The effect of foot immersion and neck cooling on cardiac autonomic function in older adults exposed to indoor overheating : a randomized crossover trial.

Foot immersion and neck cooling are recommended cooling strategies for protecting heat-vulnerable persons during heat waves. While we recently showed that these strategies do not limit core temperature increases in older adults during prolonged heat exposure, we did observe small reductions in heart rate. Expanding on these findings, we examined the effects of foot immersion with and without neck cooling on cardiac autonomic function. Seventeen adults (9 females; 65-81 years) underwent 3 randomized, 6-hour exposures to 38°C and 35% relative humidity with: no cooling (control), foot immersion (20°C water), or foot immersion with a wet towel (20°C) around the neck. Cardiac autonomic responses were measured at baseline and end-exposure. These included heart rate variability, cardiac and systolic blood pressure responses to standing, indexed via the 30:15 ratio and supine-to-standing systolic pressure change, respectively, and baroreflex sensitivity during repeated sit-to-stand maneuvers. The 30:15 ratio was 0.04 [95% CI: 0.01, 0.07] greater with foot immersion and neck cooling (1.08 (0.04)) relative to control (1.04 (0.06); P=0.018). Similarly, standing systolic pressure was elevated 9 [0, 17] mm Hg with foot immersion and neck cooling (P=0.043). That said, neither difference remained statistically significant after adjusting for multiplicity (Padjusted≥0.054). No differences in 30:15 ratio or standing systolic pressure were observed with foot immersion alone, while heart rate variability and baroreflex sensitivity were unaffected by either cooling intervention. While foot immersion with neck cooling potentially improved cardiac autonomic responses in older adults exposed to simulated indoor overheating, these effects were small and of questionable clinical importance.

Time to reach equilibrium deep body temperatures in young and older adults resting in the heat: A descriptive secondary analysis.

It is commonly thought that steady-state thermoregulatory responses are achieved within 30-90 min of compensable heat stress. However, this assumption is based on measurements of whole-body heat exchange during exercise, which stabilize (equilibrate) more rapidly than deep body temperatures, especially under resting conditions. To support the design of ecologically relevant heat exposure studies, we quantified equilibrium times for deep body temperature, as indexed by rectal temperature, in young and older adults resting in the heat. We also evaluated the lag in rectal temperature equilibrium relative to whole-body heat storage (direct calorimetry). Equilibrium times were estimated with data from two laboratory-based trials (NCT04353076 and NCT04348630) in which 83 adults aged 19-80 years (34 female) were exposed to simulated heat wave conditions for 8-9 hours. When assessed on the group level, it took rectal temperature 3.3 [bootstrap 95%CI: 2.9 to 3.9] hours to reach thermal equilibrium (<0.05°C/hour rate of change) in young adults exposed to 40°C, 9% relative humidity (RH). In older adults, who were exposed to a greater range of conditions (31-40°C, 9-45% RH), equilibrium times were longer, ranging from 4.4 [3.8 to 5.3] to 5.2 [4.9 to 5.4] hours. Furthermore, rectal temperature equilibrium was delayed 0.9 [0.5 to 1.4] and 1.8 [0.9 to 2.7] hours compared to whole-body heat storage in young and older adults, respectively (only assessed in 40°C, 9% RH). Individual level equilibrium times ranged from 1-8 hours. These findings highlight the importance of ecologically relevant exposure durations in translational research assessing the physiological impacts of hot weather.

Pretreatment of microneedles enhances passive transdermal administration of pilocarpine and pilocarpine-induced sweat production in humans.

The development of an effective transdermal drug delivery protocol to eccrine sweat glands is important for the advancement of research on the human sweating response. We investigated whether microneedle treatment prior to the application of pilocarpine, a hydrophilic and sudorific agent that does not induce sweating due to a limited percutaneous passive diffusion by skin application alone, augments sweat production. We applied three microneedle arrays to forearm skin sites simultaneously (n = 20). Upon removal of the microneedles, 1 % pilocarpine was applied to each site for 5-, 15-, and 30-min for the assessment of sweat gland function. In parallel, pilocarpine was administered by transdermal iontophoresis (5-min) at a separate site. Sweat rate was assessed continuously via the ventilated capsule technique. Pilocarpine augmented sweat rate at the 15- and 30-min periods as compared to the application at 5-min. The sweating responses induced by the 15- and 30-min application of pilocarpine were equivalent to âˆ¼ 80 % of that measured at the iontophoretically treated sites. Notably, we observed a correlation in sweat rate between these two transdermal drug delivery methods. Altogether, our findings show that pre-treatment of microneedle arrays can enhance transdermal delivery efficiency of pilocarpine to human eccrine sweat glands.

The BDNF Val66Met polymorphism and health-related quality of life in youth with obesity.

The brain derived-neurotrophic factor (BDNF) Val66Met polymorphism causes functional changes in BDNF, and is associated with obesity and some psychiatric disorders, but its relationship to health-related quality of life (HRQoL) remains unknown. This study examined, in youth with obesity, whether carriers of the BDNF Val66met polymorphism Met-alleles (A/A or G/A) differed from noncarriers (G/G) on HRQoL. The participants were 187 adolescents with obesity. Ninety-nine youth were carriers of the homozygous Val/Val (G/G) alleles, and 88 were carriers of the Val/Met (G/A) or Met/Met (A/A) alleles. Blood samples were drawn in the morning after an overnight fast for genotyping. HRQoL was measured using the Pediatric-Quality of Life core version. Compared to carriers of the Val66Met Val (G/G) alleles, carriers of the Met-Alleles reported significantly higher physical -HRQoL (p = 0.02), school-related HRQoL, (p = 0.05), social-related HRQoL (p = 0.05), and total HRQoL (p = 0.03), and a trend for Psychosocial-HRQoL. Research is needed to confirm our findings and determine whether carriers of the BDNF Val66Met homozygous Val (G/G) alleles may be at risk of diminished HRQoL, information that can influence interventions in a high-risk population of inactive youth with obesity.

Seasonal changes in hydration in free-living Japanese children and adolescents.

Changes in hydration status occur throughout the day affecting physiological and behavioural functions. However, little is known about the hydration status of free-living Japanese children and the seasonality of this response. We evaluated hydration status estimated by urine osmolality (Uosm) in 349 children (189 boys and 160 girls, 9.5 ± 2.6 years, range: 6-15 years) upon waking at home and during a single school day in spring (April) and summer (July). Further, we assessed the efficacy of employing self-assessment of urine colour (UC; based on an 8-point scale) by children to monitor their hydration status. Early morning Uosm was greater in the spring (903 ± 220 mOsm L-1; n = 326) as compared to summer (800 ± 244 mOsm L-1; n = 125) (P = 0.003, paired t test, n = 104). No differences, however, were observed in Uosm during the school day (P = 0.417, paired t test, n = 32). While 66% and 50% of children were considered underhydrated (Uosm ≥ 800 mOsm L-1) upon waking in the spring and summer periods, respectively, more children were underhydrated (∼12%) during the school day. Self-reported UC was similar between seasons as assessed in the morning and school day (P ≥ 0.101, paired t test), which differed from the pattern of responses observed with Uosm. We showed that a significant number of Japanese children are likely underhydrated especially in the spring period. Children do not detect seasonal changes in hydration from self-assessed UC, limiting its utility to manage hydration status in children.

Exploring the contribution of inter-individual factors to the development of physiological heat strain in older adults exposed to simulated indoor overheating.

Older adults are at elevated risk of heat-related mortality due to age-associated declines in thermoregulatory and cardiovascular function. However, the inter-individual factors that exacerbate physiological heat strain during heat exposure remain unclear, making it challenging to identify more heat-vulnerable subgroups. We therefore explored factors contributing to inter-individual variability in physiological responses of older adults exposed to simulated hot weather. Thirty-seven older adults (61-80 years, 16 females) rested for 8 h in 31 and 36 °C (45% relative humidity). Core (rectal) temperature, heart rate (HR), HR variability, mean arterial pressure (MAP), and cardiac autonomic responses to standing were measured at baseline and end-exposure. Bootstrapped least absolute shrinkage and selection operator regression was used to evaluate whether variation in these responses was related to type 2 diabetes (T2D, n = 10), hypertension (n = 18), age, sex, body morphology, habitual physical activity levels, and/or heat-acclimatization. T2D was identified as a predictor of end-exposure HR (with vs. without: 13 beats/min (bootstrap 95% confidence interval: 6, 23)), seated MAP (-7 mmHg (-18, 1)), and the systolic pressure response to standing (20 mmHg (4, 36)). HR was also influenced by sex (female vs. male: 8 beats/min (1, 16)). No other predictors were identified. The inter-individual factors explored did not meaningfully contribute to the variation in body temperature responses in older adults exposed to simulated indoor overheating. By contrast, cardiovascular responses were exacerbated in females and individuals with T2D. These findings improve understanding of how inter-individual differences contribute to heat-induced physiological strain in older persons.

Impact of a simulated multiday heatwave on nocturnal physiology, behavior, and sleep: A 10-day confinement study.

This study investigated the impact of a multiday heatwave on nocturnal physiology, behavior, and sleep under controlled conditions with comprehensive monitoring of environmental factors and participant activities. Seven young healthy males were confined for ten days in controlled conditions that ranged between hot-to-warm (day:35.4°C, night:26.3°C) during nights 4-6 and temperate (day:25.4°C, night:22.3°C) before (nights 1-3) and after (nights 7-10) the heatwave. Measurements included core and skin temperatures, heart rate, sympathovagal balance, vasomotion indicators, urine samples, blanket coverage, subjective sleep assessments, and partial polysomnography. The average nocturnal core temperature was 0.2°C higher during and after the heatwave compared to the pre-heatwave period, with this difference being more pronounced (+0.3°C) in the first two hours of sleep (p<0.001). For every 0.1°C rise in overnight core temperature, the total sleep time decreased by 14 minutes (pseudo-R2=0.26, p=0.01). The elevated core temperatures occurred despite the participants exhibiting evident thermoregulatory behavior, as they covered 30% less body surface during the heatwave compared to pre- and post-heatwave periods (p<0.001). During the heatwave, mean skin temperature at bedtime was 1.3°C higher than pre-heatwave and 0.8°C higher than post-heatwave periods (p<0.001). No differences in other responses, including heart rate and vasomotion indicators, were observed. The paper details a 20-minute sleepwalking episode that was coupled with marked changes in sleepwalker's thermophysiological responses. In conclusion, the simulated heatwave resulted in higher overnight core temperature which was associated with reduced total sleep time. Behavioral thermoregulation during sleep may serve as a defense against these effects, though more research is needed.

Markers of enterocyte damage, microbial translocation, and systemic inflammation following 9 h of heat exposure in young and older adults.

Heat stress induced damage to the gastrointestinal barrier can induce local and systemic inflammatory reactions implicated in heat-stroke. Gastrointestinal barrier damage has been shown to be greater in older relative to young adults following hyperthermia. However, comparisons between young and older adults have been limited to brief exposures (3 h), which may not reflect the duration of heat stress experienced during heat waves. We therefore evaluated markers of intestinal epithelial damage (log transformed intestinal fatty acid binding protein, IFABPLOG), microbial translocation (soluble cluster of differentiation 14, sCD14LOG), and systemic inflammation (tumour necrosis factor alpha, TNF-αLOG; interleukin 6, IL-6LOG; C-reactive protein, CRP) in 19 young (interquartile range: 21-27 years; 10 females) and 37 older (68-73 years; 10 females) adults before and after 9 h of rest in 40 °C (9% relative humidity). The magnitude of the increase in IFABPLOG was 0.38 log pg/mL (95% CI, 0.10, 0.65 log pg/mL) greater in the older relative to young cohort (P = 0.049) after 9 h heat exposure. At baseline both IL-6LOG and CRP concentrations were higher in the older (IL-6: 2.67 (1.5) log pg/mL, CRP: 0.28 (1.5) mg/mL) relative to the young (IL-6: 1.59 log pg/mL, SD 1.2; CRP: 0.11 mg/mL, SD 1.7) group (both P ≤ 0.001). The change in IL-6 and CRP was similar between groups following 9 h heat exposure (IL-6: P = 0.053; CRP: P = 0.241). Neither sCD14LOG and TNF-αLOG were different between groups at baseline nor altered after 9 h heat exposure. Our data indicate that age may modify intestinal epithelial injury following 9 h of passive heat exposure.

Impacts of age, type 2 diabetes, and hypertension on circulating neutrophil gelatinase-associated lipocalin and kidney injury molecule-1 after prolonged work in the heat in men.

PURPOSE: Prolonged work in the heat increases the risk of acute kidney injury (AKI) in young men. Whether aging and age-associated chronic disease may exacerbate the risk of AKI remains unclear. METHODS: We evaluated plasma neutrophil gelatinase-associated lipocalin (NGAL) and serum kidney injury molecule-1 (KIM1) before and after 180 min of moderate-intensity work (200 W/m2) in temperate (wet-bulb globe temperature [WBGT] 16 °C) and hot (32 °C) environments in healthy young (n = 13, 22 years) and older men (n = 12, 59 years), and older men with type 2 diabetes (T2D; n = 9, 60 years) or hypertension (HTN; n = 9, 60 years). RESULTS: There were no changes in NGAL or KIM1 concentrations following prolonged work in temperate conditions in any group. Despite a similar work tolerance, the relative change in NGAL was greater in the older group when compared to the young group following exercise in the hot condition (mean difference + 82 ng/mL; p < 0.001). Baseline concentrations of KIM1 were ~ 22 pg/mL higher in the older relative to young group, increasing by ~ 10 pg/mL in each group after exercise in the heat (both p ≤ 0.03). Despite a reduced work tolerance in the heat in older men with T2D (120 ± 40 min) and HTN (108 ± 42 min), elevations in NGAL and KIM1 were similar to their healthy counterparts. CONCLUSION: Age may be associated with greater renal stress following prolonged work in the heat. The similar biomarker responses in T2D and HTN compared to healthy older men, alongside reduced exercise tolerance in the heat, suggest these individuals may exhibit greater vulnerability to heat-induced AKI if work is prolonged.

An exploratory survey of on-site heat stress management practices in the Canadian mining industry.

With climate change fueling more frequent and intense periods of hot weather, heat stress management programs are becoming increasingly important for protecting the health and safety of workers in the Canadian mining industry. While the inclusion of heat-mitigation measures such as those provided by the American College of Governmental Industrial Hygienists (ACGIH) Threshold Limit Values (TLVs) are commonly employed by industry, there is a need to develop more comprehensive industry-specific measures for heat stress prevention and management. To better understand current heat management practices and identify opportunities for improvement, an exploratory survey of 51 employees responsible for health and safety at underground mining (n = 35), and surface operations (n = 16) (e.g., open-pit mining, milling, smelting, and exploration site) was conducted in Canada. The respondents answered 50 questions related to workplace heat stress management, including descriptors of the workplace environment, perceived heat stress hazard, administration of heat stress management programming, heat stress emergency procedures, environmental monitoring strategies, and knowledge of mining-specific regulations related to heat stress. Twenty-four managers (47%) reported that heat-related illnesses led to restricted duty or lost time claims at their site, with a median of 5 [IQR: 2-10, max: 30] reportable heat-related illnesses occurring per site annually. Many also felt that heat-related illnesses are under-reported by their workforce (n = 36, 71%). Most sites reported established heat stress management programs to prevent heat illness (n = 43, 84%), typically based on the TLVs (n = 38, 75%). Although some organizations do conduct pre-task evaluations for heat stress (n = 30, 59%), more than half do not conduct post-job evaluations (n = 28, 55%) or pre-employment screening for heat stress vulnerability (n = 3, 6%). While our findings indicate that the health and safety managers recognize the hazard posed by heat and have stated practices to help address the hazard, we also observed inconsistencies in heat stress management programming across the sample. Developing and adopting a standard heat stress management and reporting system would be an important step toward protecting workers from existing and emerging threats from extreme heat and climate change.

Impaired autophagy following ex vivo cooling of simulated hypothermic temperatures in peripheral blood mononuclear cells from young and older adults.

Hypothermia is a critical consequence of extreme cold exposure that increases the risk of cold-related injury and death in humans. While the initiation of cytoprotective mechanisms including the process of autophagy and the heat shock response (HSR) is crucial to cellular survival during periods of stress, age-related decrements in these systems may underlie cold-induced cellular vulnerability in older adults. Moreover, whether potential sex-related differences in autophagic regulation influence the human cold stress response remain unknown. We evaluated the effect of age and sex on mechanisms of cytoprotection (autophagy and the HSR) and cellular stress (apoptotic signaling and the acute inflammatory response) during ex vivo hypothermic cooling. Venous blood samples from 20 healthy young (10 females; mean [SD]: 22 [2] years) and 20 healthy older (10 females; 66 [5] years) adults were either isolated immediately (baseline) for peripheral blood mononuclear cells (PBMCs) or exposed to water bath temperatures maintained at 37, 35, 33, 31, or 4 °C for 90 min before PBMC isolation. Proteins associated with autophagy, apoptosis, the HSR, and inflammation were analyzed via Western blotting. Indicators of autophagic initiation and signaling (LC3, ULK1, and beclin-2) and the HSR (HSP90 and HSP70) increased when exposed to hypothermic temperatures in young and older adults (all p ≤ 0.007). Sex-related differences were only observed with autophagic initiation (ULK1; p = 0.015). However, despite increases in autophagic initiators ULK1 and beclin-2 (all p < 0.001), this was paralleled by autophagic dysfunction (increased p62) in all groups (all p < 0.001). Further, apoptotic (cleaved-caspase-3) and inflammatory (IL-6 and TNF-α) signaling increased in all groups (all p < 0.001). We demonstrated that exposure to hypothermic conditions is associated with autophagic dysfunction, irrespective of age or sex, although there may exist innate sex-related differences in cytoprotection in response to cold exposure as evidenced through altered autophagic initiation.

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

Type 2 diabetes (T2D) 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) yr; V̇o2peak 32.3 (7.6) mL·kg-1·min-1; n = 26; HbA1c 5.1%-9.1%] and without diabetes [Control; aged 61 (5) yr; 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 with 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). Furthermore, 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 with the limbs.NEW & NOTEWORTHY This study evaluates the influence of exercise intensity on decrements in whole body sweating associated with type 2 diabetes. Furthermore, it investigates whether diabetes-related sweating impairments were exhibited uniformly or heterogeneously across body regions. We found that whole body sweating was attenuated in the type 2 diabetes group relative to control participants during moderate- and vigorous-intensity exercise but not light-intensity exercise; impairments were largely mediated by reduced sweating at the trunk rather than the limbs.

"Death Is a Possibility for Those without Shelter": A Thematic Analysis of News Coverage on Homelessness and the 2021 Heat Dome in Canada.

Among the most vulnerable to the health-harming effects of heat are people experiencing homelessness. However, during the 2021 Heat Dome, the deadliest extreme heat event (EHE) recorded in Canada to date, people experiencing homelessness represented the smallest proportion of decedents (n = 3, 0.5%)-despite the impacted region (British Columbia) having some of the highest rates of homelessness in the country. Thus, we sought to explore the 2021 Heat Dome as a media-based case study to identify potential actions or targeted strategies that were initiated by community support agencies, individuals and groups, and communicated in the news during this EHE that may have aided in the protection of this group or helped minimize the mortality impacts. Using media articles collated for a more extensive investigation into the effects of the 2021 Heat Dome (n = 2909), we identified a subset which included content on people experiencing homelessness in Canada (n = 274, 9%). These articles were thematically analysed using NVivo. Three main themes were identified: (i) public warnings issued during the 2021 Heat Dome directly addressed people experiencing homelessness, (ii) community support services explicitly targeting this population were activated during the heat event, and (iii) challenges and barriers faced by people experiencing homelessness during extreme heat were communicated. These findings suggest that mass-media messaging and dedicated on-the-ground initiatives led by various organizations explicitly initiated to support individuals experiencing homelessness during the 2021 Heat Dome may have assisted in limiting the harmful impacts of the heat on this community.

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.

GH and IGF-1 in skin interstitial fluid and blood are associated with heat loss responses in exercising young adults.

PURPOSE: Sweat glands and cutaneous vessels possess growth hormone (GH) and insulin-like growth factor 1 (IGF-1) receptors. Here, we assessed if exercise increases GH and IGF-1 in skin interstitial fluid, and whether baseline and exercise-induced increases in GH and IGF-1 concentrations in skin interstitial fluid/blood are associated with heat loss responses of sweating and cutaneous vasodilation. METHODS: Sixteen young adults (7 women) performed a 50-min moderate-intensity exercise bout (50% VO2peak) during which skin dialysate and blood samples were collected. In a sub-study (n = 7, 4 women), we administered varying concentrations of GH (0.025-4000 ng/mL) and IGF-1 (0.000256-100 µg/mL) into skin interstitial fluid via intradermal microdialysis. Sweat rate (ventilated capsule) and cutaneous vascular conductance (CVC) were measured continuously for both studies. RESULTS: Exercise increased sweating and CVC (both P < 0.001), paralleled by increases of serum GH and skin dialysate GH and IGF-1 (all P ≤ 0.041) without changes in serum IGF-1. Sweating was positively correlated with baseline dialysate and serum GH levels, as well as exercise-induced increases in serum GH and IGF-1 (all P ≤ 0.044). Increases in CVC were not correlated with any GH and IGF-1 variables. Exogenous administration of GH and IGF-1 did not modulate resting sweat rate and CVC. CONCLUSION: (1) Exercise increases GH and IGF-1 levels in the skin interstitial fluid, (2) exercise-induced sweating is associated with baseline GH in skin interstitial fluid and blood, as well as exercise-induced increases in blood GH and IGF-1, and (3) cutaneous vasodilation during exercise is not associated with GH and IGF-1 in skin interstitial fluid and blood.

"Breaking down in tears, soaked in sweat, and sick from the heat": Media-based composite narratives of first responders working during the 2021 Heat Dome.

BACKGROUND: During the summer of 2021, a deadly, unprecedented multiday Heat Dome engulfed western Canada. As a result of this extreme heat event (EHE), emergency dispatchers received an unparalleled increase in incoming 911 calls for ambulance, police, and fire (as first responders) services to attend to hundreds of heat-vulnerable community members succumbing to the heat. With 103 all-time heat records broken during this EHE and indoor temperatures of nearly 40°C, the first responders attending these calls faced extensive job demands and highly challenging operating conditions. Initial investigations have explored the health system-level impacts; however, little has been done to explore the impact on the first responders themselves. Therefore, this study aimed to improve our understanding of EHEs' impacts on the operational capabilities and health of first responders, specifically police, fire, ambulance, and dispatch services. METHODS: A systematized review and content analysis of media articles published on the 2021 Heat Dome in Canada was conducted (n = 2909), and four media-based composite narratives were developed highlighting police, fire, ambulance, and dispatch services. The Job Demands-Resources (JD-R) model was applied as a theoretical framework for occupational burnout. RESULTS: The media-based composite narratives highlighted that first responders faced record-breaking call volumes, increased mental-health-related claims, and exhaustive heat-related physiological stress. Using the JD-R model as a theoretical framework for occupational burnout, we identified three measures of stressful job demand: work overload (e.g., the surge in call volume, firefighters responding to medical emergencies), emotional demands (e.g., severe medical emergencies, sudden deaths, unresponsive patients, distraught family members), and physical demands (e.g., resuscitation in personal protective equipment, heat-related illness). CONCLUSION: The experiences described underscore the importance of supporting first responders during work in extreme heat conditions. These findings have important implications for addressing rising rates of burnout during and following public health crises, such as EHEs, a problem that is increasingly being recognized as a threat to the Canadian public healthcare system.

Agreement between measured and self-reported physiological strain in males and females during simulated occupational heat stress.

RATIONALE: Monitoring physiological strain is recommended to safeguard workers during heat exposure, but is logistically challenging. The perceptual strain index (PeSI) is a subjective estimate thought to reflect the physiological strain index (PSI) that requires no physiological monitoring. However, sex is known to influence perceptions of heat stress, potentially limiting the utility of the PeSI. OBJECTIVES: The objective of this study was to assess whether sex modifies the relationship between PeSI and PSI. METHODS: Thirty-four adults (15 females) walked on a treadmill (moderate intensity; ~200 W/m2) for 180 min or until termination (volitional fatigue, rectal temperature ≥39.5°C) in 16°C, 24°C, 28°C, and 32°C wet-bulb globe temperatures. Rectal temperature and heart rate were recorded to calculate PSI (0-10 scale). Rating of perceived exertion and thermal sensation were recorded to calculate PeSI (0-10 scale). Relationships between PSI and PeSI were evaluated via linear mixed models. Mean bias (95% limits of agreement [LoA]) between PSI and PeSI was assessed via Bland-Altman analysis. Mean absolute error between measures was calculated by summing absolute errors between the PeSI and the PSI and dividing by the sample size. FINDINGS: PSI increased with PeSI (p < 0.01) but the slope of this relation was not different between males and females (p = 0.83). Mean bias between PSI and PeSI was small (-0.4 points), but the 95% LoA (-3.5 to 2.7 points) and mean absolute error were wide (1.3 points). IMPACT: Our findings indicate that sex does not appreciably impact the agreement between the PeSI and PSI during simulated occupational heat stress. The PeSI is not a suitable surrogate for the PSI in either male or female workers.

Greater hyperthermia in men with type 2 diabetes does not lead to higher serum levels of cellular stress biomarkers following exercise-heat stress.

Type 2 diabetes (T2D) is associated with worsening age-related impairments in heat loss, causing higher core temperature during exercise. We evaluated whether these thermoregulatory impairments occur with altered serum protein responses to heat stress by measuring cytoprotection, inflammation, and tissue damage biomarkers in middle-aged-to-older men (50-74 years) with (n = 16) and without (n = 14) T2D following exercise in 40°C. There were no changes in irisin, klotho, HSP70, sCD14, TNF-α, and IL-6, whereas NGAL (+539 pg/mL, p = 0.002) and iFABP (+250 pg/mL, p < 0.001) increased similarly across groups. These similar response patterns occurred despite elevated core temperature in individuals with T2D, suggesting greater heat vulnerability.

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.

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.