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.

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

It is commonly thought that steady-state thermoregulatory responses are achieved within 30-90 min of compensable heat stress. However, this assumption is based on measurements of whole body heat exchange during exercise, which stabilize (equilibrate) more rapidly than deep body temperatures, especially under resting conditions. To support the design of ecologically relevant heat exposure studies, we quantified equilibrium times for deep body temperature, as indexed by rectal temperature, in young and older adults resting in the heat. We also evaluated the lag in rectal temperature equilibrium relative to whole body heat storage (direct calorimetry). Equilibrium times were estimated with data from two laboratory-based trials (NCT04353076 and NCT04348630) in which 83 adults aged 19-80 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.

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

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

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

Type 2 diabetes (T2D) is associated with reduced whole body sweating during exercise-heat stress. However, it is unclear if this impairment is related to exercise intensity and whether it occurs uniformly across body regions. We evaluated whole body (direct calorimetry) and local (ventilated-capsule technique; chest, back, forearm, thigh) sweat rates in physically active men with type 2 diabetes [T2D; aged 59 (7) yr; V̇o2peak 32.3 (7.6) mL·kg-1·min-1; n = 26; HbA1c 5.1%-9.1%] and without diabetes [Control; aged 61 (5) yr; V̇o2peak 37.5 (5.4) mL·kg-1·min-1; n = 26] during light- (∼40% V̇o2peak), moderate- (∼50% V̇o2peak), and vigorous- (∼65% V̇o2peak) intensity exercise (elicited by fixing metabolic heat production at ∼150, 200, 250 W·m-2, respectively) in 40°C, ∼17% relative humidity. Whole body sweating was ∼11% (T2D: Control mean difference [95% confidence interval]: -37 [-63, -12] g·m-2·h-1) and ∼13% (-50 [-76, -25] g·m-2·h-1) lower in the T2D compared with the Control group during moderate- and vigorous- (P ≤ 0.001) but not light-intensity exercise (-21 [-47, 4] g·m-2·h-1; P = 0.128). Consequently, the diabetes-related reductions in whole body sweat rate were 2.3 [1.6, 3.1] times greater during vigorous relative to light exercise (P < 0.001). Furthermore, these diabetes-related impairments in local sweating were region-specific during vigorous-intensity exercise (group × region interaction: P = 0.024), such that the diabetes-related reduction in local sweat rate at the trunk (chest, back) was 2.4 [1.2, 3.7] times greater than that at the limbs (thigh, arm). In summary, when assessed under hot, dry conditions, diabetes-related impairments in sweating are exercise intensity-dependent and greater at the trunk compared with the limbs.NEW & NOTEWORTHY This study evaluates the influence of exercise intensity on decrements in whole body sweating associated with type 2 diabetes. Furthermore, it investigates whether diabetes-related sweating impairments were exhibited uniformly or heterogeneously across body regions. We found that whole body sweating was attenuated in the type 2 diabetes group relative to control participants during moderate- and vigorous-intensity exercise but not light-intensity exercise; impairments were largely mediated by reduced sweating at the trunk rather than the limbs.

Myths and methodologies: Considerations for evaluating the time course of thermoregulatory adaptation during heat acclimation.

Since the early 1900s, repeated heat exposure has been used as a method to induce physiological adaptations that enhance our ability to tolerate heat stress during athletic and occupational pursuits. Much of this work has been dedicated to quantifying the time course of adaptation and identifying the minimum duration of acclimation required to optimise performance or enhance safety. To achieve this, investigators have typically applied classical (constant load) heat acclimation, whereby 60-90 min exercise is performed at the same absolute or relative intensity in a hot environment for 3-24 days, with adaptations evaluated using an identical forcing function test before and after. This approach has provided a foundation from which to develop our understanding of changes in thermoregulatory function, but it has several, frequently overlooked shortcomings, which have resulted in misconceptions concerning the time course of adaptation. It is frequently suggested that most of the thermoregulatory adaptations during heat acclimation occur within a week, but this is an oversimplification and a predictable artefact of the experimental designs used. Consequently, the time course of complete human adaptation to heat remains poorly understood and appears to vary considerably due to numerous individual factors. The purpose of this communication is to highlight the key methodological considerations required when interpreting the existing literature documenting adaptation over time. We also propose potential means by which to improve the way we induce and quantify the magnitude of adaptation to expedite discovery.

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.

Brain-derived neurotrophic factor in older adults exposed to simulated indoor overheating.

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.

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.

Agreement between measured and self-reported physiological strain in young adults and older adults with and without common chronic diseases during simulated occupational heat stress.

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/m2) 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.

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.

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.

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

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

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

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

Finite element model of female thermoregulation with geometry based on medical images.

INTRODUCTION: this study describes the development of a female finite element thermoregulatory model (FETM) METHOD: the female body model was developed from medical image datasets of a median U.S. female and was constructed to be anatomically correct. The body model preserves the geometric shapes of 13 organs and tissues, including skin, muscles, fat, bones, heart, lungs, brain, bladder, intestines, stomach, kidneys, liver, and eyes. Heat balance within the body is described by the bio-heat transfer equation. Heat exchange at the skin surface includes conduction, convection, radiation, and sweat evaporation. Vasodilation, vasoconstriction, sweating, and shivering are controlled by afferent and efferent signals to and from the skin and hypothalamus. RESULTS: the model was validated with measured physiological data during exercise and rest in thermoneutral, hot, and cold conditions. Validations show the model predicted the core temperature (rectal and tympanic temperatures) and mean skin temperatures with acceptable accuracy (within 0.5 °C and 1.6 °C, respectively) CONCLUSION: this female FETM predicted high spatial resolution temperature distribution across the female body, which provides quantitative insights into human thermoregulatory responses in females to non-uniform and transient environmental exposure.

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.

Effect of extracellular hyperosmolality on sweat rate during metaboreflex activation in passively heated young men.

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/kgH2O, 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 cm2). 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/cm2 [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.

The impact of age, type 2 diabetes and hypertension on heart rate variability during rest and exercise at increasing levels of heat stress.

PURPOSE: In older adults with type 2 diabetes (T2D) and hypertension (HTN), cardiac autonomic modulation is markedly attenuated during exercise-heat stress. However, the extent to which this impairment is evident under increasing levels of heat stress remains unknown. METHODS: We examined heart rate variability (HRV), a surrogate of cardiac autonomic modulation, during incremental exercise-heat stress exposures in young (20-30 years) and middle-aged-to-older individuals (50-70 years) without and with T2D and HTN. Thirteen young and healthy (Young, n = 13) and 37 older men without (Older, n = 14) and with HTN (n = 13) or T2D (n = 10) performed 180-min treadmill walking at a fixed metabolic rate (~ 200 W/m2; ~ 3.5 METs) in a differing wet-bulb globe temperature (WBGT; 16 °C, 24 °C, 28 °C, and 32 °C). Electrocardiogram (ECG) and core temperature measurements were recorded throughout. Data were analysed using 5-min averaged epochs following 60-min exercise, which represented the last common timepoint across groups and conditions. RESULTS: Ageing did not significantly reduce HRV during increasing exercise-heat stress (all p > 0.050). However, T2D and HTN modified HRV during exercise-heat stress such that Detrended Fluctuation Analysis (DFA) α1 (p = 0.012) and the cardiac sympathetic index (p = 0.037) were decreased compared to Older in all except the warmest WBGT condition (32 °C). CONCLUSION: Our unique observations indicate that, relative to their younger counterparts, HRV in healthy older individuals is not perturbed during exercise heat-stress. However, relative to their age-matched healthy counterparts, HRV is reduced during exercise-heat stress in individuals with age-associated chronic conditions, indicative of cardiac autonomic dysfunction.

Cooling strategies for firefighters: Effects on physiological, physical, and visuo-motor outcomes following fire-fighting tasks in the heat.

OBJECTIVES: Due to the nature of firefighting, most effective cooling interventions to reduce heat strain and optimise performance are not practically viable. This study quantified the effects of two practical cooling strategies, co-designed with subject-matter experts, on physiological strain and physical, perceptual, and visuo-motor performance during simulated firefighting in the heat. DESIGN: Randomised cross-over. METHODS: On three occasions 14 firefighters completed an 80-min simulation in a hot-humid environment (32.0[0.9]°C, 59[3]%RH) including two 20-min firefighting tasks in full protective clothing, each followed by 20-min seated recovery. Recovery involved removal of protective clothing and one of three interventions - control (CON; ambient-temperature water consumption), basic (BASIC; cool-water consumption, ambient-forearm immersion/towels, fan), and advanced (ADV; ice-slushy consumption, cool-forearm immersion/ice packs, misting-fan). Thermal (core temperature) and cardiovascular (heart rate, arterial pressure) responses were measured throughout, whilst physical (handgrip/balance), visuo-motor (reaction time/memory recall) and perceptual (fatigue/thermal sensation/comfort) measures were assessed pre- and post-trial. RESULTS: Compared to CON, core temperature was lower in BASIC and ADV following the second task (ADV: 37.7[0.4]; BASIC: 38.0[0.4]; CON: 38.3[0.4]°C) and recovery protocol (ADV: 37.5[0.3]; BASIC: 37.7 [0.3] CON: 38.3[0.4]°C). This was paralleled by lowered heart rate, rate pressure product, and thermal sensation following the recovery protocols, in the ADV and BASIC condition compared to CON (p < .05). No physical or visuo-motor outcomes differed significantly between conditions. CONCLUSION: Whilst these observations need to be extended to field conditions, our findings demonstrate that two novel cooling interventions developed in collaboration with subject-matter experts offered benefits for reducing thermal strain and optimising firefighter safety.