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.

The intensity-dependent effects of exercise and superimposing environmental heat stress on autophagy in peripheral blood mononuclear cells from older men.

Autophagy is a vital cellular process, essential to maintaining cellular function during acute physiological stressors including exercise and heat stress. We previously showed that autophagy occurs during exercise in an intensity-dependent manner in peripheral blood mononuclear cells (PBMCs) from young men, with elevated responses in the heat. However, given autophagy declines with age, it is unclear whether a similar pattern of response occurs in older adults. Therefore, we evaluated autophagy and the cellular stress response [i.e., apoptosis, inflammation, and the heat shock response (HSR)] in PBMCs from 10 healthy older men [mean (SD): aged 70 yr (5)] in response to 30 min of semirecumbent cycling at low, moderate, and vigorous intensities [40, 55, and 70% maximal oxygen consumption (V̇o2max), respectively] in a temperate (25°C) environment, with an additional vigorous-intensity bout (70% of V̇o2max) performed in a hot environment (40°C). Responses were evaluated before and after exercise, as well as throughout a 6-h seated recovery period performed in the same environmental conditions as the respective exercise bout. Proteins were assessed via Western blot. Although we observed elevations in mean body temperature with each increase in exercise intensity, autophagy was only stimulated during vigorous-intensity exercise, where we observed elevations in LC3-II (P < 0.05). However, when the same exercise was performed in the heat, the LC3-II response was attenuated, which was accompanied by significant p62 accumulation (P < 0.05). Altogether, our findings demonstrate that older adults exhibit autophagic impairments when the same vigorous-intensity exercise is performed in hot environments, potentially underlying heat-induced cellular vulnerability in older men.NEW & NOTEWORTHY We demonstrate that autophagic stimulation occurs in response to short-duration (30-min) vigorous-intensity exercise in peripheral blood mononuclear cells from older adults; however, no changes in autophagy occur during low- or moderate-intensity exercise. Moreover, older adults exhibit autophagic impairments when the same vigorous-intensity exercise is performed in hot ambient conditions. When paired with an attenuated heat shock response, as well as elevated apoptotic responses, older men may exhibit greater cellular vulnerability to exertional heat stress.

Dose-dependent nonthermal modulation of whole body heat exchange during dynamic exercise in humans.

To maintain heat balance during exercise, humans rely on skin blood flow and sweating to facilitate whole body dry and evaporative heat exchange. These responses are modulated by the rise in body temperature (thermal factors), as well as several nonthermal factors implicated in the cardiovascular response to exercise (i.e., central command, mechanoreceptors, and metaboreceptors). However, the way these nonthermal factors interact with thermal factors to maintain heat balance remains poorly understood. We therefore used direct calorimetry to quantify the effects of dose-dependent increases in the activation of these nonthermal stimuli on whole body dry and evaporative heat exchange during dynamic exercise. In a randomized crossover design, eight participants performed 45-min cycling at a fixed metabolic heat production (200 W/m2) in warm, dry conditions (30°C, 20% relative humidity) on four separate occasions, differing only in the level of lower-limb compression applied via bilateral thigh cuffs pressurized to 0, 30, 60, or 90 mmHg. This model provoked increments in nonthermal activation while ensuring the heat loss required to balance heat production was matched across trials. At end-exercise, dry heat loss was 2 W/m2 [1, 3] lower per 30-mmHg pressure increment (P = 0.006), whereas evaporative heat loss was elevated 5 W/m2 [3, 7] with each pressure increment (P < 0.001). Body heat storage and esophageal temperature did not differ across conditions (both P ≥ 0.600). Our findings indicate that the nonthermal factors engaged during exercise exert dose-dependent, opposing effects on whole body dry and evaporative heat exchange, which do not significantly alter heat balance.NEW & NOTEWORTHY To maintain heat balance during exercise, humans rely on skin blood flow and sweating to facilitate dry and evaporative heat exchange. These responses are modulated by body temperatures (thermal factors) and several nonthermal factors (e.g., central command, metaboreceptors), although the way thermal and nonthermal factors interact to regulate body temperature is poorly understood. We demonstrate that nonthermal factors exert dose-dependent, opposing effects on dry and evaporative heat loss, without altering heat storage during dynamic exercise.

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.

Effect of sportswear on performance and physiological heat strain during prolonged running in moderately hot conditions.

INTRODUCTION: This study examined the impact of different upper-torso sportswear technologies on the performance and physiological heat strain of well-trained and national-level athletes during prolonged running in moderately hot conditions. METHODS: A randomized crossover design was employed in which 20 well-trained (n = 16) and national-level (n = 4) athletes completed four experimental trials in moderately hot conditions (35°C, 30% relative humidity). In each trial, participants ran at 70% of their peak oxygen uptake (70% V̇O2peak ) for 60 min, while wearing a different upper-body garment: cotton t-shirt, t-shirt with sweat-wicking fabric, compression t-shirt, and t-shirt with aluminum dots lining the inside of the upper back of the garment. Running speed was adjusted to elicit the predetermined oxygen consumption associated with 70% V̇O2peak . Physiological (core and skin temperatures, total body water loss, and urine specific gravity) and perceptual (thermal comfort and sensation, ratings of perceived exertion, and garment cooling functionality) parameters along with running speed at 70% V̇O2peak were continuously recorded. RESULTS: No significant differences were observed between the four garments for running speed at 70% V̇O2peak , physiological heat strain, and perceptual responses (all p > 0.05). The tested athletes reported larger areas of perceived suboptimal cooling functionality in the cotton t-shirt and the t-shirt with aluminum dots relative to the sweat-wicking and compression t-shirts (d: 0.43-0.52). CONCLUSION: There were not differences among the tested garments regarding running speed at 70% V̇O2peak , physiological heat strain, and perceptual responses in well-trained and national-level endurance athletes exercising in moderate heat.

Recommended water immersion duration for the field treatment of exertional heat stroke when rectal temperature is unavailable.

INTRODUCTION: The recommended treatment for exertional heat stroke is immediate, whole-body immersion in < 10 °C water until rectal temperature (Tre) reaches ≤ 38.6 °C. However, real-time Tre assessment is not always feasible or available in field settings or emergency situations. We defined and validated immersion durations for water temperatures of 2-26 °C for treating exertional heat stroke. METHODS: We compiled data for 54 men and 18 women from 7 previous laboratory studies and derived immersion durations for reaching 38.6 °C Tre. The resulting immersion durations were validated against the durations of cold-water immersion used to treat 162 (98 men; 64 women) exertional heat stroke cases at the Falmouth Road Race between 1984 and 2011. RESULTS: Age, height, weight, body surface area, body fat, fat mass, lean body mass, and peak oxygen uptake were weakly associated with the cooling time to a safe Tre of 38.6 °C during immersions to 2-26 °C water (R2 range: 0.00-0.16). Using a specificity criterion of 0.9, receiver operating characteristics curve analysis showed that exertional heat stroke patients must be immersed for 11-12 min when water temperature is ≤ 9 °C, and for 18-19 min when water temperature is 10-26 °C (Cohen's Kappa: 0.32-0.75, p < 0.001; diagnostic odds ratio: 8.63-103.27). CONCLUSION: The reported immersion durations are effective for > 90% of exertional heat stroke patients with pre-immersion Tre of 39.5-42.8 °C. When available, real-time Tre monitoring is the standard of care to accurately diagnose and treat exertional heat stroke, avoiding adverse health outcomes associated with under- or over-cooling, and for implementing cool-first transport second exertional heat stroke policies.

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.

Changes in surrogate markers of intestinal epithelial injury and microbial translocation in young and older men during prolonged occupational heat stress in temperate and hot conditions.

PURPOSE: Exertional heat stress can cause damage to the intestinal epithelium and disrupt gastrointestinal barrier integrity, leading to microbial translocation (MT) linked to the development of heat stroke. This study aimed to assess age-related differences in markers of intestinal epithelial injury and MT following non-heat stress and high-heat stress exercise in healthy young and older men. METHODS: Markers of intestinal epithelial injury (intestinal fatty acid-binding protein-'IFABP') and MT (soluble cluster of differentiation 14-'sCD14'; and lipopolysaccharide-binding protein-'LBP') were assessed in healthy young (18-30 y, n = 13) and older (50-70 y) men (n = 12). Blood samples were collected before, after 180 min of moderate-intensity (metabolic rate: 200 W/m2) walking and following 60 min recovery in either a non-heat stress [temperate: 21.9 °C, 35% relative humidity (RH)] or high-heat stress (hot: 41.4 °C, 35% RH) environment. RESULTS: There were no differences in IFABP and sCD14 between the young and older groups in the temperate condition, while LBP was greater in the older group (+ 0.66 ug/mL; + 0.08 to + 1.24 ug/mL). In the hot condition, the older group experienced greater increases in IFABP compared to the young group (+ 712 pg/mL/hr; + 269 to + 1154 pg/mL/hr). However, there were no clear between-group differences for sCD14 (+ 0.24 ug/mL/hr, - 0.22 to + 0.70 ug/mL/hr) or LBP (+ 0.86 ug/mL/hr, - 0.73 to + 2.46 ug/mL/hr). CONCLUSION: While older men may experience greater intestinal epithelial injury following exercise in the heat; this did not lead to a greater magnitude of microbial translocation relative to their younger counterparts.

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.

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.

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.

Hot Topic: A Systematic Review and Content Analysis of Heat-Related Messages During the 2021 Heat Dome in Canada.

CONTEXT: During the summer of 2021, western Canada experienced a deadly heat event. From the first heat alert to postevent reporting, thousands of media articles were published that reference the heat event. However, a gap remains in understanding how this communication chain-from the release of a public heat alert to information shared through media outlets to the public-currently operates to disseminate heat-related messaging across Canada. OBJECTIVE: To understand the role of digital media in delivering heat-health messaging during an extreme heat event in Canada. DESIGN: A qualitative content analysis was conducted using Canadian news articles published on the 2021 Heat Dome between June 2021 and February 2022 (n = 2909). The coding frame was designed to align with the basic framework for information gathering used in journalism (who, what, where, when, and how) and included both concept-driven and data-driven codes. RESULTS: Overall, 2909 unique media articles discussing the 2021 Heat Dome were identified, with the majority (74%) published by online news agencies (how). The highest article count was on June 29, 2021 (n = 159), representing 5% of the total data set (n = 2909) spanning 260 days (when); 57% of the identified locations were in British Columbia (where). Although we found that the top voices providing media-based heat-health messages are government officials (who), only 23% of articles included heat-health messaging that aligns with the government health alert bulletins released during extreme heat. In addition, heat-health messaging frequently included contradictory content, inconsistent language, or incorrect advice (what). CONCLUSION: The findings demonstrate clear opportunities to improve health communication related to extreme heat, perhaps most importantly, including updates to mass media messaging educating the public on heat-protective behaviors.

Reliability of laser-Doppler flowmetry derived measurements of forearm and calf cutaneous vasodilation during gradual local heating in young adults.

OBJECTIVES: Evaluate reliability of laser-Doppler flowmetry derived cutaneous vasodilation on the upper and lower limbs during gradual local heating. METHODS: In twenty-eight young adults (21 (SD 3) years, 14 females), absolute cutaneous vascular conductance (CVCabs) and CVC normalized to maximum vasodilation at 44 °C (%CVCmax) were assessed at two adjacent sites on each of the forearm and calf during gradual local skin heating (33-42 °C at 1 °C·5 min-1) for two identical trials (∼1 week apart). Responses were assessed for baseline, the steady-state heating plateau at 42 °C and the span (i.e. plateau-baseline). RESULTS: Between-day reliability was characterized as measurement consistency across trials. Within-day reliability was characterized as within-limb measurement consistency across adjacent skin sites. Between- and within-day absolute reliability (coefficient of variation) generally improved with heating, from poor (>25 %) at baseline to good (<10 %) for %CVCmax and moderate (10-25 %) for CVCabs for plateau and span. However, relative reliability (intraclass correlation coefficient) was generally not acceptable (<0.70) for any condition. Responses were generally consistent for females and males and there were no major forearm and calf differences. CONCLUSIONS: Consistency of CVC estimates improved during gradual local heating with negligible limb and sex differences, which are important considerations for experimental design and interpretation.

Involvement of nitric oxide synthase and reactive oxygen species in TRPA1-mediated cutaneous vasodilation in young and older adults.

OBJECTIVE: To investigate the nitric oxide synthase (NOS) and reactive oxygen species (ROS) contributions of the cutaneous vasodilator response to transient receptor potential ankyrin-1 channel (TRPA1) activation in young and older adults. MATERIALS AND METHODS: In sixteen young (20 ± 2 years, 8 females) and sixteen older adults (61 ± 5 years, 8 females), cutaneous vascular conductance normalized to maximum vasodilation (%CVCmax) was assessed at four dorsal forearm skin sites continuously perfused via microdialysis with: 1) vehicle solution (Control, 2 % dimethyl sulfoxide, 2 % Ringer, 96 % propylene glycol), 2) 10 mM Ascorbate (non-specific ROS inhibitor), 3) 10 mM L-NAME (non-specific NOS inhibitor), or 4) Ascorbate+L-NAME. The TRPA1 agonist cinnamaldehyde was co-administered at all sites [0 % (baseline), 2.9 %, 8.8 %, 26.4 %; ≥ 30 min per dose]. RESULTS: %CVCmax was not different between groups for Control, L-NAME, and Ascorbate (all p > 0.05). However, there were significant main dose effects for each site wherein %CVCmax was greater than baseline from 2.9 % to 26.4 % cinnamaldehyde for Control and Ascorbate, and at 26.4 % cinnamaldehyde for L-NAME and Ascorbate+L-NAME (all p < 0.05). For Ascorbate+L-NAME, there was a significant main group effect, wherein perfusion was 6 %CVCmax [95% CI: 2, 11, p < 0.05] greater in the older compared to the young group across all cinnamaldehyde doses. There was a significant main site effect for area under the curve wherein L-NAME and Ascorbate+L-NAME were lower than Control and Ascorbate across groups (all p < 0.05). CONCLUSION: The NOS-dependent cutaneous vasodilator response to TRPA1 activation is maintained in older adults, with no detectable contribution of ascorbate-sensitive ROS in either age group.

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.

Serum klotho concentrations in older men with hypertension or type 2 diabetes during prolonged exercise in temperate and hot conditions.

PURPOSE: Klotho is a cytoprotective protein that increases during acute physiological stressors (e.g., exercise heat stress), although age-related declines in klotho may underlie cellular vulnerability to heat stress. The present study aimed to compare serum klotho in healthy older men and men with type 2 diabetes (T2D) or hypertension (HTN) during prolonged exercise in temperate or hot conditions. METHODS: We evaluated serum klotho in 12 healthy older men (mean [SD]; 59 years [4]), 10 men with HTN (60 years [4]), and 9 men with T2D (60 years [5]) before and after 180 min of moderate-intensity (fixed metabolic rate of 200 W/m2; ~ 3.4 METs) exercise and 60 min of recovery in temperate (wet-bulb globe temperature (WBGT) 16 °C) and hot (WBGT 32 °C) environments. Core temperature (rectal), heart rate (HR), and heart rate reserve (HRR) were measured continuously while klotho was measured at the end of baseline, exercise, and recovery. RESULTS: Total exercise duration was reduced during the hot condition in older men with HTN and T2D than healthy older men (both p ≤ 0.049), despite similar core temperatures, HR, and HRR. Klotho was higher than rest following exercise in the heat in healthy older men (+ 191 pg/mL [189]; p < 0.001) and responses were greater (p = 0.036) than men with HTN (+ 118 pg/mL [49]; p = 0.030), although klotho did not increase in men with T2D (+ 4 pg/mL [71]; p ≥ 0.638). CONCLUSION: Given klotho's role in cytoprotection, older men with HTN and especially T2D may be at increased cellular vulnerability to prolonged exercise or physically demanding exercise in the heat.

Impacts of age, diabetes, and hypertension on serum endothelial monocyte-activating polypeptide-II after prolonged work in the heat.

BACKGROUND: With rising temperature extremes, older workers are becoming increasingly vulnerable to heat-related injuries because of age- and disease-associated decrements in thermoregulatory function. Endothelial monocyte-activating polypeptide-II (EMAP-II) is a proinflammatory cytokine that has not yet been well-characterized during heat stress, and which may mediate the inflammatory response to high levels of physiological strain. METHODS: We evaluated serum EMAP-II concentrations before and after 180 min of moderate-intensity work (200 W/m2 ) in temperate (wet-bulb globe temperature [WBGT] 16°C) and hot (WBGT 32°C) environments in heat-unacclimatized, healthy young (n = 13; mean [SD]; 22 [3] years) and older men (n = 12; 59 [4] years), and unacclimatized older men with hypertension (HTN) (n = 10; 60 [4] years) or type 2 diabetes (T2D) (n = 9; 60 [5] years). Core temperature and heart rate were measured continuously. RESULTS: In the hot environment, work tolerance time was lower in older men with HTN and T2D compared to healthy older men (both p < 0.049). While core temperature and heart rate reserve increased significantly (p < 0.001), they did not differ across groups. End-exercise serum EMAP-II concentrations were higher in young men relative to their older counterparts due to higher baseline levels (both p ≤ 0.02). Elevations in serum EMAP-II concentrations were similar between healthy older men and older men with HTN, while serum EMAP-II concentrations did not change in older men with T2D following prolonged work in the heat. CONCLUSION: Serum EMAP-II concentrations increased following prolonged moderate-intensity work in the heat and this response is influenced by age and the presence of HTN or T2D.

Continuous Monitoring of Entropy Production and Entropy Flow in Humans Exercising under Heat Stress.

Complex living systems, such as the human organism, are characterized by their self-organized and dissipative behaviors, where irreversible processes continuously produce entropy internally and export it to the environment; however, a means by which to measure human entropy production and entropy flow over time is not well-studied. In this article, we leverage prior experimental data to introduce an experimental approach for the continuous measurement of external entropy flow (released to the environment) and internal entropy production (within the body), using direct and indirect calorimetry, respectively, for humans exercising under heat stress. Direct calorimetry, performed with a whole-body modified Snellen calorimeter, was used to measure the external heat dissipation from the change in temperature and relative humidity between the air outflow and inflow, from which was derived the rates of entropy flow of the body. Indirect calorimetry, which measures oxygen consumption and carbon dioxide production from inspired and expired gases, was used to monitor internal entropy production. A two-compartment entropy flow model was used to calculate the rates of internal entropy production and external entropy flow for 11 middle-aged men during a schedule of alternating exercise and resting bouts at a fixed metabolic heat production rate. We measured a resting internal entropy production rate of (0.18 ± 0.01) W/(K·m2) during heat stress only, which is in agreement with published measurements. This research introduces an approach for the real-time monitoring of entropy production and entropy flow in humans, and aims for an improved understanding of human health and illness based on non-equilibrium thermodynamics.