Performing exercise, especially in hot conditions, can heat the body, causing significant increases in internal body temperature. To offset this increase, powerful and highly developed autonomic ...thermoregulatory responses (i.e., skin blood flow and sweating) are activated to enhance whole body heat loss; a response mediated by temperature-sensitive receptors in both the skin and the internal core regions of the body. Independent of thermal control of heat loss, nonthermal factors can have profound consequences on the body's ability to dissipate heat during exercise. These include the activation of the body's sensory receptors (i.e., baroreceptors, metaboreceptors, mechanoreceptors, etc.) as well as phenotypic factors such as age, sex, acclimation, fitness, and chronic diseases (e.g., diabetes). The influence of these factors extends into recovery such that marked impairments in thermoregulatory function occur, leading to prolonged and sustained elevations in body core temperature. Irrespective of the level of hyperthermia, there is a time-dependent suppression of the body's physiological ability to dissipate heat. This delay in the restoration of postexercise thermoregulation has been associated with disturbances in cardiovascular function which manifest most commonly as postexercise hypotension. This review examines the current knowledge regarding the restoration of thermoregulation postexercise. In addition, the factors that are thought to accelerate or delay the return of body core temperature to resting levels are highlighted with a particular emphasis on strategies to manage heat stress in athletic and/or occupational settings.
To assess potential mechanisms responsible for the lower sudomotor thermosensitivity in women during exercise, we examined sex differences in sudomotor function and skin blood flow (SkBF) during ...exercise performed at progressive increases in the requirement for heat loss. Eight men and eight women cycled at rates of metabolic heat production of 200, 250, and 300 W/m(2) of body surface area, with each rate being performed sequentially for 30 min. The protocol was performed in a direct calorimeter to measure evaporative heat loss (EHL) and in a thermal chamber to measure local sweat rate (LSR) (ventilated capsule), SkBF (laser-Doppler), sweat gland activation (modified iodine-paper technique), and sweat gland output (SGO) on the back, chest, and forearm. Despite a similar requirement for heat loss between the sexes, significantly lower increases in EHL and LSR were observed in women (P ≤ 0.001). Sex differences in EHL and LSR were not consistently observed during the first and second exercise periods, whereas EHL (348 ± 13 vs. 307 ± 9 W/m(2)) and LSR on the back (1.61 ± 0.07 vs. 1.20 ± 0.09 mg · min(-1) · cm(-2)), chest (1.33 ± 0.06 vs. 1.08 ± 0.09 mg · min(-1) · cm(-2)), and forearm (1.53 ± 0.07 vs. 1.20 ± 0.06 mg · min(-1) · cm(-2), men vs. women) became significantly greater in men during the last exercise period (P < 0.05). At each site, differences in LSR were solely due to a greater SGO in men, as opposed to differences in sweat gland activation. In contrast, no sex differences in SkBF were observed throughout the exercise period. The present study demonstrates that sex differences in sudomotor function are only evidenced beyond a certain requirement for heat loss, solely through differences in SGO. In contrast, the lower EHL and LSR in women are not paralleled by a lower SkBF response.
•Heatwaves are associated with stark elevations in morbidity and mortality.•Older adults are at particular risk of multiple pathophysiological conditions.•Aging and disease elicit impaired ...physiological responses to heat stress.•These impairments can lead to acute and chronic injury in sensitive bodily systems.•Research is needed to better delineate health impacts of heatwaves in older adults.
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.
Although a number of studies have examined potential differences in temperature regulation between males and females during heat stress, conclusions have remained limited as to whether reported ...differences are due to confounding physical characteristics or to actual differences in the physiological variables of temperature regulation. Recent observations suggest that sex differences in temperature regulation, particularly in sudomotor activity, go beyond those associated with physical characteristics. Females have recently been shown to have a lower sudomotor activity, as well as a lower thermosensitivity of the response compared to males during exercise performed at a fixed rate of metabolic heat production. Furthermore, sex differences in local and whole‐body sudomotor activity are only evident above a certain combination of environmental conditions and rate of metabolic heat production. In contrast, both the onset threshold and thermosensitivity of cutaneous vasodilatation are similar between males and females. In theory, differences in the thermosensitivity of sudomotor activity could be related to either a central (neural activity/integration) and/or peripheral (effector organ) modulation of temperature regulation. Based on recent findings, sex differences in sudomotor activity appear to be mediated peripherally, although a central modulation has yet to be conclusively ruled out. Here we present a brief yet comprehensive review of the current state of knowledge pertaining to sex differences in temperature regulation during exercise in the heat.
Key points
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A relative exercise intensity (%) protocol is often used to compare absolute whole‐body sweat rates (WBSRs) during exercise between participants of different aerobic capacity.
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Under ...conditions permitting full evaporation, heat balance theory suggests that exercise intensity should be fixed to elicit the same rate of evaporation required for heat balance (Ereq).
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Whole‐body direct calorimetry was employed to measure WBSRs throughout 90 min of exercise across a range of air temperatures and rates of metabolic heat production.
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Irrespective of ambient temperature and metabolic heat production, Ereq alone described ∼90% of all variability in WBSR during steady‐state and non‐steady‐state exercise, whereas <2% of variation was independently described by %.
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To perform an unbiased comparison of WBSRs (but not necessarily core temperature) between different individuals/groups under conditions allowing full evaporation, future studies should consider using a fixed Ereq irrespective of the % incurred.
Although the requirements for heat dissipation during exercise are determined by the necessity for heat balance, few studies have considered them when examining sweat production and its potential modulators. Rather, the majority of studies have used an experimental protocol based on a fixed percentage of maximum oxygen uptake (%). Using multiple regression analysis, we examined the independent contribution of the evaporative requirement for heat balance (Ereq) and % to whole‐body sweat rate (WBSR) during exercise. We hypothesised that WBSR would be determined by Ereq and not by %. A total of 23 males performed two separate experiments during which they exercised for 90 min at different rates of metabolic heat production (200, 350, 500 W) at a fixed air temperature (30°C, n= 8), or at a fixed rate of metabolic heat production (290 W) at different air temperatures (30, 35, 40°C, n= 15 and 45°C, n= 7). Whole‐body evaporative heat loss was measured by direct calorimetry and used to calculate absolute WBSR in grams per minute. The conditions employed resulted in a wide range of Ereq (131–487 W) and % (15–55%). The individual variation in non‐steady‐state (0–30 min) and steady‐state (30–90 min) WBSR correlated significantly with Ereq (P < 0.001). In contrast, % correlated negatively with the residual variation in WBSR not explained by Ereq, and marginally increased (∼2%) the amount of total variability in WBSR described by Ereq alone (non‐steady state: R2= 0.885; steady state: R2= 0.930). These data provide clear evidence that absolute WBSR during exercise is determined by Ereq, not by %. Future studies should therefore use an experimental protocol which ensures a fixed Ereq when examining absolute WBSR between individuals, irrespective of potential differences in relative exercise intensity.
Occupational heat strain (ie, the effect of environmental heat stress on the body) directly threatens workers' ability to live healthy and productive lives. We estimated the effects of occupational ...heat strain on workers' health and productivity outcomes.
Following PRISMA guidelines for this systematic review and meta-analysis, we searched PubMed and Embase from database inception to Feb 5, 2018, for relevant studies in any labour environment and at any level of occupational heat strain. No restrictions on language, workers' health status, or study design were applied. Occupational heat strain was defined using international health and safety guidelines and standards. We excluded studies that calculated effects using simulations or statistical models instead of actual measurements, and any grey literature. Risk of bias, data extraction, and sensitivity analysis were performed by two independent investigators. Six random-effects meta-analyses estimated the prevalence of occupational heat strain, kidney disease or acute kidney injury, productivity loss, core temperature, change in urine specific gravity, and odds of occupational heat strain occurring during or at the end of a work shift in heat stress conditions. The review protocol is available on PROSPERO, registration number CRD42017083271.
Of 958 reports identified through our systematic search, 111 studies done in 30 countries, including 447 million workers from more than 40 different occupations, were eligible for analysis. Our meta-analyses showed that individuals working a single work shift under heat stress (defined as wet-bulb globe temperature beyond 22·0 or 24·8°C depending on work intensity) were 4·01 times (95% CI 2·45–6·58; nine studies with 11 582 workers) more likely to experience occupational heat strain than an individual working in thermoneutral conditions, while their core temperature was increased by 0·7°C (0·4–1·0; 17 studies with 1090 workers) and their urine specific gravity was increased by 14·5% (0·0031, 0·0014–0·0048; 14 studies with 691 workers). During or at the end of a work shift under heat stress, 35% (31–39; 33 studies with 13 088 workers) of workers experienced occupational heat strain, while 30% (21–39; 11 studies with 8076 workers) reported productivity losses. Finally, 15% (11–19; ten studies with 21 721 workers) of individuals who typically or frequently worked under heat stress (minimum of 6 h per day, 5 days per week, for 2 months of the year) experienced kidney disease or acute kidney injury. Overall, this analysis include a variety of populations, exposures, and occupations to comply with a wider adoption of evidence synthesis, but resulted in large heterogeneity in our meta-analyses. Grading of Recommendations, Assessment, Development and Evaluation analysis revealed moderate confidence for most results and very low confidence in two cases (average core temperature and change in urine specific gravity) due to studies being funded by industry.
Occupational heat strain has important health and productivity outcomes and should be recognised as a public health problem. Concerted international action is needed to mitigate its effects in light of climate change and the anticipated rise in heat stress.
EU Horizon 2020 research and innovation programme.
Despite previous reviews and commentaries, significant misconceptions remain concerning deep-body (core) and skin temperature measurement in humans. Therefore, the authors have assembled the ...pertinent Laws of Thermodynamics and other first principles that govern physical and physiological heat exchanges. The resulting review is aimed at providing theoretical and empirical justifications for collecting and interpreting these data. The primary emphasis is upon deep-body temperatures, with discussions of intramuscular, subcutaneous, transcutaneous and skin temperatures included. These are all turnover indices resulting from variations in local metabolism, tissue conduction and blood flow. Consequently, inter-site differences and similarities may have no mechanistic relationship unless those sites have similar metabolic rates, are in close proximity and are perfused by the same blood vessels. Therefore, it is proposed that a gold standard deep-body temperature does not exist. Instead, the validity of each measurement must be evaluated relative to one's research objectives, whilst satisfying equilibration and positioning requirements. When using thermometric computations of heat storage, the establishment of steady-state conditions is essential, but for clinically relevant states, targeted temperature monitoring becomes paramount. However, when investigating temperature regulation, the response characteristics of each temperature measurement must match the forcing function applied during experimentation. Thus, during dynamic phases, deep-body temperatures must be measured from sites that track temperature changes in the central blood volume.
•Thermodynamic principles govern physical and biological heat exchanges.•Inter-site tissue temperatures may be unrelated unless perfused by the same blood vessel.•Measurement validity must be evaluated relative to one's research objectives.•Measurement sensitivity must match the forcing function that disturbs homoeostasis.•During dynamic phases, measurements should track central blood temperature.
Older adults typically experience greater levels of thermal strain during physical efforts in the heat compared to young individuals. While this may be related to an age-dependent reduction in ...whole-body sweating, no study has clearly delineated at what age this occurs. In the present study, we report direct measurements of human heat dissipation during physical activity in the heat in males ranging in age from 20-70 years. Eighty-five males performed four 15-min bouts of cycling separated by 15-min rest periods, in a calorimeter regulated to 35°C and 20% relative humidity. Direct calorimetry was used to measure total heat loss (whole-body evaporative heat loss and dry heat exchange). We also used indirect calorimetry as a continuous measure of metabolic heat production. Body heat storage was calculated as the temporal summation of heat production and total heat loss over the experimental session. Whole-body sweat rate (WBSR) was calculated from measurements of evaporative heat loss. Males were divided into five age categories for the analysis of WBSR and body heat storage: 20-31 years (n = 18), 40-44 years (n = 15), 45-49 years (n = 15), 50-55 years (n = 21) and 56-70 years (n = 16). Relative to young males, WBSR was reduced in males aged 56-70 during each exercise (all P<0.05), in males aged 50-55 during the second (P = 0.031) and third exercises (P = 0.028) and in males aged 45-49 during the final exercise bout (P = 0.046). Although not significantly different, 40-44 years old males also had a lower rate of heat loss compared to younger males. Over the sum of two hours, the change in body heat content was greater in males 40-70 years compared to young males (all P<0.05). Our findings suggest that middle-aged and older adults have impairments in heat dissipation when doing physical activity in the heat, thus possibly increasing their risk of heat-related illness under such conditions.
Direct calorimetry is the gold standard means of measuring human metabolic rate and its use has been fundamental for understanding metabolism in health and disease. While metabolic rate is now more ...commonly estimated indirectly from measures of the oxygen consumed during respiration, direct calorimetry provides the user with the unique capacity to quantify the heat produced from aerobic and anaerobic metabolism by measuring heat exchange between the body and the environment. This review provides a brief historical overview of the fundamental concepts which underlie direct calorimetry, of pioneer scientists which developed these concepts into functional pieces of equipment and the subsequent use of direct calorimetry to advance our understanding of energy balance, nutrition, and the pathogenesis of metabolic diseases. Attention is directed to seminal studies that successfully employed direct calorimetry to verify that the law of energy conservation also applies to human beings and to establish the validity of indirect calorimetry. Finally, we discuss the more recent use of direct calorimetry for the measurement of whole-body heat exchange and body heat storage in the study of human thermoregulation.
Non‐technical summary The human body controls its temperature through coordinated physiological processes. Prior to the current study, it remained unknown if differences between males and females ...existed in these processes. The results from the current study show that females have a lower whole‐body sweat response during exercise in the heat compared to males, which results in a greater increase in body temperature. The physiological process responsible for the lower whole‐body sweat rate was a lower thermosensitivity of the response, meaning a lower increase in sweat production for a given increase in body temperature. Knowledge of sex‐related differences in the physiology of temperature regulation may lead to better improvements in heat exposure guidelines for industrial, military and athletic settings.
It is unclear whether true physiological differences exist in temperature regulation between males and females during exercise, independently of differences in physical characteristics and metabolic heat production. Therefore, we examined differences in the onset threshold and thermosensitivity of whole‐body sudomotor activity and cutaneous vascular conductance between males and females matched for body mass and surface area. Nine males and nine females performed 90 min of exercise at each of the following intensities in a warm/dry environment: 50% of maximum oxygen consumption () and at a fixed rate of metabolic heat production equal to 500 W. Evaporative heat loss (EHL, direct calorimetry) and cutaneous vascular conductance (CVC, laser‐Doppler) were measured continuously. Mean body temperature was calculated from the measurements of oesophageal and mean skin temperatures. During exercise at 50%, a lower rate of sudomotor activity was observed in females (385 ± 12 vs. 512 ± 24 W, P < 0.001). However, irrespective of sex, individual EHL values were strongly associated with metabolic heat production (R2= 0.82, P < 0.001). Nonetheless, a lower rate of EHL was observed in females when exercise was performed at 500 W of metabolic heat production (419 ± 7 vs. 454 ± 11 W, P= 0.032). Furthermore, a lower increase in EHL per increase in mean body temperature was observed in females (553 ± 77 vs. 795 ± 85 W °C−1, P= 0.051), with no differences in the onset threshold (36.77 ± 0.06 vs. 36.61 ± 0.11°C, P= 0.242). In contrast, no differences were observed in CVC. Collectively, these findings demonstrate that females have a lower thermosensitivity of the whole‐body sudomotor response compared to males during exercise in the heat performed at a fixed rate of metabolic heat production.