 W·m-2, respectively) in 40°C, ~17% relative humidity. Whole-body sweating was ~11% (T2D-Control mean difference [95% confidence interval]: -37 [-63, -12] g·m-2·h-1) and ~13% (-50 [-76, -25] g·m-2·h-1) lower in the T2D compared to the Control group during moderate- and vigorous- (p≤0.001), but not light-intensity exercise (-21 [-47, 4] g·m-2·h-1; p=0.128). Consequently, the diabetes-related reductions in whole-body sweat rate were 2.3 [1.6, 3.1] times greater during vigorous relative to light exercise (p<0.001). Further, these diabetes-related impairments in local sweating were region-specific during vigorous-intensity exercise (group × region interaction: p=0.024), such that the diabetes-related reduction in local sweat rate at the trunk (chest, back) was 2.4 [1.2, 3.7] times greater than that at the limbs (thigh, arm). In summary, when assessed under hot, dry conditions, diabetes-related impairments in sweating are exercise intensity-dependent and greater at the trunk compared to the limbs.

Effect of daylong exposure to indoor overheating on autophagy and the cellular stress response in older adults.

To protect vulnerable populations during heat waves, public health agencies recommend maintaining indoor air temperature below ∼24-28 °C. While we recently demonstrated that maintaining indoor temperatures ≤26 °C mitigates the development of hyperthermia and cardiovascular strain in older adults, the cellular consequences of prolonged indoor heat stress are poorly understood. We therefore evaluated the cellular stress response in 16 adults (six females) aged 66-78 years during 8 h rest in ambient conditions simulating homes maintained at 22 °C (control) and 26 °C (indoor temperature upper limit proposed by health agencies), as well as non-air-conditioned domiciles during hot weather and heat waves (31 and 36 °C, respectively; all 45% relative humidity). Western blot analysis was used to assess changes in proteins associated with the cellular stress response (autophagy, apoptosis, acute inflammation, and heat shock proteins) in peripheral blood mononuclear cells harvested prior to and following exposure. Following 8 h exposure, no cellular stress response-related proteins differed significantly between the 26 and 22 °C conditions (all, P ≥ 0.056). By contrast, autophagy-related proteins were elevated following exposure to 31 °C (p62: 1.5-fold; P = 0.003) and 36 °C (LC3-II, LC3-II/I, p62; all ≥2.0-fold; P ≤ 0.002) compared to 22 °C. These responses were accompanied by elevations in apoptotic signaling in the 31 and 36 °C conditions (cleaved-caspase-3: 1.8-fold and 3.7-fold, respectively; P ≤ 0.002). Furthermore, HSP90 was significantly reduced in the 36 °C compared to 22 °C condition (0.7-fold; P = 0.014). Our findings show that older adults experience considerable cellular stress during prolonged exposure to elevated ambient temperatures and support recommendations to maintain indoor temperatures ≤26 °C to prevent physiological strain in heat-vulnerable persons.

Effects of Daylong Exposure to Indoor Overheating on Thermal and Cardiovascular Strain in Older Adults: A Randomized Crossover Trial.

BACKGROUND: Health agencies recommend that homes of heat-vulnerable occupants (e.g., older adults) be maintained below 24-28°C to prevent heat-related mortality and morbidity. However, there is limited experimental evidence to support these recommendations. OBJECTIVE: To aid in the development of evidence-based guidance on safe indoor temperatures for temperate continental climates, we evaluated surrogate physiological outcomes linked with heat-related mortality and morbidity in older adults during simulated indoor overheating. METHODS: Sixteen older adults [six women; median age: 72 y, interquartile range (IQR): 70-73 y; body mass index: 24.6 (IQR: 22.1-27.0) kg/m2] from the Ottawa, Ontario, Canada, region (warm summer continental climate) completed four randomized, 8-h exposures to conditions experienced indoors during hot weather in continental climates (e.g., Ontario, Canada; 64 participant exposures). Ambient conditions simulated an air-conditioned environment (22°C; control), proposed indoor temperature upper limits (26°C), and temperatures experienced in homes without air-conditioning (31°C and 36°C). Core temperature (rectal) was monitored as the primary outcome; based on previous recommendations, between-condition differences >0.3°C were considered clinically meaningful. RESULTS: Compared with 22°C, core temperature was elevated to a meaningful extent in 31°C [+0.7°C; 95% confidence interval (CI): 0.5, 0.8] and 36°C (+0.9°C; 95% CI: 0.8, 1.1), but not 26°C (+0.2°C, 95% CI: 0.0, 0.3). Increasing ambient temperatures were also associated with elevated heart rate and reduced arterial blood pressure and heart rate variability at rest, as well as progressive impairments in cardiac and blood pressure responses to standing from supine. DISCUSSION: Core temperature and cardiovascular strain were not appreciably altered following 8-h exposure to 26°C but increased progressively in conditions above this threshold. These data support proposals for the establishment of a 26°C indoor temperature upper limit for protecting vulnerable occupants residing in temperate continental climates from indoor overheating. https://doi.org/10.1289/EHP13159.

Hormonal intrauterine devices and heat exchange during exercise.

Synthetic progestins in oral contraceptives are thought to blunt heat dissipation by reducing skin blood flow and sweating. However, whether progestin-releasing intrauterine devices (IUDs) modulate heat loss during exercise-heat stress is unknown. We used direct calorimetry to measure whole-body total (dry + evaporative) heat loss in young, physically active women (mean (SD); aged 24 (4) years, V ̇ O 2 peak ${\dot V_{{{\mathrm{O}}_{\mathrm{2}}}{\mathrm{peak}}}}$ 39.3 (5.3) ml/kg/min) with (IUD; n = 19) and without (Control; n = 17) IUDs in the follicular and luteal phases of the menstrual cycle during light- and moderate-intensity exercise at fixed rates of heat production (∼175 and ∼275 W/m2 ) in 30°C, ∼21% relative humidity. Between-group and -phase differences were evaluated using traditional hypothesis testing and statistical equivalence testing within pre-determined bounds (±11 W/m2 ; difference required to elicit a ±0.3°C difference in core temperature over 1 h) in each exercise bout. Whole-body total heat loss was statistically equivalent between groups within ±11 W m-2 (IUD-Control [90% CIs]; Light: -2 [-8, 5] W/m2 , P = 0.007; Moderate: 0 [-6, 6] W/m2 , P = 0.002), as were dry and evaporative heat loss (P ≤ 0.023), except for evaporative heat loss during moderate-intensity exercise (equivalence: P = 0.063, difference: P = 0.647). Whole-body total and evaporative heat loss were not different between phases (P ≥ 0.267), but dry heat loss was 3 [95% CIs: 1, 5] W/m2 greater in the luteal phase (P ≤ 0.022). Despite this, all whole-body heat loss outcomes were equivalent between phases (P ≤ 0.003). These findings expand our understanding of the factors that modulate heat exchange in women and provide valuable mechanistic insight of the role of endogenous and exogenous female sex hormones in thermoregulation. KEY POINTS: Progestin released by hormonal intrauterine devices (IUDs) may negatively impact heat dissipation during exercise by blunting skin blood flow and sweating. However, the influence of IUDs on thermoregulation has not previously been assessed. We used direct calorimetry to show that IUD users and non-users display statistically equivalent whole-body dry and evaporative heat loss, body heat storage and oesophageal temperature during moderate- and high-intensity exercise in a warm, dry environment, indicating that IUDs do not appear to compromise exercise thermoregulation. However, within IUD users and non-users, dry heat loss was increased and body heat storage and oesophageal temperature were reduced in the luteal compared to the follicular phase of the menstrual cycle, though these effects were small and unlikely to be practically meaningful. Together, these findings expand our understanding of the factors that modulate heat exchange in women and have important practical implications for the design of future studies of exercise thermoregulation.

Intradermal Microdialysis: An Approach to Investigating Novel Mechanisms of Microvascular Dysfunction in Humans.

The cutaneous vasculature is an accessible tissue that can be used to assess microvascular function in humans. Intradermal microdialysis is a minimally invasive technique used to investigate mechanisms of vascular smooth muscle and endothelial function in the cutaneous circulation. This technique allows for the pharmacological dissection of the pathophysiology of microvascular endothelial dysfunction as indexed by decreased nitric oxide-mediated vasodilation, an indicator of cardiovascular disease development risk. In this technique, a microdialysis probe is placed in the dermal layer of the skin, and a local heating unit with a laser Doppler flowmetry probe is placed over the probe to measure the red blood cell flux. The local skin temperature is clamped or stimulated with direct heat application, and pharmacological agents are perfused through the probe to stimulate or inhibit intracellular signaling pathways in order to induce vasodilation or vasoconstriction or to interrogate mechanisms of interest (co-factors, antioxidants, etc.). The cutaneous vascular conductance is quantified, and mechanisms of endothelial dysfunction in disease states can be delineated.

Association between haemoglobin A1c and whole-body heat loss during exercise-heat stress in physically active men with type 2 diabetes.

NEW FINDINGS: What is the central question of this study? Is the impairment in heat dissipation during exercise observed in men with type 2 diabetes related to glycaemic control (indexed by glycated haemoglobin; haemoglobin A1c )? What is the main finding and its importance? No association was found between haemoglobin A1c (range: 5.1-9.1%) and whole-body heat loss in men with type 2 diabetes during exercise in the heat. However, individuals with elevated haemoglobin A1c exhibited higher body core temperature and heart rate responses. Thus, while haemoglobin A1c is not associated with heat loss per se, it may still have important implications for physiological strain during exercise. ABSTRACT: Type 2 diabetes is associated with a reduced capacity to dissipate heat. It is unknown whether this impairment is related to glycaemic control (indexed by glycated haemoglobin; haemoglobin A1c ) is unknown. We evaluated the association between haemoglobin A1c and whole-body heat loss (via direct calorimetry), body core temperature, and heart rate in 26 physically active men with type 2 diabetes (43-73 years; HbA1c 5.1-9.1%) during exercise at increasing rates of metabolic heat production (∼150, 200, 250 W m-2 ) in the heat (40°C, ∼17% relative humidity). Haemoglobin A1c was not associated with whole-body heat loss (P = 0.617), nor the increase in core temperature from pre-exercise (P = 0.347). However, absolute core temperature and heart rate were elevated ∼0.2°C (P = 0.014) and ∼6 beats min-1 (P = 0.049), respectively, with every percentage point increase in haemoglobin A1c . Thus, while haemoglobin A1c does not appear to modify diabetes-related reductions in capacity for heat dissipation, it may still have important implications for physiological strain during exercise-heat stress.

Sex differences in adaptation to intermittent post-exercise sauna bathing in trained middle-distance runners.

BACKGROUND: The purpose of this study was to investigate the effect of sex on the efficacy of intermittent post-exercise sauna bathing to induce heat acclimation and improve markers of temperate exercise performance in trained athletes. METHODS: Twenty-six trained runners (16 female; mean ± SD, age 19 ± 1 years, V̇O2max F: 52.6 ± 6.9 mL⋅kg-1⋅min-1, M: 64.6 ± 2.4 mL⋅kg-1⋅min-1) performed a running heat tolerance test (30 min, 9 km⋅h-1/2% gradient, 40 °C/40%RH; HTT) and temperate (18 °C) exercise tests (maximal aerobic capacity [V̇O2max] and lactate profile) pre and post 3 weeks of normal exercise training plus 29 ± 1 min post-exercise sauna bathing (101-108 °C) 3 ± 1 times per week. RESULTS: Females and males exhibited similar reductions (interactions p > 0.05) in peak rectal temperature (- 0.3 °C; p < 0.001), skin temperature (- 0.9 °C; p < 0.001) and heart rate (- 9 beats·min-1; p = 0.001) during the HTT at post- vs pre-intervention. Only females exhibited an increase in active sweat glands on the forearm (measured via modified iodine technique; F: + 57%, p < 0.001; M: + 1%, p = 0.47). Conversely, only males increased forearm blood flow (measured via venous occlusion plethysmography; F: + 31%, p = 0.61; M: + 123%; p < 0.001). Females and males showed similar (interactions p > 0.05) improvements in V̇O2max (+ 5%; p = 0.02) and running speed at 4 mmol·L-1 blood lactate concentration (+ 0.4 km·h-1; p = 0.001). CONCLUSIONS: Three weeks of post-exercise sauna bathing effectively induces heat acclimation in females and males, though possibly amid different thermoeffector adaptations. Post-exercise sauna bathing is also an effective ergogenic aid for both sexes.

Intermittent post-exercise sauna bathing improves markers of exercise capacity in hot and temperate conditions in trained middle-distance runners.

PURPOSE: This study investigated whether intermittent post-exercise sauna bathing across three-weeks endurance training improves exercise heat tolerance and exercise performance markers in temperate conditions, compared to endurance training alone. The subsidiary aim was to determine whether exercise-heat tolerance would further improve following 7-Weeks post-exercise sauna bathing. METHODS: Twenty middle-distance runners (13 female; mean ± SD, age 20 ± 2 years, [Formula: see text]O2max 56.1 ± 8.7 ml kg-1 min-1) performed a running heat tolerance test (30-min, 9 km h-1/2% gradient, 40 °C/40%RH; HTT) and temperate (18 °C) exercise tests (maximal aerobic capacity [[Formula: see text]O2max], speed at 4 mmol L-1 blood lactate concentration ([La-]) before (Pre) and following three-weeks (3-Weeks) normal training (CON; n = 8) or normal training with 28 ± 2 min post-exercise sauna bathing (101-108 °C, 5-10%RH) 3 ± 1 times per week (SAUNA; n = 12). Changes from Pre to 3-Weeks were compared between-groups using an analysis of co-variance. Six SAUNA participants continued the intervention for 7 weeks, completing an additional HTT (7-Weeks; data compared using a one-way repeated-measures analysis of variance). RESULTS: During the HTT, SAUNA reduced peak rectal temperature (Trec; - 0.2 °C), skin temperature (- 0.8 °C), and heart rate (- 11 beats min-1) more than CON at 3-Weeks compared to Pre (all p < 0.05). SAUNA also improved [Formula: see text]O2max (+ 0.27 L-1 min-1; p = 0.02) and speed at 4 mmol L-1 [La-] (+ 0.6 km h-1; p = 0.01) more than CON at 3-Weeks compared to Pre. Only peak Trec (- 0.1 °C; p = 0.03 decreased further from 3-Weeks to 7-Weeks in SAUNA (other physiological variables p > 0.05). CONCLUSIONS: Three-weeks post-exercise sauna bathing is an effective and pragmatic method of heat acclimation, and an effective ergogenic aid. Extending the intervention to seven weeks only marginally improved Trec.

Nine-, but Not Four-Days Heat Acclimation Improves Self-Paced Endurance Performance in Females.

Although emerging as a cost and time efficient way to prepare for competition in the heat, recent evidence indicates that "short-term" heat acclimation (<7 days) may not be sufficient for females to adapt to repeated heat stress. Furthermore, self-paced performance following either short-term, or longer (>7 days) heat acclimation has not been examined in a female cohort. Therefore, the aim of this study was to investigate self-paced endurance performance in hot conditions following 4- and 9-days of a high-intensity isothermic heat acclimation protocol in a female cohort. Eight female endurance athletes (mean ± SD, age 27 ± 5 years, mass 61 ± 5 kg, VO2peak 47 ± 6 ml⋅kg⋅min-1) performed 15-min self-paced cycling time trials in hot conditions (35°C, 30%RH) before (HTT1), and after 4-days (HTT2), and 9-days (HTT3) isothermic heat acclimation (HA, with power output manipulated to increase and maintain rectal temperature (T rec) at ∼38.5°C for 90-min cycling in 40°C, 30%RH) with permissive dehydration. There were no significant changes in distance cycled (p = 0.47), mean power output (p = 0.55) or cycling speed (p = 0.44) following 4-days HA (i.e., from HTT1 to HTT2). Distance cycled (+3.2%, p = 0.01; +1.8%, p = 0.04), mean power output (+8.1%, p = 0.01; +4.8%, p = 0.05) and cycling speed (+3.0%, p = 0.01; +1.6%, p = 0.05) were significantly greater in HTT3 than in HTT1 and HTT2, respectively. There was an increase in the number of active sweat glands per cm2 in HTT3 as compared to HTT1 (+32%; p = 0.02) and HTT2 (+22%; p < 0.01), whereas thermal sensation immediately before HTT3 decreased ("Slightly Warm," p = 0.03) compared to ratings taken before HTT1 ("Warm") in 35°C, 30%RH. Four-days HA was insufficient to improve performance in the heat in females as observed following 9-days HA.