Search

Background: Health agencies recommend that homes of heat-vulnerable occupants (e.g., older adults) be maintained below 24-28[degrees]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/[m.sup.2]] 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[degrees]C; control), proposed indoor temperature upper limits (26[degrees]C), and temperatures experienced in homes without air-conditioning (31[degrees]C and 36[degrees]C). Core temperature (rectal) was monitored as the primary outcome; based on previous recommendations, between-condition differences >0.3[degrees]C were considered clinically meaningful. Results: Compared with 22[degrees]C, core temperature was elevated to a meaningful extent in 31[degrees]C [+0.7[degrees]C; 95% confidence interval (CI): 0.5, 0.8] and 36[degrees]C (+0.9[degrees]C; 95% CI: 0.8, 1.1), but not 26[degrees]C (+0.2[degrees]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[degrees]C but increased progressively in conditions above this threshold. These data support proposals for the establishment of a 26[degrees]C indoor temperature upper limit for protecting vulnerable occupants residing in temperate continental climates from indoor overheating. https://doi.org/10.1289/EHP13159, Introduction In the summer of 2021, an unprecedented heat wave in the Pacific Northwest of North America broke national temperature records in Canada by 5[degrees]C and resulted in the deaths [...]

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. [ABSTRACT FROM AUTHOR]

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 h in 31 and 36 °C (45% relative humidity). Core (rectal) temperature, heart rate (HR), HR variability, mean arterial pressure (MAP), and cardiac autonomic responses to standing were measured at baseline and end-exposure. Bootstrapped least absolute shrinkage and selection operator 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% confidence interval: 6, 23)), seated MAP (−7 mmHg (−18, 1)), and the systolic pressure response to standing (20 mmHg (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 heat-induced physiological strain in older persons. [ABSTRACT FROM AUTHOR]

Background: Health agencies, including the U.S. Centers for Disease Control and Prevention and the World Health Organization, recommend that heat-vulnerable older adults without home air-conditioning should visit cooling centers or other air-conditioned locations (e.g., a shopping mall) during heat waves. However, experimental evidence supporting the effectiveness of brief air-conditioning is lacking. OBJECTIVE: We evaluated whether brief exposure to an air-conditioned environment, as experienced in a cooling center, was effective for limiting physiological strain in older adults during a daylong laboratory-based heat wave simulation. Methods: Forty adults 64-79 years of age underwent a 9-h simulated heat wave (heat index: 37[degrees]C) with (cooling group, n = 20) or without (control group, n = 20) a cooling intervention consisting of 2-h rest in an air-conditioned room (~ 23[degrees]C, hours 5-6). Core and skin temperatures, whole-body heat exchange and storage, cardiovascular function, and circulating markers of acute inflammation were assessed. Results: Core temperature was 0.8[degrees]C (95% CI: 0.6, 0.9) lower in the cooling group compared with the control group at the end of the cooling intervention (p < 0.001; hour 6), and it remained 0.3[degrees]C (95% CI: 0.2, 0.4) lower an hour after returning to the heat (p < 0.001; hour 7). Despite this, core temperatures in each group were statistically equivalent at hours 8 and 9, within [+ or -] 0.3[degrees]C (p [less than or equal to] 0.005). Cooling also acutely reduced demand on the heart and improved indices of cardiovascular autonomic function (p [less than or equal to] 0.021); however, these outcomes were not different between groups at the end of exposure (p [greater than or equal to] 0.58). Discussion: Brief air-conditioning exposure during a simulated heat wave caused a robust but transient reduction in core temperature and cardiovascular strain. These findings provide important experimental support for national and international guidance that cooling centers are effective for limiting physiological strain during heat waves. However, they also show that the physiological impacts of brief cooling are temporary, a factor that has not been considered in guidance issued by health agencies. https://doi.org/10.1289/EHP11651, Introduction The planet is warming at an unprecedented rate, (1) giving rise to more frequent and severe heat waves and increasing yearly heat-related fatalities. (2) Older adults ([greater than or [...]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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, V̇O2peak${\dot V_{{{\mathrm{O}}_{\mathrm{2}}}{\mathrm{peak}}}}$ 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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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 FROM AUTHOR]