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With mines extending deeper and rising surface temperatures, workers are exposed to hotter environments. This study aimed to characterize heat stress and strain in the Canadian mining industry and evaluate the utility of the Heat Strain Score Index (HSSI), combined with additional self-reported adverse health outcomes. An exploratory web-based survey was conducted among workers ( n  = 119) in the Canadian mining industry. The survey included 74 questions on workers' risk perception, strategies for heat stress management, and the HSSI-a validated tool to classify workplace heat stress based on various workplace factors and indicators of heat strain. Most workers reported that heat stress is an occupational hazard associated with their duties and tasks (89%). Based on the HSSI, 22% of respondents were classified as high risk, 42% at moderate risk, and 36% at low risk for heat stress and heat strain. Those with higher HSSI scores self-reported more heat-related adverse signs and symptoms with a higher prevalence of self-reported heat-related illness ( p  < 0.01). Despite workers reporting various self-initiated practices (e.g., drinking water) and management-enforced heat mitigation practices (e.g., rest breaks), many workers reported still having experienced signs or symptoms of heat stress (86%) and heat-related illnesses (37%). The study found elevated heat stress and strain levels among a sample of workers in the Canadian mining industry despite workers employing various heat-mitigating strategies. Heat stress management programs considering mining-specific factors and challenges are needed to safeguard worker health and safety.

We evaluated enterocyte damage (IFABP), microbial translocation (sCD14), and inflammatory responses (TNF-α, IL-6, CRP) in 16 older adults (66-78 years) during 8 hours rest in conditions simulating homes maintained at 22°C (control), the 26°C indoor temperature upper limit proposed by health agencies, and homes without air-conditioning during heatwaves (31°C, 36°C). Relative to 22°C, IFABP was elevated ~181 pg/mL after exposure to 31°C (P=0.07), and by ~378 pg/mL (P<0.001) after exposure to 36°C. No differences were observed for sCD14, TNF-α, IL-6, or CRP (all P≥0.26). Our data supports recommendations to maintain indoor temperatures ≤26°C to preserve gastrointestinal barrier integrity in heat-vulnerable persons.

Purpose: Exercise-induced heat acclimation can mitigate age-related reductions in heat-loss capacity, though performing repeated bouts of strenuous exercise in the heat may be untenable for many older adults. While short-term passive heat acclimation (e.g., ≤7 days of warm-water immersion) enhances whole-body heat loss in young adults, evidence of its efficacy in older adults is lacking. Thus, we examined whether 7-days warm-water immersion would improve whole-body heat loss in older adults., Methods: Twelve habitually active older men (median [IQR] age: 68 [64-73] years; peak oxygen uptake (V̇O2peak): 34.1 [29.4-36.1] mLO2·kg-1·min-1) completed 7 consecutive days of ~90-minutes warm-water immersion (~40 °C) with core (rectal) temperature clamped at ~38.5 °C for the final 60 minutes. Before and after the warm-water immersion intervention, whole-body total (evaporative + dry) heat loss was measured via direct calorimetry during three, 30-minute bouts of cycling at increasing fixed rates of metabolic heat production (150, 200, 250 W·m-2), each separated by 15-minutes rest, in a hot-dry environment (40 °C, ~13% relative humidity). Rectal temperature and heart rate were measured continuously., Results: Following 7 days of warm-water immersion, whole-body total heat loss was elevated by 23 [95% confidence interval: 14, 31] W·m-2 across exercise bouts (acclimation-effect: P < 0.001; interaction: P = 0.598). This was paralleled by reductions in core temperature and heart rate of 0.3 [0.2, 0.4] °C and 11 [8, 14] beats·min-1 (both, acclimation-effect: P < 0.001; interaction: P = 0.288), respectively., Conclusions: Seven consecutive days of warm-water immersion improved whole-body heat loss and reduced core temperature and cardiovascular strain across light-to-vigorous intensity exercise in habitually active older men. Passive heat acclimation may be an efficacious alternative to exercise-heat acclimation to improve heat-loss capacity. Studies are warranted to assess effectiveness in more heat-vulnerable populations., Competing Interests: Conflict of Interest and Funding Source: This study was supported by the Natural Sciences and Engineering Council of Canada (all funds held by Dr. Glen P. Kenny-RGPIN-2020-03891); G.P.K is supported by a University of Ottawa Industry Research Chair. K.T.J, F.K.O, R.D.M, B.J.R, N.J.K, N.V.K, and J.J.M are supported by the Human and Environmental Physiology Research Unit, University of Ottawa. R.D.M was supported by a Canadian Institutes of Health Research Postdoctoral Fellowship. F.K.O and J.J.M were supported by a Mitacs Accelerate Fellowship (IT30924). A.D.F is supported by the University of Thessaly, Greece. The authors declare no conflicts of interest., (Copyright © 2025 by the American College of Sports Medicine.)

Heart rate variability (HRV) has shown potential as a tool for monitoring thermal strain, but there is limited data to support its efficacy in older adults during prolonged heat exposures. We compared HRV between young (19-31 years, n  = 20) and older (61-78 years, n  = 39) adults during 9 h of heat exposure (40 °C, 9% RH). We also explored whether heart rate (HR) and/or HRV could be used to distinguish older adults who achieved elevated thermal strain, defined as either (1) an increase in core temperature >1.0 °C (occurring in 39%, 15/39) or (2) a reduction in systolic blood pressure >10 mm Hg (occurring in 67%, 26/39). Percentage of age-predicted maximal HR and percentage of heart rate reserve (HRR) were higher, whereas standard deviation of normal RR intervals, the square root of the mean of squared differences between successive RR intervals (RMSSD), high frequency power (HF), and cardiac vagal index (CVI) were lower in older compared to young adults during heat exposure ( P  ≤ 0.004). In older adults, increases in core temperature were correlated with percentage of age-predicted maximal HR, percentage of HRR, RMSSD, and CVI ( P  ≤ 0.031), whereas changes in systolic blood pressure were not significantly associated with HR or HRV indices ( P  ≥ 0.327). Receiver operating characteristic curve analysis indicated that HR and HRV indices had generally poor ability to identify older adults with elevated thermal strain (area under the curve ≤0.65). Age-related differences in HRV, consistent with vagal withdrawal among older adults, remained during daylong heat exposure, but marked heterogeneity of response likely contributed to HRV providing limited discriminatory value in identifying changes in core temperature or blood pressure in older adults., Competing Interests: The authors declare there are no competing interests.

While monitoring physiological strain is recommended to safeguard workers during heat exposure, it is logistically challenging. The perceptual strain index (PeSI) is a subjective estimate thought to reflect the physiological strain index (PSI) that requires no direct monitoring. However, advanced age and chronic diseases (hypertension/type 2 diabetes [T2D]) influence the perception of heat stress, potentially limiting the utility of the PeSI. We therefore assessed whether the relation and agreement between the PeSI and PSI during simulated work in various environmental conditions is modified by age and T2D/hypertension. Thirteen young adults and 37 older adults without ( n  = 14) and with T2D ( n  = 10) or hypertension ( n  = 13) walked on a treadmill (∼200 W/m 2 ) for 180 min or until termination (volitional fatigue, rectal temperature ≥39.5 °C) in 16, 24, 28, 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). The relation between hourly PSI and PeSI was assessed via linear mixed models. Mean bias (95% limits of agreement [LoA]) between PSI and PeSI was assessed via Bland-Altman analysis. PSI increased with PeSI ( p  < 0.001), but the slope of this relation was not different between young and older adults ( p  = 0.189) or as a function of chronic disease (within older adults; p  = 0.183). The mean bias between PSI and PeSI was small (0.02), but the 95% LoA was wide (-3.3-3.4). Together, a linear relation between PeSI and PSI was observed but agreement between these measures varied considerably across individuals and thus PeSI should not be used as a surrogate marker of PSI. Caution should be taken when utilizing the PeSI to estimate physiological strain on workers.

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 h 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 (SD: 0.04)) relative to control (1.04 (0.06); P  = 0.018). Similarly, standing systolic blood pressure was elevated 9 [0, 17] mmHg with foot immersion and neck cooling ( P  = 0.043). That said, neither difference remained statistically significant after adjusting for multiplicity ( P adjusted  ≥ 0.054). No differences in 30:15 ratio or standing systolic blood 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., Competing Interests: GPK, RDM, JJM, PB, and RJS reported receiving grants from the Canadian Institutes of Health Research and Health Canada. No other disclosures are declared by the authors.

Purpose: Brain-derived neurotrophic factor (BDNF) is a neuroprotective growth factor that increases in young adults during short, intense bouts of passive heat stress. However, this may not reflect the response in heat-vulnerable populations exposed to air temperatures more consistent with indoor overheating during hot weather and heatwaves, especially as the BDNF response to acute stressors may diminish with increasing age. We therefore evaluated the ambient and body temperature-dependent responses of BDNF in older adults during daylong passive heating., Methods: Sixteen older adults (6 females; aged 66-78 years) completed 8-h exposure to four randomized ambient conditions simulating those experienced indoors during hot weather and heatwaves in continental climates: 22 °C (air-conditioning; control), 26 °C (health-agency-recommended indoor temperature limit), 31 °C, and 36 °C (non-airconditioned home); all 45% relative humidity. To further investigate upstream mechanisms of BDNF regulation during thermal strain, we also explored associations between BDNF and circulating heat shock protein 70 (HSP70; taken as an indicator of the heat shock response)., Results: Circulating BDNF was elevated by ~ 28% (1139 [95%CI: 166, 2112] pg/mL) at end-exposure in the 36 °C compared to the 22 °C control condition (P = 0.026; 26 °C-and 31 °C-22 °C differences: P ≥ 0.090), increasing 90 [22, 158] pg/mL per 1 °C rise in ambient temperature (linear trend: P = 0.011). BDNF was also positively correlated with mean body temperatures (P = 0.013), which increased 0.12 [0.10, 0.13]°C per 1 °C rise in ambient temperature (P < 0.001). By contrast, serum HSP70 did not change across conditions (P ≥ 0.156), nor was it associated with BDNF (P = 0.376)., Conclusion: Our findings demonstrate a progressive increase in circulating BDNF during indoor overheating in older adults., (© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

While foot immersion and neck cooling have been recommended for protecting heat-vulnerable groups, recent evidence does not support their efficacy for mitigating increases in physiological heat strain in older adults. However, their influence on self-reported environmental symptoms and mood-state remains unclear. Seventeen older adults (nine females, median [interquartile range] age: 72 [69-74]) completed three randomized heat exposures (6-h; 38°C, 35% relative humidity) with no cooling (control), foot immersion to mid-calf in 20°C water for the final 40-min of each hour (foot immersion), or foot immersion with a wet towel (20°C) around the neck (foot immersion with neck cooling). Core temperature, skin temperature, and heart rate areas under the curve (AUC) were assessed as indicators of cumulative physiological strain. Environmental symptom scores (68-item environmental symptoms questionnaire) and mood disturbance (40-item profile of mood states questionnaire) were evaluated at end-heating (adjusted for pre-exposure). Core temperature AUC was not different between conditions ( p  = 0.418). However, the skin temperature and heart rate AUCs were 11.8°C · h [95% confidence interval: 8.1, 15.5] and 12.5 bpm · h [0.1, 24.8] lower for foot immersion and 16.6°C · h [12.9, 20.3] and 19.6 bpm · h [7.2, 32.0] lower for foot immersion with neck cooling compared to control ( p  ≤ 0.032). Environmental symptom scores were 0.8-fold [0.6, 1.0] lower for both foot immersion with and without neck cooling, compared to control (both p  = 0.036). Mood disturbance was not different between conditions (both p  ≥ 0.275). Foot immersion with and without neck cooling reduces self-reported environmental symptoms in older adults despite having little effect on physiological heat strain., Competing Interests: No potential conflict of interest was reported by the author(s)., (© 2024 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.)

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., Competing Interests: None declared.

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 yr (34 female) were exposed to simulated heat-wave conditions for 8-9 h. When assessed at the group level, it took rectal temperature 3.3 [bootstrap 95% confidence interval: 2.9-3.9] h to reach thermal equilibrium (<0.05°C/h 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°C-40°C, 9-45% RH), equilibrium times were longer, ranging from 4.4 [3.8-5.3] to 5.2 [4.9-5.4] h. Furthermore, rectal temperature equilibrium was delayed 0.9 [0.5-1.4] and 1.8 [0.9-2.7] h compared with whole body heat storage in young and older adults, respectively (only assessed in 40°C, 9% RH). Individual-level equilibrium times ranged from 1 to 8 h. These findings highlight the importance of ecologically relevant exposure durations in translational research assessing the physiological impacts of hot weather. NEW & NOTEWORTHY Deep body (rectal) temperature took 3-5 h on average and up to 6-8 h at the individual level to reach thermal equilibrium in young and older adults resting in the heat. Furthermore, stable rectal temperatures were delayed by up to 2 h relative to the achievement of heat balance (0 kJ/min rate of heat storage). We provide the first quantification of the temporal profiles of thermal strain during extended rest in conditions simulating hot weather.

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, IFABP LOG ), microbial translocation (soluble cluster of differentiation 14, sCD14 LOG ), and systemic inflammation (tumour necrosis factor alpha, TNF-α LOG ; interleukin 6, IL-6 LOG ; 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 IFABP LOG 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-6 LOG 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 sCD14 LOG and TNF-α LOG 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., Competing Interests: None to declare.

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., Competing Interests: No conflict of interest, financial or otherwise, are declared by the author(s).

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; V̇o 2peak 32.3 (7.6) mL·kg -1 ·min -1 ; n = 26; HbA 1c 5.1%-9.1%] and without diabetes [Control; aged 61 (5) yr; V̇o 2peak 37.5 (5.4) mL·kg -1 ·min -1 ; n = 26] during light- (∼40% V̇o 2peak ), moderate- (∼50% V̇o 2peak ), and vigorous- (∼65% V̇o 2peak ) 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.

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.

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/m 2 ) 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., (© 2024 The Authors. American Journal of Industrial Medicine published by Wiley Periodicals LLC.)

We investigated the utility of heart rate (HR) and heart rate variability (HRV) for identifying individuals who may terminate work early due to excessive heat strain. Forty-eight men and women (median = 36 years; Q1 = 20 years; Q3 = 54 years) attempted 180 min of moderate-intensity work at a fixed metabolic rate (∼200 W/m 2 ; ∼3.5 METs) in a hot environment (wet-bulb globe temperature: 32 °C). Receiver operating characteristics (ROC) curves were used to identify the ability of indices of HR (absolute HR, percentage of maximum HR, percentage of HR reserve) and HRV (root-mean-square of successive differences (RMSSD), high-frequency power, and detrended fluctuation analysis component alpha 1 (DFA α 1 )) to discriminate between participants who completed the 180 min work bout or terminated prematurely. Participants who terminated work prematurely ( n  = 26) exhibited higher HR and percentage of HR measures, as well as reduced RMSSD and DFA α 1 after the first hour of work compared to participants who completed the bout. The discriminative utility of HR and HRV indices was strongest within the first hour of work, with percentage of HR reserve demonstrating excellent discriminative power (ROC area under curve (AUC) of 0.8). Stratifying participants by age and sex improved ROC AUC point estimates for most indices, particularly in female participants. The study provides preliminary evidence supporting the use of noninvasive cardiac monitoring for predicting work tolerance in healthy individuals exposed to occupational heat stress. HR and percentage of HR reserve were suggested to discriminate work termination most effectively. Further investigations are warranted to explore the influence of individual factors and refine the discriminative thresholds for early identification of excessive occupational heat strain., Competing Interests: No conflict of interest, financial or otherwise, is declared by the author(s). The results of the present study do no constitute endorsement by ACSM. The results of the study are presented clearly, honestly, and without fabrication, falsification, or inappropriate data manipulation. All data are available from the corresponding author upon reasonable request.

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., Competing Interests: Declaration of interests GPK and RDM receive funding from the Canadian Institutes of Health Research and Health Canada. SRN receives funding from the Canadian Institutes of Health Research. NVK declares no competing interests., (Copyright © 2024 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY-NC-ND 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

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., Competing Interests: The authors declare no conflicts of interest., (Copyright © 2023 The Authors. Published by Wolters Kluwer Health, Inc.)

Older adults are at greater risk of heat-related morbidity and mortality during heat waves, which is commonly linked to impaired thermoregulation. However, little is known about the influence of increasing age on the relation between thermal strain and perceptual responses during daylong heat exposure. We evaluated thermal and perceptual responses in 20 young (19-31 yr) and 39 older adults (20 with hypertension and/or type 2 diabetes; 61-78 yr) resting in the heat for 9 h (heat index: 37°C). Body core and mean skin temperature areas under the curve (AUC, hours 0-9 ) were assessed as indicators of cumulative thermal strain. Self-reported symptoms (68-item environmental symptoms questionnaire) and mood disturbance (40-item profile of mood states questionnaire) were assessed at end-heating (adjusted for prescores). Body core temperature AUC was 2.4°C·h [1.0, 3.7] higher in older relative to young adults ( P < 0.001), whereas mean skin temperature AUC was not different (-0.5°C·h [-4.1, 3.2] P = 0.799). At end-heating, self-reported symptoms were not different between age groups (0.99-fold [0.80, 1.23], P = 0.923), with or without adjustment for body core or mean skin temperature AUC (both P ≥ 0.824). Mood disturbance was 0.93-fold [0.88, 0.99] lower in older, relative to young adults ( P = 0.031). Older adults with and without chronic health conditions experienced similar thermal strain, yet those with these conditions reported lower symptom scores and mood disturbance compared with young adults and their age-matched counterparts (all P ≤ 0.026). Although older adults experienced heightened thermal strain during the 9-h heat exposure, they did not experience greater self-reported symptoms or mood disturbance relative to young adults. NEW & NOTEWORTHY Despite experiencing greater cumulative thermal strain during 9 h of passive heat exposure, older adults reported similar heat-related symptoms and lower mood disturbance than young adults. Furthermore, self-reported symptoms and mood disturbance were lower in older adults with common age-associated health conditions than young adults and healthy age-matched counterparts. Perceptual responses to heat in older adults can underestimate their level of thermal strain compared with young adults, which may contribute to their increased heat vulnerability.

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 / m 2 ] 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.

The heat-related health burden is expected to persist and worsen in the coming years due to an aging global population and climate change. Defining the breadth and depth of our understanding of age-related changes in thermoregulation can identify underlying causes and strategies to protect vulnerable individuals from heat. We conducted the first systematic quantitative literature review to provide context to the historical experimental research of healthy older adults - compared to younger adults or unhealthy age matched cases - during exogenous heat strain, focusing on factors that influence thermoregulatory function (e.g. co-morbidities). We identified 4,455 articles, with 147 meeting eligibility criteria. Most studies were conducted in the US (39%), Canada (29%), or Japan (12%), with 71% of the 3,411 participants being male. About 71% of the studies compared younger and older adults, while 34% compared two groups of older adults with and without factors influencing thermoregulation. Key factors included age combined with another factor (23%), underlying biological mechanisms (18%), age independently (15%), influencing health conditions (15%), adaptation potential (12%), environmental conditions (9%), and therapeutic/pharmacological interventions (7%). Our results suggest that controlled experimental research should focus on the age-related changes in thermoregulation in the very old, females, those with overlooked chronic heat-sensitive health conditions (e.g. pulmonary, renal, mental disorders), the impact of multimorbidity, prolonged and cumulative effects of extreme heat, evidence-based policy of control measures (e.g. personal cooling strategies), pharmaceutical interactions, and interventions stimulating protective physiological adaptation. These controlled studies will inform the directions and use of limited resources in ecologically valid fieldwork studies., Competing Interests: Disclosure statement The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

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/m 2 ) 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/m 2 [1, 3] lower per 30-mmHg pressure increment ( P = 0.006), whereas evaporative heat loss was elevated 5 W/m 2 [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.

Heat waves can cause dangerous elevations in body temperature that can compromise cellular function and increase the risk of heat stroke and major cardiovascular events. Visiting a cooling center or other air-conditioned location is commonly recommended by health agencies to protect heat-vulnerable older persons but the associated cellular effects remain underexplored. We evaluated cellular stress responses in peripheral blood mononuclear cells (PBMC) from 19 older adults [71 (SD 2) yr; 9 females] before and after a 9-h heat exposure [40.3°C and 9.3% relative humidity (RH)], with participants moved to a cool room (∼23°C) for hours 5 and 6 (cooling group). Responses were compared with 17 older adults [72 (4) yr; 7 females] who remained in the heat for the entire 9 h (control group). Changes in proteins associated with autophagy, apoptotic signaling, acute inflammation, and the heat shock response (HSR) were assessed via Western blot. Although both groups experienced similar elevations in physiological strain before the cooling center intervention, brief cooling resulted in stark albeit transient reductions in core temperature and heart rate. At end-exposure, autophagy proteins LC3-II and p62 were elevated 1.9-fold [95% CI: 1.2, 2.8] and 2.3-fold [1.4, 3.8], respectively, in the control group relative to cooling group. This was paired with a 2.8-fold [1.6, 4.7] greater rise in apoptotic protein cleaved-caspase-3 in the control group compared with the cooling group. Our findings indicate that 2 h of ambient cooling midway through a 9-h simulated heat wave may preserve autophagy and mitigate heat-induced cellular stress in older adults. NEW & NOTEWORTHY Heat waves can lead to dangerous elevations in body temperature, increasing the risk of life-threatening health conditions. Visiting a cooling center or other air-conditioned location is commonly recommended to protect heat-vulnerable older persons, although the effects on the cellular stress response remain unknown. We found that 2 h of ambient cooling midway through a 9 h simulated heat wave preserves autophagy, a vital cellular survival mechanism, and mitigates accompanying pathways of cellular stress in older adults.

Public health agencies recommend that older adults without home air-conditioning visit cooling centres to mitigate physiological strain from high ambient temperatures during heat waves. However, there is little evidence regarding their influence on self-reported environmental symptoms and mood-state after returning to the heat., Methods: Forty adults (64-79 years) underwent a daylong laboratory-based indoor overheating simulation (9-hours, heat index: 37 °C) with (cooling, n = 20) or without (control, n = 20) a 2-hour air-conditioning intervention (hours 5-6). Mean skin and core temperature areas under the curve (AUC, hours 0-9) were used to assess cumulative thermal strain. Group differences in total symptom scores and subjective heat illness (68-item environmental symptoms questionnaire) as well as total mood disturbance and energy index (40-item profile of mood states questionnaire) were evaluated at end-heating (adjusted for pre-exposure scores)., Results: Cooling reduced mean skin and core temperature AUCs by 4.0 [0.1, 0.8] and 1.6 [0.4, 2.8] °C·hour compared to control (both p < 0.048). However, at end-heating neither mean skin nor core temperatures differed between groups (both p > 0.999). Total symptom scores and subjective heat illness were 0.58-fold [0.44, 0.77] and 0.56-fold [0.40, 0.78] lower in the cooling compared to control group (both p < 0.001). Mood disturbance was 0.91-fold [0.83, 0.99] lower for cooling than control (p = 0.036), although energy index was not different between groups (p = 0.141)., Conclusion: Cooling centres can have sustained positive effects on perceived thermal strain and mood-state in older adults after returning to the heat. However, continued vigilance and use of appropriate countermeasures to mitigate physiological strain from indoor overheating should be encouraged as body temperatures can rapidly return to pre-cooling levels., Competing Interests: Declaration of Competing Interest No conflicts of interest, financial or otherwise, are declared by the authors., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Aging is associated with an elevated risk of heat-related mortality and morbidity, attributed, in part, to declines in thermoregulation. However, comparisons between young and older adults have been limited to brief exposures (1-4 h), which may not adequately reflect the duration or severity of the heat stress experienced during heat waves. We therefore evaluated physiological responses in 20 young (19-31 yr; 10 females) and 39 older (61-78 yr; 11 females) adults during 9 h of rest at 40°C and 9% relative humidity. Whole body heat exchange and storage were measured with direct calorimetry during the first 3 h and final 3 h. Core temperature (rectal) was monitored continuously. The older adults stored 88 kJ [95% confidence interval (CI): 29, 147] more heat over the first 3 h of exposure ( P = 0.006). Although no between-group differences were observed after 3 h [young: 37.6°C (SD 0.2°C) vs. older: 37.7°C (0.3°C); P = 0.216], core temperature was elevated by 0.3°C [0.1, 0.4] (adjusted for baseline) in the older group at hour 6 [37.6°C (0.2°C) vs. 37.9°C (0.2°C); P < 0.001] and by 0.2°C [0.0, 0.3] at hour 9 [37.7°C (0.3°C) vs. 37.8°C (0.3°C)], although the latter comparison was not significant after multiplicity correction ( P = 0.061). Our findings indicate that older adults sustain greater increases in heat storage and core temperature during daylong exposure to hot dry conditions compared with their younger counterparts. This study represents an important step in the use of ecologically relevant, prolonged exposures for translational research aimed at quantifying the physiological and health impacts of hot weather and heat waves on heat-vulnerable populations. NEW & NOTEWORTHY We found greater increases in body heat storage and core temperature in older adults than in their younger counterparts during 9 h of resting exposure to hot dry conditions. Furthermore, the age-related increase in core temperature was exacerbated in older adults with common heat-vulnerability-linked health conditions (type 2 diabetes and hypertension). Impairments in thermoregulatory function likely contribute to the increased risk of heat-related illness and injury seen in older adults during hot weather and heat waves.

With rising global temperatures, heat-related mortality is increasing, particularly among older adults. Although this is often attributed to declines in thermoregulatory function, little is known regarding the effect of age on the cellular processes associated with mitigating heat-induced cytotoxicity. We compared key components of the cellular stress response in 19 young (19-31 yr; 10 female) and 37 older adults (61-78 yr; 10 female) during 9 h of heat exposure (40°C, 9% relative humidity). Mean body temperature (T body ) was calculated from core and skin temperatures. Changes in proteins associated with autophagy, apoptotic signaling, acute inflammation, and the heat shock response were assessed via Western blot in peripheral blood mononuclear cells harvested before and after exposure. T body increased by 1.5 (SD 0.3)°C and 1.7 (0.3)°C in the young and older adults, respectively. We observed similar elevations in autophagy-related proteins (LC3-II and LC3-II/I) in young and older adults (both P ≥ 0.121). However, the older adults displayed signs of autophagic dysfunction, evidenced by a 3.7-fold [95% CI: 2.4, 5.6] greater elevation in the selective autophagy receptor p62 ( P < 0.001). This was paired with elevations in apoptotic responses, with a 1.7-fold [1.3, 2.3] increase in cleaved caspase-3 in the older relative to young adults ( P < 0.001). Older adults also exhibited diminished heat shock protein 90 responses (0.7-fold [0.5, 0.9] vs. young, P = 0.011) and, at any given level of thermal strain (T body area under the curve), elevated tumor necrosis factor-α (1.5-fold [1.0, 2.5] vs. young, P = 0.008). Attenuated autophagic responses may underlie greater vulnerability to heat-induced cellular injury in older adults. NEW & NOTEWORTHY We demonstrate for the first time that peripheral blood mononuclear cells from older adults exhibit signs of autophagic impairments during daylong (9 h) heat exposure relative to their younger counterparts. This was paired with greater apoptotic signaling and inflammatory responses, and an inability to stimulate components of the heat shock response. Thus, autophagic dysregulation during prolonged heat exposure may contribute to age-related heat vulnerability during hot weather and heat waves.

Background: Health agencies, including the U.S. Centers for Disease Control and Prevention and the World Health Organization, recommend that heat-vulnerable older adults without home air-conditioning should visit cooling centers or other air-conditioned locations (e.g., a shopping mall) during heat waves. However, experimental evidence supporting the effectiveness of brief air-conditioning is lacking., Objective: We evaluated whether brief exposure to an air-conditioned environment, as experienced in a cooling center, was effective for limiting physiological strain in older adults during a daylong laboratory-based heat wave simulation., Methods: Forty adults 64-79 years of age underwent a 9-h simulated heat wave (heat index: 37°C) with (cooling group, n = 20 ) or without (control group, n = 20 ) a cooling intervention consisting of 2-h rest in an air-conditioned room ( ∼ 23 ° C , hours 5-6). Core and skin temperatures, whole-body heat exchange and storage, cardiovascular function, and circulating markers of acute inflammation were assessed., Results: Core temperature was 0.8°C (95% CI: 0.6, 0.9) lower in the cooling group compared with the control group at the end of the cooling intervention ( p < 0.001 ; hour 6), and it remained 0.3°C (95% CI: 0.2, 0.4) lower an hour after returning to the heat ( p < 0.001 ; hour 7). Despite this, core temperatures in each group were statistically equivalent at hours 8 and 9, within ± 0.3 ° C ( p ≤ 0.005 ). Cooling also acutely reduced demand on the heart and improved indices of cardiovascular autonomic function ( p ≤ 0.021 ); however, these outcomes were not different between groups at the end of exposure ( p ≥ 0.58 )., Discussion: Brief air-conditioning exposure during a simulated heat wave caused a robust but transient reduction in core temperature and cardiovascular strain. These findings provide important experimental support for national and international guidance that cooling centers are effective for limiting physiological strain during heat waves. However, they also show that the physiological impacts of brief cooling are temporary, a factor that has not been considered in guidance issued by health agencies. https://doi.org/10.1289/EHP11651.

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 A 1c )? What is the main finding and its importance? No association was found between haemoglobin A 1c (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 A 1c exhibited higher body core temperature and heart rate responses. Thus, while haemoglobin A 1c 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 A 1c ) is unknown. We evaluated the association between haemoglobin A 1c 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; HbA 1c 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 A 1c 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 A 1c . Thus, while haemoglobin A 1c 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., (© 2022 The Authors. Experimental Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society.)

Adverse Childhood Experiences (ACEs) are known to contribute to later mental health. Conversely, Benevolent Childhood Experiences (BCEs) may buffer against mental health difficulties. The importance of ACEs and BCEs for mental health of both parents and children may be most obvious during periods of stress, with potential consequences for functioning of the family. Subgroups of ACEs and BCEs in parents during the COVID-19 pandemic were investigated and validated in relation to indices of parent, child, and family well-being. In May 2020, ACEs/BCEs were assessed in 547 parents of 5-18-year-old children from the U.K., U.S., Canada, and Australia. Subgroups of parents with varying levels of ACEs and BCEs were identified via latent class analysis. The subgroups were validated by examining associations between class membership and indices of parent and child mental health and family well-being. Four latent classes were identified: low-ACEs/high-BCEs, moderate-ACEs/high-BCEs, moderate-ACEs/low-BCEs, and high-ACEs/moderate-BCEs. Regardless of the extent of BCEs, there was an increased risk of parent and child mental health difficulties and family dysfunction among those reporting moderate-to-high levels of ACEs. Parents' history of adversity may influence the mental health of their family. These findings highlight the importance of public health interventions for preventing early-life adversity.

New Findings: What is the central question of this study? Does acute intradermal administration of the antioxidant ascorbate augment local forearm cutaneous vasodilatation and sweating via nitric oxide synthase (NOS)-dependent mechanisms during exercise-heat stress in older adults with uncomplicated controlled hypertension? What is the main finding and its importance? Relative to the control site, ascorbate had no effect on forearm cutaneous vascular conductance (CVC) and sweat rate, although CVC was reduced with NOS inhibition in older adults with hypertension. Acute local administration of ascorbate to forearm skin does not modulate heat loss responses during exercise-heat stress in older adults with hypertension., Abstract: Nitric oxide synthase (NOS) contributes to the heat loss responses of cutaneous vasodilatation and sweating during exercise. However, the contribution of NOS may be attenuated in individuals with uncomplicated, controlled hypertension due to elevated oxidative stress, which can reduce NO bioavailability. We evaluated the hypothesis that the acute local intradermal administration of the antioxidant ascorbate would enhance cutaneous vasodilatation and sweating via NOS-dependent mechanisms during an exercise-heat stress in adults with hypertension. Habitually active adults who were normotensive (n = 14, 7 females, 62 ± 4 years) or had uncomplicated, controlled hypertension (n = 13, 6 females, 62 ± 5 years) performed 30 min of moderate-intensity (50% of their pre-determined peak oxygen uptake) semi-recumbent cycling in the heat (35°C, 20% relative humidity). Cutaneous vascular conductance (CVC) and sweat rate were assessed at four forearm skin sites continuously perfused with (1) lactated Ringer solution (Control), (2) 10 mM antioxidant ascorbate, (3) 10 mM N G -nitro-l-arginine methyl ester (l-NAME), a non-selective NOS inhibitor, or (4) a combination of ascorbate and l-NAME. Relative to Control, no effect of ascorbate was observed on CVC or sweating in either group (P = 0.619). However, l-NAME reduced CVC relative to Control in both groups (P ≤ 0.038). No effect of any treatment on sweating was observed (P ≥ 0.306). Thus, acute local administration of ascorbate to forearm skin does not enhance the activation of heat loss responses of cutaneous vasodilatation and sweating in older adults, and those with hypertension during an exercise-heat stress., (© 2022 The Authors. Experimental Physiology © 2022 The Physiological Society.)

Aging is associated with attenuated sweat gland function, which has been suggested to occur in a peripheral-to-central manner. However, evidence supporting this hypothesis remains equivocal. We revisited this hypothesis by evaluating the sweat rate across the limbs and trunk in young and older men during whole-body, passive heating. A water-perfused suit was used to raise and clamp esophageal temperature at 0.6°C (low-heat strain) and 1.2°C (moderate-heat strain) above baseline in 14 young (24 (SD 5) years) and 15 older (69 (4) years) men. Sweat rate was measured at multiple sites on the trunk (chest, abdomen) and limbs (biceps, forearm, quadriceps, calf) using ventilated capsules (3.8 cm 2 ). Sweat rates, expressed as the average of 5 min of stable sweating at low- and moderate-heat strain, were compared between groups (young, older) and regions (trunk, limbs) within each level of heat strain using a linear mixed-effects model with nested intercepts (sites nested within region nested within participant). At low-heat strain, the age-related reduction in sweat rate (older-young values) was greater at the trunk (0.65 mg/cm 2 /min [95% CI 0.44, 0.86]) compared to the limbs (0.42 mg/cm 2 /min [0.22, 0.62]; interaction: p = 0.010). At moderate-heat strain, sweat rate was lower in older compared to young (main effect: p = 0.025), albeit that reduction did not differ between regions (interaction: p = 0.888). We conclude that, contrary to previous suggestions, the age-related decline in sweat rate was greater at the trunk compared to the limbs at low-heat strain, with no evidence of regional variation in that age-related decline at moderate-heat strain., (© 2022 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.)

Heat-stress-induced dehydration is associated with extracellular hyperosmolality. To counteract the associated stress, cells employ cytoprotective mechanisms, including autophagy; however, the autophagic response to hyperosmotic stress has yet to be evaluated in humans. Thus, we investigated autophagy and associated cellular stress pathways [the heat shock response (HSR), apoptosis, and the acute inflammatory response] to isosmotic and hyperosmotic conditions with and without hyperthermia in 12 young men (mean [SD]; 25 [5] yr). Participants received a 90-min intravenous infusion of either isosmotic (ISO; 0.9% NaCl; serum osmolality of 293 [4] mosmol/kgH 2 O) or hyperosmotic (HYP; 3.0% NaCl; 300 [6] mosmol/kgH 2 O) saline, followed by passive whole body heating using water perfused suit to increase esophageal temperature by ∼0.8°C. Peripheral blood mononuclear cells were harvested at baseline (preinfusion), postinfusion, and after heating, and changes in protein content were analyzed via Western blotting. Post infusion, the LC3-II/I ratio was higher in HYP compared with ISO infusion ( P < 0.001), although no other protein changes were observed (all P > 0.050). Following passive heating, autophagy increased in HYP, as demonstrated by an increase in LC3-II from baseline ( P = 0.004) and an elevated LC3-II/I ratio compared with ISO ( P = 0.035), and a decrease in p62 when compared with the ISO condition ( P = 0.019). This was accompanied by an elevation in cleaved caspase-3 following heating in the HYP condition ( P < 0.010); however, the HSR and acute inflammatory response did not change under any condition (all P > 0.050). Taken together, our findings indicate that serum hyperosmolality induces autophagy and apoptotic signaling during mild hyperthermia with minimal autophagic activation during normothermia. NEW & NOTEWORTHY We demonstrate that a physiologically relevant increase in serum osmolality causes minimal activation of the autophagic response. However, the combined stressors of serum hyperosmolality and mild hyperthermia causes activation of both autophagy and apoptotic signaling. Thus, changes in osmotic homeostasis appear to influence the cell's cytoprotective ability during periods of heat stress, highlighting the importance of considering osmotic status when examining autophagic responses in vivo.

Metaboreflex activation augments sweating during mild-to-moderate hyperthermia in euhydrated (isosmotic isovolemic) individuals. Recent work indicates that extracellular hyperosmolality may augment metaboreflex-mediated elevations in sympathetic nervous activity. Our primary objective was, therefore, to test the hypothesis that extracellular hyperosmolality would exacerbate metaboreflex-mediated increases in sweat rate. On two separate occasions, 12 young men [means (SD): 25 (5) yr] received a 90-min intravenous infusion of either 0.9% saline (isosmotic condition, ISO) or 3.0% saline (hyperosmotic condition, HYP), resulting in a postinfusion serum osmolality of 290 (3) and 301 (7) mosmol/kgH 2 O, respectively. A whole body water perfusion suit was then used to increase esophageal temperature by 0.8°C above resting. Participants then performed a metaboreflex activation protocol consisting of 90-s isometric handgrip exercise (40% of their predetermined maximum voluntary contraction), followed by 150 s of brachial occlusion (trapping produced metabolites within the limb). Metaboreflex-induced sweating was quantified as the change in global sweat rate (from preisometric handgrip exercise to brachial occlusion), estimated as the surface area-weighted average of local sweat rate on the abdomen, axilla, chest, bicep, quadriceps, and calf, measured using ventilated capsules (3.8 cm 2 ). We also explored whether this response differed between body regions. The change in global sweat rate due to metaboreflex activation was significantly greater in HYP compared with ISO (0.03 mg/min/cm 2 [95% confidence interval: 0.00, 0.06]; P = 0.047), but was not modulated by body region (site × condition interaction: P = 0.679). These findings indicate that extracellular hyperosmolality augments metaboreflex-induced increases in global sweat rate, with no evidence for region-specific differences.

Observed individual variability in cardiac baroreflex sensitivity (cBRS) and heart rate variability (HRV) is extensive, especially during exposure to stressors such as heat. A large part of the observed variation may be related to the reliability (consistency) of the measurement. We therefore examined the test-retest reliability of cBRS and HRV measurements on three separate occasions in 14 young men (age: 24 (SD 5) years), at rest and during whole-body heating (water-perfused suit) to raise and clamp oesophageal temperature 0.6°C, 1.2°C and 1.8°C above baseline. Beat-to-beat measurements of RR interval and systolic blood pressure (BP) were obtained for deriving HRV (from RR), and cBRS calculated via (i) the spontaneous method, α coefficients and transfer function analysis at each level of heat strain, and (ii) during forced oscillations via squat-stand manoeuvres (0.1 Hz) before and after heating. Absolute values and changes in all cBRS estimates were variable but generally consistent with reductions in parasympathetic activity. cBRS estimates demonstrated poor absolute reliability (coefficient of variation ≥25%), but relative reliability (intraclass correlation coefficient; ICC) of some frequency estimates was acceptable (ICC ≥0.70) during low-heat strain (ICC: 0.56-0.74). After heating, forced oscillations in BP demonstrated more favourable responses than spontaneous oscillations (better reliability, lower minimum detectable change). Absolute reliability of HRV estimates were poor, but relative reliability estimates were often acceptable (≥0.70). Our findings illustrate how measurement consistency of cardiac autonomic modulation estimates are altered during heat stress, and we demonstrate the possible implications on research design and data interpretation., (© 2020 The Authors. Experimental Physiology © 2020 The Physiological Society.)

Laser-Doppler flowmetry (LDF) is commonly used to assess cutaneous vasodilatation responses, but its reliability (i.e. consistency) during whole-body passive heating is unknown. We therefore assessed the reliability of LDF-derived indices of cutaneous vasodilatation during incremental whole-body heating. Fourteen young men (age: 24 (SD 5) years) completed three identical trials, each separated by 1 week. During each trial, a water-perfused suit was used to raise and clamp oesophageal temperature at 0.6°C (low-heat strain; LHS) and 1.2°C (moderate-heat strain; MHS) above baseline. LDF-derived skin blood flow (SkBF) was measured at three dorsal mid-forearm sites, with local skin temperature clamped at 34°C. Data were expressed as absolute cutaneous vascular conductance (CVC abs ; SkBF/mean arterial pressure) and normalised to maximal conductance (%CVC max ) achieved via simultaneous local skin heating to 44°C and increasing oesophageal temperature to 1.8°C above baseline. Between-day reliability was characterised as measurement consistency across trials, while within-day reliability was characterised as measurement consistency across adjacent skin sites during each trial. Between- and within-day absolute reliability (coefficient of variation) generally improved with increasing heat strain, changing from poor (>25%) at baseline, poor-to-moderate (15-34%) at LHS, and moderate (10-25%) at MHS. Generally, these estimates were more consistent when expressed as %CVC max . Conversely, relative reliability was mostly acceptable (intraclass correlation coefficient ≥0.70) during LHS and when data were expressed as CVC abs . These findings indicate that the consistency of LDF-derived CVC estimates during heat stress depends on the level of heat strain and method of data expression, which should be considered when designing and interpreting experiments., (© 2020 The Authors. Experimental Physiology © 2020 The Physiological Society.)

The ventilated capsule technique is widely used to measure time-dependent changes in sweating in humans. However, evaluations of its reliability (consistency) have been restricted to the forearm, despite extensive regional heterogeneity in the sweating response. Given the importance of such information for experimental design, statistical analysis and interpretation, we determined the reliability of local sweat rate at nine sites during whole-body passive (resting) heating. On three separate occasions, a water-perfused suit was used to increase and clamp oesophageal temperature 0.6, 1.2 and 1.8°C above baseline in 14 young men [24 (SD 5) years of age], while sweat rate was measured at the forehead, chest, abdomen, biceps, forearm, hand, quadriceps, calf and foot using ventilated capsules (3.8 cm 2 ). Absolute and relative reliability were determined via the coefficient of variation (CV) and intraclass correlation coefficient (ICC), respectively. At low heat strain (0.6°C), almost all sites had acceptable relative reliability (ICC ≥ 0.70) and moderate absolute reliability (CV < 25%). At moderate heat strain (1.2°C), only the abdomen, hand, quadriceps and foot had acceptable relative reliability, whereas the forehead, abdomen, forearm, hand and quadriceps had moderate absolute reliability. At high heat strain (1.8°C), relative reliability was acceptable at the abdomen, quadriceps, calf and foot, whereas the chest, abdomen, forearm, hand, quadriceps, calf and foot had moderate absolute reliability. Our findings indicate that the measurement site and level of heat strain impact the consistency of local sweat rate measured via the ventilated capsule technique, and we demonstrate the possible implications for research design and data interpretation., (© 2020 The Authors. Experimental Physiology © 2020 The Physiological Society.)

With the increasing threat of climate change and the accompanying rise in the frequency and severity of extreme heat events, there are growing health concerns for heat-vulnerable elderly adults. Elderly adults are at increased risk of developing heat-related injuries, in part due to age-related declines in thermoregulatory and cellular function. Regarding the latter, the process of autophagy is activated as a cellular protective mechanism to counter heat-induced stress, but the extent that heat stress activates autophagy in elderly adults is not known. Further, the interplay between autophagy, the heat shock response (HSR), the acute inflammatory response, and apoptosis remains poorly understood in elderly adults. Therefore, the purpose of this study was to examine changes in autophagy, the HSR, inflammation, and apoptosis following increasing levels of ex vivo heat stress representative of physiologically relevant increases in body core temperatures (37-41 °C). Whole blood from 20 elderly adults (72 ± 4 years; 14 men, 6 women) was heated (via water immersion) to temperatures representative of normal resting conditions (normothermia; 37 °C), in addition to moderate and severe heat stress conditions (39, and 41 °C, respectively) for 90 min. Peripheral blood mononuclear cells (PBMC) were isolated and protein markers of autophagy, the HSR, acute inflammation, and apoptosis were examined. No significant increases in markers of autophagy or the HSR were observed following any temperature condition. However, an increase in acute inflammation was observed above baseline following moderate heat stress (39 °C), with further increases in inflammation and apoptosis observed during severe heat stress (41 °C). Our findings indicate that PBMCs from elderly adults do not exhibit increases in autophagy or the HSR following severe heat stress, potentially contributing to the elevated risk of cellular dysfunction seen in elderly adults during heat stress., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Purpose: Current occupational heat stress guidelines rely on time-weighted averaging to quantify the metabolic demands of variable-intensity work. However, variable-intensity work may be associated with impairments in whole-body total heat loss (dry + evaporative heat loss), especially in older workers, which exacerbate heat strain relative to constant-intensity work eliciting the same time-weighted average metabolic rate. We, therefore, used direct calorimetry to evaluate whether variable-intensity work would cause decrements in the average rate of whole-body total heat loss that augment body heat storage and core temperature compared with constant-intensity work in young and older men., Methods: Eight young (19-31 yr) and eight older (54-65 yr) men completed four trials involving 90 min of work (cycling) eliciting an average metabolic heat production of ~200 W·m in dry-heat (40°C, 20% relative humidity). One trial involved constant-intensity work (CON), whereas the others involved 10-min cycles of variable-intensity work: 5-min low-intensity and 5-min high-intensity (VAR 5:5), 6-min low-intensity and 4-min very high-intensity (VAR 6:4), and 7-min low- and 3-min very, very high-intensity (VAR 7:3). Metabolic heat production, total heat loss, body heat storage (heat production minus total heat loss), and core (rectal) temperature were measured throughout., Results: When averaged over each 90-min work period, metabolic heat production, total heat loss, and heat storage were similar between groups and conditions (all P ≥ 0.152). Peak core temperature (average of final 10 min) was also similar between groups and conditions (both P ≥ 0.111)., Conclusions: Whole-body total heat loss, heat storage, and core temperature were not significantly influenced by the partitioning of work intensity in young or older men, indicating that time-weighted averaging appears to be appropriate for quantifying the metabolic demands of variable-intensity work to assess occupational heat stress.

Purpose: Time-weighted averaging is used in occupational heat stress guidelines to estimate the metabolic demands of variable-intensity work. However, compared to constant-intensity work of the same time-weighted average metabolic rate, variable-intensity work may cause decrements in total heat loss (dry + evaporative heat loss) that exacerbate heat storage in women. We therefore used direct calorimetry to assess whole-body total heat loss and heat storage (metabolic heat production minus total heat loss) in women and men during constant- and variable-intensity work of equal average intensity., Methods: Ten women [mean (SD); 31 (11) years] and fourteen men [30 (8) years] completed two trials involving 90-min of constant- and variable-intensity work (cycling) eliciting an average metabolic heat production of ~ 200 W/m 2 in dry-heat (40 °C, ~ 15% relative humidity). External work was fixed at ~ 40 W/m 2 for constant-intensity work, and alternated between ~ 15 and ~ 60 W/m 2 (5-min each) for variable-intensity work., Results: When expressed as a time-weighted average over each work period, total heat loss did not differ between men and women (mean difference [95% CI]; 4 W/m 2 [- 11, 20]; p = 0.572) or between constant- and variable-intensity work (1 W/m 2 [- 3, 5]; p = 0.642). Consequently, heat storage did not differ significantly between men and women (- 4 W/m 2 [- 17, 8]; p = 0.468) or between constant- and variable-intensity work (0 W/m 2 [- 3, 3]; p = 0.834)., Conclusion: Neither whole-body heat loss nor heat storage was modulated by the partitioning of work intensity, indicating that time-weighted averaging is appropriate for estimating metabolic demand to assess occupational heat stress in women.

Key Points: In humans, hypohydration attenuates sweat secretion and attenuates whole-body heat loss, probably to mitigate further fluid losses and thereby support blood pressure regulation. Recently, however, we demonstrated that the hypohydration-mediated reduction in net whole-body heat exchange (evaporative heat loss - dry heat gain) was blunted in middle-aged compared to younger men during moderate exercise in dry heat; albeit, the underpinning mechanisms could not be determined. Here we evaluated the hypothesis that those findings stemmed from a diminished influence of extracellular hyperosmolality on net whole-body heat exchange in middle-aged-to-older compared to young men. Consistent with that hypothesis, extracellular hyperosmolality induced by an intravenous infusion of hypertonic saline (3% NaCl) reduced net heat exchange and augmented rectal temperature to a greater extent in the young compared to middle-aged-to-older men. Thus, age-related differences in the influence of hypohydration on thermoregulatory function appear to be due to blunted sensitivity to hyperosmolality with ageing., Abstract: We recently demonstrated that sweating-induced hypohydration attenuated whole-body heat dissipation to a greater extent in young compared to middle-aged men during exercise-heat stress. Here, we evaluated whether this divergent response stemmed from an attenuated influence of extracellular hyperosmolality on heat exchange with ageing. To achieve this, ten young (mean (SD): 25 (5) years) and ten middle-aged-to-older (61 (5) years) men completed two trials involving a 90-min intravenous infusion of isosmotic saline (0.9% NaCl; ISO) or hyperosmotic saline (3.0% NaCl; HYP) followed by 60 min of cycling at a fixed metabolic heat production of 250 W/m 2 (∼50% peak aerobic power) in dry heat (40°C, ∼17% relative humidity). Whole-body net heat exchange (evaporative heat loss - dry heat gain) was measured via direct calorimetry. Rectal temperature was monitored continuously. Heat exchange was attenuated in HYP compared to ISO in the young (233 (20) vs. 251 (17) W/m 2 ; P = 0.002) but not older group (229 (16) vs. 227 (20) W/m 2 ; P = 0.621). Further, heat exchange was lower in the middle-aged-to-older vs. young men in ISO (P = 0.034) but not in HYP (P = 0.623). Similarly, end-exercise rectal temperature was greater in HYP relative to ISO in the young (38.3 (0.4)°C vs. 37.9 (0.3)°C; P = 0.015) but not the middle-aged-to-older men (38.3 (0.3)°C vs. 38.2 (0.2)°C; P = 0.652). Compared to the young, rectal temperature was greater in the middle-aged-to-older during ISO (P = 0.035) whereas no between-group difference was observed in HYP (P = 0.746). Our findings indicate that ageing blunts the effect of extracellular hyperosmolality on thermoregulatory function during exercise-heat stress., (© 2020 The Authors. The Journal of Physiology © 2020 The Physiological Society.)

Prepubertal children (6-12 yr) differ from adults in various morphological and physiological factors that may influence thermoregulatory function; however, experimental evidence of meaningful child-adult differences in heat strain during exercise-heat stress is sparse, despite numerous studies. Although we appreciate the challenges associated with performing such comparisons, part of that discrepancy may be due to the methods used. Nonetheless, a focused discussion of these methodological considerations and their implications for current understanding remains unavailable. This is an important knowledge gap given the threat to health posed by rising global temperatures and the ongoing focus on improving physical activity levels in children. The aims of this methodological review were, therefore, to (i) review the theoretical basis for child-adult differences in thermoregulatory function, (ii) describe previous comparisons of exercise thermoregulation between prepubertal children and adults, (iii) discuss two methodological issues associated with that research, which, in our view, make it difficult to present empirical evidence related to child-adult differences in thermoregulatory function and associated heat strain, (iv) provide potential solutions to these issues, and (v) propose pertinent areas for further research.

More frequent and intense periods of extreme heat (heatwaves) represent the most direct challenge to human health posed by climate change. Older adults are particularly vulnerable, especially those with common age-associated chronic health conditions (e.g., cardiovascular disease, hypertension, obesity, type 2 diabetes, chronic kidney disease). In parallel, the global population is aging and age-associated disease rates are on the rise. Impairments in the physiological responses tasked with maintaining homeostasis during heat exposure have long been thought to contribute to increased risk of health disorders in older adults during heatwaves. As such, a comprehensive overview of the provisional links between age-related physiological dysfunction and elevated risk of heat-related injury in older adults would be of great value to healthcare officials and policy makers concerned with protecting heat-vulnerable sectors of the population from the adverse health impacts of heatwaves. In this narrative review, we therefore summarize our current understanding of the physiological mechanisms by which aging impairs the regulation of body temperature, hemodynamic stability and hydration status. We then examine how these impairments may contribute to acute pathophysiological events common during heatwaves (e.g., heatstroke, major adverse cardiovascular events, acute kidney injury) and discuss how age-associated chronic health conditions may exacerbate those impairments. Finally, we briefly consider the importance of physiological research in the development of climate-health programs aimed at protecting heat-vulnerable individuals., (Copyright © 2020 The Authors. Published by Elsevier Ltd.. All rights reserved.)

In studies of human thermoregulation, ingestible temperature pills are being increasingly used as a convenient alternative to more clinically relevant indices of deep-body (core) temperature (e.g., rectal temperature). It remains unclear whether the time between pill ingestion and the measurement period influences the validity of telemetry pills as a surrogate index of core temperature. We therefore assessed the influence of pill ingestion timing on the agreement between rectal temperature (criterion method) and ingestible pill temperature during exercise-heat stress. To achieve this, nine young men (21-31 years) completed two trials involving 15-min rest, 90-min exercise at an average metabolic heat production of 200 W/m 2 (~40% peak oxygen consumption), and 45-min recovery. Core temperature was measured throughout using rectal temperature and four telemetric temperature pills (VitalSense®) ingested 12, 6, 3 and 1 h(s) prior to the start of each trial. Data from the two trials were combined and averaged over the final 10-min of rest, exercise, and recovery for analysis. Our primary finding was that the mean squared difference between rectal temperature and each pill did not differ significantly across ingestion times during rest, exercise or recovery (p = 0.056), with those errors ranging from 0.1-0.2°C, 0.2-0.2°C, 0.1-0.2°C, and 0.1-0.2°C for the pills ingested 12, 6, 3, and 1 h(s) before data collection, respectively. While there is a need for larger confirmatory studies, our findings indicate that pill ingestion timing does not significantly influence the validity of telemetry pill temperature as an index of core temperature., Competing Interests: No conflict of interest, financial or otherwise, are declared by the author(s)., (© 2020 Informa UK Limited, trading as Taylor & Francis Group.)

Susceptibility to heat illness during physically demanding work in hot environments is greater on the second of two consecutive workdays. While it has been demonstrated that heat storage is exacerbated on the second compared to first workday in older workers (50-65 yr), the effects on heart rate variability (HRV), an established surrogate of cardiac autonomic modulation, remain unclear. This study evaluated HRV in older workers on the day following prolonged work in the heat. Electrocardiogram was recorded in nine older (53-64 yr) males at rest, during three 30-min bouts of semi-recumbent cycling at fixed rates of metabolic heat production (150, 200, 250 W/m 2 ), each separated by 15-min recovery. Experiments were conducted in hot-dry conditions (40 °C, 20% relative humidity), immediately prior to (Day 1), and on the day following (Day 2), a prolonged work simulation (∼7.5 hr) involving moderate intensity intermittent exercise in hot-dry conditions (38 °C, 34% relative humidity). Core temperature, as well as time, frequency, and nonlinear HRV indices were derived for analysis during rest, the final 5-min of exercise at the highest heat production and recovery. The change in core temperature at the end of work (mean ±SD) was significantly greater on Day 2 (1.0 °C ±0.3) relative to Day 1 (0.8 °C ±0.2; p  < 0.01). Heart rate, however, did not significantly differ between days 1 and 2 at rest (Day 1, 59 ±11 bpm; Day 2, 62 ±13 bpm), during exercise (Day 1, 113 ±21 bpm; Day 2, 114 ±18 bpm ) and at the end of recovery (Day 1, 75 ±16 bpm; Day 2, 76 ±12 bpm). Likewise, there were no significant differences in any HRV indices derived from time, frequency, and nonlinear domains (all p  > 0.05). Prolonged work in the heat did not modulate next-day heart rhythms, as reflected by HRV, despite augmented core temperature. While HRV can reflect physiological aspects of cardiac autonomic stressors, these findings indicate it does not provide a means to identify exacerbated heat strain in older workers over consecutive work shifts in the heat.

New Findings: What is the central question of this study? Does higher aerobic fitness, indexed by peak oxygen uptake ( V ̇ O 2 peak ), attenuate the age-related decline in thermoregulatory function during exercise in the heat? What is the main finding and its importance? When assessed in aerobically fit and less fit adults ( V ̇ O 2 peak : ∼30 vs. ∼50 ml kg -1  min -1 ) aged 18-66 years, a steeper decline in whole-body total heat loss (evaporative + dry heat exchange) was observed with increasing age in less aerobically fit adults. These outcomes indicate that increased aerobic fitness may attenuate the age-related decline in thermoregulatory function during exercise-heat stress., Abstract: Ageing is associated with decrements in cutaneous vasodilatation and sweating that attenuate whole-body total heat loss (evaporative + dry heat exchange) during exercise-heat stress. However, it remains uncertain whether increased aerobic fitness, as indexed by peak oxygen uptake ( V ̇ O 2 peak ), slows that age-related decline. To evaluate this possibility, we conducted a retrospective analysis of data from aerobically fit (n = 38; V ̇ O 2 peak : (mean (SD)) 49 (4) ml kg -1  min -1 ) and less fit (n = 35; V ̇ O 2 peak : 32 (3) ml kg -1  min -1 ) adults spanning a broad age range (18-65 vs. 18-66 years). Participants performed three, 30 min bouts of cycling at metabolic heat productions of 150, 200 and 250 W m -2 , each separated by 15 min recovery, in dry heat (40˚C, ∼15% relative humidity). Metabolic heat production and whole-body total heat loss were measured using indirect and direct calorimetry, respectively. Total heat loss (mean (95% CI)) declined at a rate of 5 (2, 8), 6 (3, 8) and 5 (3, 10) W m -2 per decade during exercise at metabolic heat productions of 150, 200 and 250 W m -2 , respectively, in less aerobically fit individuals (all P ≤ 0.002), due primarily to reductions in evaporative heat loss. In contrast, no significant associations between age and total heat loss were observed in aerobically fit individuals (all P ≥ 0.146). As such, the slope of the age-related reduction in total heat loss was steeper in less fit compared to fit individuals across all three exercise bouts (all P ≤ 0.029). These outcomes indicate that increased aerobic fitness attenuates the age-related decline in exercise thermoregulation., (© 2020 The Authors. Experimental Physiology © 2020 The Physiological Society.)

New Findings: What is the central question of this study? Repeated heat exposure during the summer months can enhance heat loss in humans (seasonal heat acclimatisation), but does the magnitude of that enhancement differ between young and older adults when assessed during passive heat exposure? What is the main finding and its importance? While seasonal heat acclimatisation enhanced evaporative heat loss (i.e. sweating) in both young and older adults, those improvements led to a greater reduction in body heat storage in older adults. These outcomes indicate that heat acclimatisation may confer greater thermoregulatory benefits with increasing age., Abstract: Repeated heat exposure throughout summer can enhance heat loss in humans (seasonal heat acclimatisation), although the effect of ageing on those improvements remains unclear. We therefore sought to assess thermoregulatory function in young and older adults during environmental heat exposure prior to and following seasonal heat acclimatisation, hypothesizing that the magnitude of adaptation would be greater in older relative to young adults. To achieve this, 14 young (19-27 years) and 10 older adults (55-72 years), who resided in a temperate humid-continental climate, completed a 3 h resting heat exposure (44°C, ∼30% relative humidity) in the winter-spring months as part of a larger investigation (pre-acclimatisation), before being re-evaluated using the same heat stress test following the summer months (post-acclimatisation). Whole-body dry and evaporative heat exchange, and metabolic rate were measured throughout using direct and indirect calorimetry (respectively), and used to quantify body heat storage (metabolic rate + dry heat gain - evaporative heat loss). Evaporative heat loss increased in both groups following acclimatisation, but those improvements led to a decrease in body heat storage in older (mean difference (95% CI); 213 (295, 131) kJ; P < 0.001), but not young adults (-25 (-94, 44) kJ; P = 0.458). Thus, body heat storage was greater in older compared to young adults before (222 (123, 314) kJ; P < 0.001), but not following acclimatisation (34 (-55, 123) kJ; P = 0.433). Although there is a need for larger and more controlled confirmatory studies, our findings indicate that seasonal heat acclimatisation may induce greater thermoregulatory adaptation in older compared to young adults., (© 2020 The Authors. Experimental Physiology © 2020 The Physiological Society.)

Purpose: Sweat-induced fluid loss during prolonged exercise-heat stress can compromise cardiovascular and thermoregulatory function, although its effects on cardiac autonomic modulation remain unclear. We therefore examined heart rate variability (HRV) and recovery (HRRec), as surrogates of cardiac autonomic modulation, during and after prolonged exercise in the heat with and without fluid replacement., Methods: Eleven young and healthy men performed 90 min of semi-recumbent cycling in dry heat (40°C; 20% relative humidity) at a fixed rate of metabolic heat production (600 W; ~46% V˙O2peak) followed by 40-min resting recovery without fluid replacement (No-FR; ~3.4% reduction in body mass). On a separate day, participants completed the same protocol with fluid replacement (FR; 500-700 mL timed boluses) to offset sweat losses. Esophageal temperature and ECG were recorded throughout, with measurements analyzed over 10-min averaged epochs during baseline, each 30-min interval during exercise and 20-min interval during recovery., Results: Esophageal temperature and heart rate were elevated in No-FR relative to FR throughout exercise (all P ≤ 0.02). The HRV indices reflecting vagal influence of heart rate including the cardiac vagal index (CVI = log10[16 × SD1 × SD2]) and root-mean-square of successive differences were attenuated throughout exercise relative to baseline in both conditions (all P < 0.05), with the magnitude of the reduction greater in the No-FR condition (all P < 0.05). Further, sample entropy was reduced throughout all time points measured during exercise in the No-FR relative to FR condition (all P ≤ 0.03)., Conclusions: Our unique observations indicate that while prolonged exercise heat stress attenuates the vagal influence and complexity of cardiac rhythms, that reduction is further exacerbated by fluid loss, highlighting the importance of fluid replacement in such conditions.

Lower-limb intermittent sequential pneumatic compression (ISPC) improves circulation and vascular function in elderly adults. We evaluated the hypothesis that ISPC would also augment whole-body heat loss (WBHL) in elderly adults (aged 69 ± 4 years) resting in extreme heat (40 °C). While ISPC increased mean arterial pressure (91 ± 9 mm Hg) relative to no-ISPC (83 ± 5 mm Hg; P = 0.013) at the end of the exposure, no influence on WBHL was observed (81 ± 7 and 86 ± 11 W for ISPC and no-ISPC, respectively, P = 0.310). Novelty When assessed in elderly adults during an extreme heat exposure, intermittent sequential pneumatic compression augmented mean arterial pressure but did not enhance whole-body heat loss.