Search

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 [...]

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]

Nitric oxide synthase (NOS) contributes to the heat loss responses of cutaneous vasodilatation and sweating during exercise. However, the contribution of NOS may be attenuated in individuals with uncomplicated, controlled hypertension due to elevated oxidative stress, which can reduce NO bioavailability. We evaluated the hypothesis that the acute local intradermal administration of the antioxidant ascorbate would enhance cutaneous vasodilatation and sweating via NOS-dependent mechanisms during an exercise-heat stress in adults with hypertension. Habitually active adultswho were normotensive (n = 14, 7 females, 62 ± 4 years) or had uncomplicated, controlled hypertension (n=13, 6 females, 62±5 years) performed 30 min of moderate-intensity (50% of their pre-determined peak oxygen uptake) semi-recumbent cycling in the heat (35°C, 20% relative humidity). Cutaneous vascular conductance (CVC) and sweat rate were assessed at four forearm skin sites continuously perfused with (1) lactated Ringer solution (Control), (2) 10 mM antioxidant ascorbate, (3) 10 mM NG-nitro-Larginine methyl ester (L-NAME), a non-selective NOS inhibitor, or (4) a combination of ascorbate and L-NAME. Relative to Control, no effect of ascorbate was observed on CVC or sweating in either group (P = 0.619). However, L-NAME reduced CVC relative to Control in both groups (P = 0.038). No effect of any treatment on sweating was observed (P = 0.306). Thus, acute local administration of ascorbate to forearm skin does not enhance the activation of heat loss responses of cutaneous vasodilatation and sweating in older adults, and those with hypertension during an exercise-heat stress. [ABSTRACT FROM AUTHOR]

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 (Tco, ingestible pill) and heart rate (HR) were measured continuously. Physiological strain index (PSI) was calculated from Tco 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 Tco, 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 Tco≥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. [ABSTRACT FROM AUTHOR]

Background: Previous studies of the Elevation Training Mask (ETM) describe comparisons between groups using the ETM and controls for effects on aerobic performance. However, comparisons have not been made to intermittent hypoxic training (IHT). Further, how the ETM impacts exercise economy is unknown. Therefore, we sought to determine the effects of training with the ETM compared to IHT on aerobic performance and cycling economy. Methods: Thirty participants were randomized into an ETM, IHT, or control group (n = 10 each). Pre- and post-testing occurred using a ramp VO2max test on a cycle ergometer allowing submaximal power output (PO) measures of economy. Economy was measured using POs of 100, 125, and 150W. High-intensity cycling interval training (HIIT) occurred 2x/week for 30 min/session for six weeks. Sessions were 20 min of HIIT (30s at 100% peak power output (PPO) of pre VO2max, 90s active recovery at 25W, 10 bouts) with a 5-minute warm-up and cool-down. Repeated measures ANOVA was used for statistical analyses. RESULTS: All participants improved VO2max, PPO, and PO at ventilatory threshold 2 pre- to post-training (p < 0.05). Interactions between groups showed that the RER for the IHT group increased at 100W and 125W, and decreased at RERmax pre- to post-training while the ETM group showed the opposite response (p < 0.05). Conclusion: The ETM and IHT groups performed similarly to the control at maximal and submaximal effort following six weeks of training. The IHT group, but not the ETM group, experienced an increased glycolytic energy shift during submaximal exercise. [ABSTRACT FROM AUTHOR]

Aging is associated with an elevated risk of heat-related mortality and morbidity, attributed, in part, to declines in thermoregulation. However, comparisons between young and older adults have been limited to brief exposures (1-4 h), which may not adequately reflect the duration or severity of the heat stress experienced during heat waves. We therefore evaluated physiological responses in 20 young (19-31 yr; 10 females) and 39 older (61-78 yr; 11 females) adults during 9 h of rest at 40°C and 9% relative humidity. Whole body heat exchange and storage were measured with direct calorimetry during the first 3 h and final 3 h. Core temperature (rectal) was monitored continuously. The older adults stored 88 kJ [95% confidence interval (CI): 29, 147] more heat over the first 3 h of exposure ( P = 0.006). Although no between-group differences were observed after 3 h [young: 37.6°C (SD 0.2°C) vs. older: 37.7°C (0.3°C); P = 0.216], core temperature was elevated by 0.3°C [0.1, 0.4] (adjusted for baseline) in the older group at hour 6 [37.6°C (0.2°C) vs. 37.9°C (0.2°C); P < 0.001] and by 0.2°C [0.0, 0.3] at hour 9 [37.7°C (0.3°C) vs. 37.8°C (0.3°C)], although the latter comparison was not significant after multiplicity correction ( P = 0.061). Our findings indicate that older adults sustain greater increases in heat storage and core temperature during daylong exposure to hot dry conditions compared with their younger counterparts. This study represents an important step in the use of ecologically relevant, prolonged exposures for translational research aimed at quantifying the physiological and health impacts of hot weather and heat waves on heat-vulnerable populations. NEW & NOTEWORTHY We found greater increases in body heat storage and core temperature in older adults than in their younger counterparts during 9 h of resting exposure to hot dry conditions. Furthermore, the age-related increase in core temperature was exacerbated in older adults with common heat-vulnerability-linked health conditions (type 2 diabetes and hypertension). Impairments in thermoregulatory function likely contribute to the increased risk of heat-related illness and injury seen in older adults during hot weather and heat waves.

With rising global temperatures, heat-related mortality is increasing, particularly among older adults. Although 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 yr; 10 female) and 37 older adults (61-78 yr; 10 female) during 9 h of heat exposure (40°C, 9% relative humidity). Mean body temperature (T body ) 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. T body increased by 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) in 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 (T body 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. NEW & NOTEWORTHY We demonstrate for the first time that peripheral blood mononuclear cells from older adults exhibit signs of autophagic impairments during daylong (9 h) heat exposure relative to their younger counterparts. This was paired with greater apoptotic signaling and inflammatory responses, and an inability to stimulate components of the heat shock response. Thus, autophagic dysregulation during prolonged heat exposure may contribute to age-related heat vulnerability during hot weather and heat waves.

Autophagy is essential to maintaining cellular homeostasis in all eukaryotic cells and to tolerance of acute stressors such as starvation, heat, and recovery after exercise. Limited information exists regarding the exercise intensity-dependent autophagic response in humans, and it is unknown how environmental heat stress may modulate this response. Therefore, we evaluated autophagy and accompanying pathways of cellular stress [the heat-shock response (HSR), apoptosis, and acute inflammation] in peripheral blood mononuclear cells (PBMCs) from 10 young men (mean [SD]; 22 [2] years) before, immediately after and up to 6-h postexercise recovery from 30 min of low-, moderate-, and high-intensity semirecumbent cycling [40%, 55%, and 70% of maximal oxygen consumption (V̇o 2max ), respectively] in a temperate environment (25°C) and at 70% of V̇o 2max in a hot environment (40°C). Changes in protein content were analyzed via Western blot. Each increase in exercise intensity was associated with elevations in mean body temperature. LC3-II increased after moderate-intensity exercise, with further increases after high-intensity exercise ( P < 0.05). However, an increase in beclin-2 and ULK1, with a decrease in p62 was only observed after high-intensity exercise, which was paralleled by elevated TNF-α and cleaved-caspase-3, with the HSR peaking at 6 h after exercise ( P < 0.05). When exercise was performed in the heat, greater LC3-II and cleaved-caspase-3 accumulation were observed; however, beclin-2 declined in recovery ( P < 0.05). Therefore, our findings indicate that autophagy in PBMCs during exercise may be associated with greater heat strain exhibited during increasing exercise intensities, which is modulated by exposure to heat.

The objective of this study was 1) to examine pooled effects of hypertension on nitric oxide (NO)-dependent vasodilation during local heating across multiple nonglabrous skin regions, and 2) explore regional differences. Responses were compared between 14 participants with uncomplicated hypertension controlled with medication (7 females, 61 ± 6 yr) and 14 age-matched nonhypertensive controls (6 females; 60 ± 5 yr). Cutaneous vascular conductance, normalized to maximum vasodilation (%CVC max ), was assessed at the upper chest, abdomen, dorsal forearm, thigh, and lateral calf during local heating. Across all regions, local skin temperatures were simultaneously increased from 33°C to 42°C (1°C·10 s -1 ) and held until a stable heating plateau was achieved (∼40 min), followed by continuous infusion of 20 mM of N G -nitro-l-arginine methyl ester (l-NAME; ∼40 min) at all sites until a stable l-NAME plateau was achieved. The difference between heating and l-NAME plateaus was defined as the NO-contribution. Statistical equivalence for each heating phase was determined based on equivalence bounds of ±10%CVC max for between-group differences. Pooled (all-regions) %CVC max responses were equivalent for baseline (two one-sided t tests; P < 0.001), heating plateau ( P = 0.002), l-NAME plateau ( P = 0.028), and NO-contribution ( P = 0.003). For individual regions, responses were equivalent at baseline for the abdomen, thigh, and calf, the heating plateau for the thigh, and the l-NAME plateau for the calf (all P < 0.05). Conversely, the calf heating plateau was lower in the hypertension group ( t test; P < 0.05). Local heat-induced cutaneous vasodilation was statistically equivalent between individuals with uncomplicated, controlled hypertension, and nonhypertensive age-matched adults when pooled across multiple skin sites. Conversely, individual between-region comparisons were generally too variable to permit definitive conclusions.