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To mitigate excessive rises in core temperature (>1°C) in non heat-acclimatized workers, the American Conference of Governmental Industrial Hygienists (ACGIH) provide heat stress limits (Action Limit Values; ALV), defined by the wet-bulb globe temperature (WBGT) and a worker’s metabolic rate. However, since these limits are based on data from men, their suitability for women remains unclear. We therefore assessed core temperature and heart rate in men (n=19; body surface area-to-mass ratio: 250 (SD 17) cm2/kg) and women (n=15; body surface area-to-mass ratio: 268 (SD 24) cm2/kg) aged 18-45 years during 180-min walking at a moderate metabolic rate (200 W/m2) in WBGTs below (16 and 24°C) and above (28 and 32°C) ACGIH ALV. Sex did not significantly influence (i) rises in core temperature, irrespective of WBGT, (ii) the proportion of participants with rises in core temperature >1°C in environments below ACGIH limits, and (iii) work duration before rises in core temperature exceeded 1°C or volitional termination in environments above ACGIH limits. Although further studies are needed, these findings indicate that for the purpose of mitigating rises in core temperature exceeding recommended limits (>1°C), ACGIH guidelines have comparable effectiveness in non heat-acclimatized men and women when working at a moderate metabolic rate. Novelty points • Sex did not appreciably influence thermal strain nor the proportion of participants with core temperatures exceeding recommended limits. • Sex did not significantly influence tolerance to uncompensable heat stress • Despite originating from data obtained in only men, current occupational heat stress guidance offered comparable effectiveness in men and women.

The purpose of this study was to assess the heat strain experienced by children during unstructured physical activity outdoors in a temperate continental summer climate. Eighteen children (7 girls, 12.1 ± 1.7 years) performed up to 4 h of outdoor free-play (duration: 218 ± 33 min; air temperature of 24.5 ± 3.9°C and relative humidity of 66.2 ± 9.2%). Urine specific gravity (USG) was measured pre-and post-free-play, while body core temperature (T co , ingestible pill) and heart rate (HR) were measured continuously. Physiological strain index (PSI) was calculated from T co and HR (scale: 0 (none) to 10 (very high)). Activity levels were categorized as rest, light, moderate, and vigorous based on the metabolic equivalent of task, estimated from video analysis. Most children were euhydrated pre (78%, USG ≤ 1.020), but not post-free-play (28%, USG ≤ 1.020). Mean and peak T co , HR, and PSI responses were 37.8 ± 0.3°C and 38.4 ± 0.3°C, 133 ± 14 bpm and 180 ± 12 bpm, and 4.7 ± 1.1 (low) and 7.4 ± 1.0 (high), respectively. All children reached peak T co ≥38.0°C, with seven ≥38.5°C, and the highest at 38.9°C. The children spent 58 ± 15% of free-play engaged in moderate-to-vigorous intensity physical activity. During free-play, all of the children performed moderate-to-vigorous intensity physical activity, which was associated with pronounced elevations in heat strain.

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