ABSTRACT The heat-related health burden is expected to persist and worsen in the coming years due to an aging global population and climate change. Defining the breadth and depth of our understanding of age-related changes in thermoregulation can identify underlying causes and strategies to protect vulnerable individuals from heat. We conducted the first systematic quantitative literature review to provide context to the historical experimental research of healthy older adults – compared to younger adults or unhealthy age matched cases – during exogenous heat strain, focusing on factors that influence thermoregulatory function (e.g. co-morbidities). We identified 4,455 articles, with 147 meeting eligibility criteria. Most studies were conducted in the US (39%), Canada (29%), or Japan (12%), with 71% of the 3,411 participants being male. About 71% of the studies compared younger and older adults, while 34% compared two groups of older adults with and without factors influencing thermoregulation. Key factors included age combined with another factor (23%), underlying biological mechanisms (18%), age independently (15%), influencing health conditions (15%), adaptation potential (12%), environmental conditions (9%), and therapeutic/pharmacological interventions (7%). Our results suggest that controlled experimental research should focus on the age-related changes in thermoregulation in the very old, females, those with overlooked chronic heat-sensitive health conditions (e.g. pulmonary, renal, mental disorders), the impact of multimorbidity, prolonged and cumulative effects of extreme heat, evidence-based policy of control measures (e.g. personal cooling strategies), pharmaceutical interactions, and interventions stimulating protective physiological adaptation. These controlled studies will inform the directions and use of limited resources in ecologically valid fieldwork studies.

ABSTRACT We determined the reliability of a 60-min treadmill protocol in the heat when spaced >4 weeks apart, longer than the test–retest duration of 1 week found in the literature. Nine unacclimated, trained males (age: 31 ± 8 y; VO2peak: 60 ± 6 ml∙kg−1∙min−1) undertook a 15 min self-paced time-trial pre-loaded with 45 min of running at 70% of individual ventilatory threshold (11.2 ± 0.3 km∙h−1) in 30 ± 1°C (53 ± 5% relative humidity). They repeated this following 40 ± 14 and 76 ± 26 days, with pre-trial standardization of diet and exercise for 48 h. When considering trial 1 as a familiarization, change in core temperature (∆Tcore) during the first 45 min (∆2.0 ± 0.2°C) between trials 2 and 3 yielded bias and 95% limits of agreement (LoA) of −0.10 ± 0.43°C, standard error of measurement (SEM) of 0.13°C and intraclass correlation coefficient (ICC) of 0.75, more reliable than measures of baseline Tcore (36.9 ± 0.2°C; LoA: −0.23 ± 0.90°C; SEM: 0.22°C; ICC: 0.03) and Tcore at 45 min during exercise (38.9 ± 0.4°C; LoA: 0.32 ± 1.12°C; SEM: 0.28°C; ICC: 0.15). The coefficient of variation (CV) between trials 2 and 3 for distance run during the 15 min time-trial was 2.1 ± 2.0% with LoA of 0.001 ± 0.253 km and SEM of 0.037 km. This protocol is reliable spaced ~5 weeks apart when considering the most commonly accepted limit of <5% CV for performance, reinforced by reliability of the ΔTcore being 0.1 ± 0.4°C.

ABSTRACT Purpose Utilising metadata from existing exertional and exertional-heat stress studies, the study aimed to determine if the exercise-associated increase in core body temperature can predict the change in exercise-induced gastrointestinal syndrome (EIGS) biomarkers and exercise-associated gastrointestinal symptoms (Ex-GIS). Method Endurance-trained individuals completed 2h of running exercise in temperate (21.2-30.0°C) to hot (35.0-37.2°C) ambient conditions (n=132 trials). Blood samples were collected pre- and post-exercise to determine the change in gastrointestinal integrity biomarkers and systemic inflammatory cytokines. Physiological and thermoregulatory strain variables were assessed every 10-15min during exercise. The strength of the linear relationship between maximal (M-Tre) and change (Δ Tre) in rectal temperature and EIGS variables was determined via Spearman’s rank correlation coefficients. While the strength of prediction was determined via simple and multiple linear regression analyses dependent on screened EIGS and Ex-GIS confounding factors. Results Significant positive correlations between Tre maximum (M-Tre) and change (Δ Tre) with I-FABP (rs=0.434, p<0.001; and rs=0.305, p<0.001; respectively), sCD14 (rs=0.358, p<0.001; and rs=0.362, p<0.001), systemic inflammatory response profile (SIR-Profile) (p<0.001), and total Ex-GIS (p< 0.05) were observed. M-Tre and Δ Tre significantly predicted (adjusted R2) magnitude of change in I-FABP (R2 (2,123)=0.164, p<0.001; and R2 (2,119)=0.058, p=0.011; respectively), sCD14 (R2 (2,81)=0.249, p<0.001; and R2 (2,77)=0.214, p<0.001), SIR-Profile (p<0.001) and total Ex-GIS (p<0.05). Conclusion Strong to weak correlations were observed between M-Tre and Δ Tre with plasma concentrations of I-FABP, sCD14, SIR-Profile, and Ex-GIS in response to exercise. M-Tre and Δ Tre can predict the magnitude of these EIGS variables and Ex-GIS in response to exercise.

ABSTRACT Thermal safety guidelines with upper thresholds aim to protect athletes’ health, yet evidence-based sport-specific thresholds remain unestablished. Experimenting with athletes in severely hot conditions raises ethical concerns, so we used a thermo-physiological model to validate the thresholds of guidelines for outdoor sports. First, the reproducibility of the joint system thermoregulation model (JOS-3) of core temperature has been validated for 18 sports experiments (n = 213) and 11 general exercise experiments (n = 121) using the Bland – Altman analysis. Then, core temperatures were predicted using the JOS-3 in conditions corresponding to the upper thresholds, and if the 90th–99.7th percentile core temperature value (corresponding to 0.3%–10% of the participants) exceeded 40°C, the thresholds were judged as potentially hazardous. Finally, we proposed revisions for sports with potentially hazardous thresholds. As a result, the JOS-3 could simulate core temperature increases in most experiments (27/29) for six sports and general exercises with an accuracy of 0.5°C. The current upper thresholds for marathons, triathlons, and football are potentially hazardous. Suggested revisions, based on specified percentiles, include: Football: revise from wet bulb globe temperature (WBGT) 32°C to 29–31°C or not revise. Marathon: revise from WBGT 28°C to 24–27°C. Triathlon: revise from WBGT 32.2°C to 23–26°C. If conducting sports events under the revised upper thresholds proves difficult, taking measures for a possible high incidence of heat illness becomes crucial, such as placing additional medical resources, assisting heat acclimatization and cooling strategies for participants, and rule changes such as shorter match times and increased breaks.

ABSTRACT Technological advancements in the last two decades have enabled development of a variety of mechanically supporting wearable robots (i.e. exoskeletons) that are transitioning to practice in medical and industrial settings. The feedback from industry and recent controlled studies is highlighting thermal discomfort as a major reason for the disuse of the devices and a substantial barrier to their long-term adoption. Furthermore, a brief overview of the devices and their intended applications reveals that many of the potential users are likely to face thermal comfort issues because of either high exertion or medically related high heat sensitivity. The aim of this review is to discuss these emerging thermal challenges and opportunities surrounding wearable robots. This review discusses mechanisms, potential solutions, and a platform for systematically measuring heat transfer inhibition caused by wearing of an exoskeleton. Lastly, the potential for substantial metabolic rate reduction provided by exoskeletons to reduce worker thermal strain in warm-to-hot conditions is also considered.

ABSTRACT Fine-scale personal heat exposure (PHE) information can help prevent or minimize weather-related deaths, illnesses, and reduced work productivity. Common methods to estimate heat risk do not simultaneously account for the intensity, frequency, and duration of thermal exposures, nor do they include inter-individual factors that modify physiological response. This study demonstrates new whole-body net thermal load estimations to link PHE to heat stress and strain over time. We apply a human-environment heat exchange model to examine how time-varying net thermal loads differ across climate contexts, personal attributes, and spatiotemporal scales. First, we investigate summertime climatic PHE impacts for three US cities: Phoenix, Miami, and New York. Second, we model body morphology and acclimatization for three profiles (middle-aged male/female; female >65 years). Finally, we quantify model sensitivity using representative data at synoptic and micro-scales. For all cases, we compare required and potential evaporative heat losses that can lead to dangerous thermal exposures based on (un)compensable heat stress. Results reveal misclassifications in heat stress or strain due to incomplete environmental data and assumed equivalent physiology and activities between people. Heat strain is most poorly represented by PHE alone for the elderly, non-acclimatized, those engaged in strenuous activities, and when negating solar radiation. Moreover, humid versus dry heat across climates elicits distinct thermal responses from the body. We outline criteria for inclusive PHE evaluations connecting heat exposure, stress, and strain while using physiological-based methods to avoid misclassifications. This work underlines the value of moving from “one-size-fits-all” thermal indices to “fit-for-purpose” approaches using personalized information.

ABSTRACT This study investigated the seasonal effects that working outdoors had on various parameters in mining industry workers over the course of a work-shift. Workers (n = 27) were assessed in summer (33.3 ± 4.2°C, 38 ± 18% RH; n = 13, age = 46 ± 14 y, BMI = 29.1 ± 5.7 kg/m2) and winter (23.6 ± 5.1°C, 39 ± 20% RH; n = 14, age = 44 ± 12 y, BMI = 31.2 ± 4.1 kg/m2). Core temperature and heart-rate were measured continuously (analyzed at five time points), while perceptual measures, cognitive and manual dexterity performance were assessed at various times over an 11-h shift at the start of a 14-day swing. Hydration was assessed (urine specific gravity) pre- and post-shift. Working memory was impaired in summer compared to winter (−10%; p = 0.039), however did not change throughout the shift. Processing efficiency was significantly reduced at 12 pm (−12%; p = 0.005) and 5 pm (−21%; p < 0.001) compared to 9 am, irrespective of season (p > 0.05). Manual dexterity (dominant-hand) improved over the shift (+13%, p = 0.002), but was not different between seasons. Perceived fatigue had no main effect of season or shift. Core temperature, heart-rate, thermal sensation and rating of perceived exertion increased throughout the shift, with only core temperature and thermal sensation showing a seasonal effect (summer: +0.33°C, +18%, respectively; p < 0.002). Notably, 23% of workers in summer and 64% in winter started work significantly dehydrated, with 54% and 64% in summer and winter, respectively, finishing work with significant to serious dehydration. Impairment in working memory in summer combined with high levels of dehydration over the work-shift reinforces the need for workplace education on the importance of hydration and risk of occupation heat stress. Abbreviations: Core temperature: Tc; Fly-in fly-out: FIFO; Ratings of perceived exertion: RPE; Relative humidity: RH; Urinary specific gravity: USG; Wet bulb globe temperature: WBGT.

ABSTRACT 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.

ABSTRACT We have previously identified predator odor as a potent stimulus activating thermogenesis in skeletal muscle in rats. As this may prove relevant for energy balance and weight loss, the current study investigated whether skeletal muscle thermogenesis was altered with negative energy balance, obesity propensity seen in association with low intrinsic aerobic fitness, and monogenic obesity. First, weight loss subsequent to 3 wk of 50% calorie restriction suppressed the muscle thermogenic response to predator odor. Next, we compared rats bred based on artificial selection for intrinsic aerobic fitness – high- and low-capacity runners (HCR, LCR) – that display robust leanness and obesity propensity, respectively. Aerobically fit HCR showed enhanced predator odor-induced muscle thermogenesis relative to the less-fit LCR. This contrasted with the profound monogenic obesity displayed by rats homozygous for a loss of function mutation in Melanocortin 4 receptor (Mc4rK3a,4X/K314X rats), which showed no discernable deficit in thermogenesis. Taken together, these data imply that body size or obesity per se are not associated with deficient muscle thermogenesis. Rather, the physiological phenotype associated with polygenic obesity propensity may encompass pleiotropic mechanisms in the thermogenic pathway. Adaptive thermogenesis associated with weight loss also likely alters muscle thermogenic mechanisms.