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

Older adults are at elevated risk of heat-related mortality due to age-associated declines in thermoregulatory and cardiovascular function. However, the inter-individual factors that exacerbate physiological heat strain during heat exposure remain unclear, making it challenging to identify more heat-vulnerable subgroups. We therefore explored factors contributing to inter-individual variability in physiological responses of older adults exposed to simulated hot weather. Thirty-seven older adults (61-80 years, 16 females) rested for 8 hours in 31°C and 36°C (45% relative humidity). Core (rectal) temperature, heart rate (HR) and HR variability, mean arterial pressure (MAP), and cardiac autonomic responses to standing were evaluated at baseline and end-exposure. Bootstrapped least absolute shrinkage and selection operator (LASSO) 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% CI: 6, 23]), seated MAP (-7 mm Hg [-18, 1]), and the systolic pressure response to standing (20 mm Hg [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 the development of heat-induced physiological strain in older persons.

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

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

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

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

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

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

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

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

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

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

Hormonal intrauterine devices and heat exchange during exercise.

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

The utility of heart rate and heart rate variability to identify limits of tolerance to moderate-intensity work in the heat: a secondary analysis.

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/m2; ∼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 α1)) 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 α1 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.

Metabolic Costs of Walking with Weighted Vests.

INTRODUCTION: The US Army Load Carriage Decision Aid (LCDA) metabolic model is used by militaries across the globe and is intended to predict physiological responses, specifically metabolic costs, in a wide range of dismounted warfighter operations. However, the LCDA has yet to be adapted for vest-borne load carriage, which is commonplace in tactical populations, and differs in energetic costs to backpacking and other forms of load carriage. PURPOSE: The purpose of this study is to develop and validate a metabolic model term that accurately estimates the effect of weighted vest loads on standing and walking metabolic rate for military mission-planning and general applications. METHODS: Twenty healthy, physically active military-age adults (4 women, 16 men; age, 26 ± 8 yr old; height, 1.74 ± 0.09 m; body mass, 81 ± 16 kg) walked for 6 to 21 min with four levels of weighted vest loading (0 to 66% body mass) at up to 11 treadmill speeds (0.45 to 1.97 m·s -1 ). Using indirect calorimetry measurements, we derived a new model term for estimating metabolic rate when carrying vest-borne loads. Model estimates were evaluated internally by k -fold cross-validation and externally against 12 reference datasets (264 total participants). We tested if the 90% confidence interval of the mean paired difference was within equivalence limits equal to 10% of the measured walking metabolic rate. Estimation accuracy, precision, and level of agreement were also evaluated by the bias, standard deviation of paired differences, and concordance correlation coefficient (CCC), respectively. RESULTS: Metabolic rate estimates using the new weighted vest term were statistically equivalent ( P < 0.01) to measured values in the current study (bias, -0.01 ± 0.54 W·kg -1 ; CCC, 0.973) as well as from the 12 reference datasets (bias, -0.16 ± 0.59 W·kg -1 ; CCC, 0.963). CONCLUSIONS: The updated LCDA metabolic model calculates accurate predictions of metabolic rate when carrying heavy backpack and vest-borne loads. Tactical populations and recreational athletes that train with weighted vests can confidently use the simplified LCDA metabolic calculator provided as Supplemental Digital Content to estimate metabolic rates for work/rest guidance, training periodization, and nutritional interventions.

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

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

A century of exercise physiology: concepts that ignited the study of human thermoregulation. Part 4: evolution, thermal adaptation and unsupported theories of thermoregulation.

This review is the final contribution to a four-part, historical series on human exercise physiology in thermally stressful conditions. The series opened with reminders of the principles governing heat exchange and an overview of our contemporary understanding of thermoregulation (Part 1). We then reviewed the development of physiological measurements (Part 2) used to reveal the autonomic processes at work during heat and cold stresses. Next, we re-examined thermal-stress tolerance and intolerance, and critiqued the indices of thermal stress and strain (Part 3). Herein, we describe the evolutionary steps that endowed humans with a unique potential to tolerate endurance activity in the heat, and we examine how those attributes can be enhanced during thermal adaptation. The first of our ancestors to qualify as an athlete was Homo erectus, who were hairless, sweating specialists with eccrine sweat glands covering almost their entire body surface. Homo sapiens were skilful behavioural thermoregulators, which preserved their resource-wasteful, autonomic thermoeffectors (shivering and sweating) for more stressful encounters. Following emigration, they regularly experienced heat and cold stress, to which they acclimatised and developed less powerful (habituated) effector responses when those stresses were re-encountered. We critique hypotheses that linked thermoregulatory differences to ancestry. By exploring short-term heat and cold acclimation, we reveal sweat hypersecretion and powerful shivering to be protective, transitional stages en route to more complete thermal adaptation (habituation). To conclude this historical series, we examine some of the concepts and hypotheses of thermoregulation during exercise that did not withstand the tests of time.

A century of exercise physiology: concepts that ignited the study of human thermoregulation. Part 3: Heat and cold tolerance during exercise.

In this third installment of our four-part historical series, we evaluate contributions that shaped our understanding of heat and cold stress during occupational and athletic pursuits. Our first topic concerns how we tolerate, and sometimes fail to tolerate, exercise-heat stress. By 1900, physical activity with clothing- and climate-induced evaporative impediments led to an extraordinarily high incidence of heat stroke within the military. Fortunately, deep-body temperatures > 40 °C were not always fatal. Thirty years later, water immersion and patient treatments mimicking sweat evaporation were found to be effective, with the adage of cool first, transport later being adopted. We gradually acquired an understanding of thermoeffector function during heat storage, and learned about challenges to other regulatory mechanisms. In our second topic, we explore cold tolerance and intolerance. By the 1930s, hypothermia was known to reduce cutaneous circulation, particularly at the extremities, conserving body heat. Cold-induced vasodilatation hindered heat conservation, but it was protective. Increased metabolic heat production followed, driven by shivering and non-shivering thermogenesis, even during exercise and work. Physical endurance and shivering could both be compromised by hypoglycaemia. Later, treatments for hypothermia and cold injuries were refined, and the thermal after-drop was explained. In our final topic, we critique the numerous indices developed in attempts to numerically rate hot and cold stresses. The criteria for an effective thermal stress index were established by the 1930s. However, few indices satisfied those requirements, either then or now, and the surviving indices, including the unvalidated Wet-Bulb Globe-Thermometer index, do not fully predict thermal strain.

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

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

Physiological responses to 9 hours of heat exposure in young and older adults. Part III: Association with self-reported symptoms and mood state.

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.

Elevations in serum brain-derived neurotrophic factor following occupational heat stress are not influenced by age or common chronic disease.

With global warming, workers are increasingly exposed to strenuous occupations in hot environments. Given age- and disease-associated declines in thermoregulatory function, older workers are at an elevated risk of developing heat-related injuries. Brain-derived neurotrophic factor (BDNF) is thought to confer neuroprotection during acute exercise, however, the influence of environmental heat on BDNF responses during prolonged work remains unclear. Therefore, we evaluated serum BDNF concentrations before and after 180 min of moderate-intensity treadmill walking (200 W/m2) and after 60 min of post-exercise recovery in temperate (wet-bulb globe temperature (WBGT) 16°C) and hot (WBGT 32°C) environments in 13 healthy young men (mean [SD; 22 [3] years), 12 healthy older men (59 [4] years), 10 men with hypertension (HTN) (60 [4] years), and 9 men with type 2 diabetes (T2D) (60 [5] years). In the temperate condition, all but one participant (1 HTN) completed the 180 min of exercise. While exercise tolerance in the heat was lower in older men with HTN (117 min [45]) and T2D (123 min [42]) compared to healthy older men (159 min [31]) (both p ≤ 0.049), similar end-exercise rectal temperatures (38.9°C [0.4]) were observed across groups, paralleled by similar elevations in serum BDNF across groups at end-exercise (+1106 pg/mL [203]) and end-recovery (+938 pg/mL [146]; all p ≤ 0.01) in the heat. No changes in serum BDNF were observed in the temperate condition. Our findings indicate similar BDNF responses in individuals with HTN or T2D compared to their healthy counterparts, despite exhibiting reduced tolerance to heat.

A century of exercise physiology: concepts that ignited the study of human thermoregulation. Part 2: physiological measurements.

In this, the second of four historical reviews on human thermoregulation during exercise, we examine the research techniques developed by our forebears. We emphasise calorimetry and thermometry, and measurements of vasomotor and sudomotor function. Since its first human use (1899), direct calorimetry has provided the foundation for modern respirometric methods for quantifying metabolic rate, and remains the most precise index of whole-body heat exchange and storage. Its alternative, biophysical modelling, relies upon many, often dubious assumptions. Thermometry, used for >300 y to assess deep-body temperatures, provides only an instantaneous snapshot of the thermal status of tissues in contact with any thermometer. Seemingly unbeknownst to some, thermal time delays at some surrogate sites preclude valid measurements during non-steady state conditions. To assess cutaneous blood flow, immersion plethysmography was introduced (1875), followed by strain-gauge plethysmography (1949) and then laser-Doppler velocimetry (1964). Those techniques allow only local flow measurements, which may not reflect whole-body blood flows. Sudomotor function has been estimated from body-mass losses since the 1600s, but using mass losses to assess evaporation rates requires precise measures of non-evaporated sweat, which are rarely obtained. Hygrometric methods provide data for local sweat rates, but not local evaporation rates, and most local sweat rates cannot be extrapolated to reflect whole-body sweating. The objective of these methodological overviews and critiques is to provide a deeper understanding of how modern measurement techniques were developed, their underlying assumptions, and the strengths and weaknesses of the measurements used for humans exercising and working in thermally challenging conditions.

Brief ambient cooling preserves autophagy in peripheral blood mononuclear cells from older adults during 9 h of heat exposure.

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.

A century of exercise physiology: concepts that ignited the study of human thermoregulation. Part 1: Foundational principles and theories of regulation.

This contribution is the first of a four-part, historical series encompassing foundational principles, mechanistic hypotheses and supported facts concerning human thermoregulation during athletic and occupational pursuits, as understood 100 years ago and now. Herein, the emphasis is upon the physical and physiological principles underlying thermoregulation, the goal of which is thermal homeostasis (homeothermy). As one of many homeostatic processes affected by exercise, thermoregulation shares, and competes for, physiological resources. The impact of that sharing is revealed through the physiological measurements that we take (Part 2), in the physiological responses to the thermal stresses to which we are exposed (Part 3) and in the adaptations that increase our tolerance to those stresses (Part 4). Exercising muscles impose our most-powerful heat stress, and the physiological avenues for redistributing heat, and for balancing heat exchange with the environment, must adhere to the laws of physics. The first principles of internal and external heat exchange were established before 1900, yet their full significance is not always recognised. Those physiological processes are governed by a thermoregulatory centre, which employs feedback and feedforward control, and which functions as far more than a thermostat with a set-point, as once was thought. The hypothalamus, today established firmly as the neural seat of thermoregulation, does not regulate deep-body temperature alone, but an integrated temperature to which thermoreceptors from all over the body contribute, including the skin and probably the muscles. No work factor needs to be invoked to explain how body temperature is stabilised during exercise.

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

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