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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., Competing Interests: None declared.

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., Competing Interests: No conflict of interest, financial or otherwise, are declared by the author(s).

Older adults are at greater risk of heat-related morbidity and mortality during heat waves, which is commonly linked to impaired thermoregulation. However, little is known about the influence of increasing age on the relation between thermal strain and perceptual responses during daylong heat exposure. We evaluated thermal and perceptual responses in 20 young (19-31 yr) and 39 older adults (20 with hypertension and/or type 2 diabetes; 61-78 yr) resting in the heat for 9 h (heat index: 37°C). Body core and mean skin temperature areas under the curve (AUC, hours 0-9 ) were assessed as indicators of cumulative thermal strain. Self-reported symptoms (68-item environmental symptoms questionnaire) and mood disturbance (40-item profile of mood states questionnaire) were assessed at end-heating (adjusted for prescores). Body core temperature AUC was 2.4°C·h [1.0, 3.7] higher in older relative to young adults ( P < 0.001), whereas mean skin temperature AUC was not different (-0.5°C·h [-4.1, 3.2] P = 0.799). At end-heating, self-reported symptoms were not different between age groups (0.99-fold [0.80, 1.23], P = 0.923), with or without adjustment for body core or mean skin temperature AUC (both P ≥ 0.824). Mood disturbance was 0.93-fold [0.88, 0.99] lower in older, relative to young adults ( P = 0.031). Older adults with and without chronic health conditions experienced similar thermal strain, yet those with these conditions reported lower symptom scores and mood disturbance compared with young adults and their age-matched counterparts (all P ≤ 0.026). Although older adults experienced heightened thermal strain during the 9-h heat exposure, they did not experience greater self-reported symptoms or mood disturbance relative to young adults. NEW & NOTEWORTHY Despite experiencing greater cumulative thermal strain during 9 h of passive heat exposure, older adults reported similar heat-related symptoms and lower mood disturbance than young adults. Furthermore, self-reported symptoms and mood disturbance were lower in older adults with common age-associated health conditions than young adults and healthy age-matched counterparts. Perceptual responses to heat in older adults can underestimate their level of thermal strain compared with young adults, which may contribute to their increased heat vulnerability.

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°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 ° 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°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°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 ± 0.3 ° C ( p ≤ 0.005 ). Cooling also acutely reduced demand on the heart and improved indices of cardiovascular autonomic function ( p ≤ 0.021 ); however, these outcomes were not different between groups at the end of exposure ( p ≥ 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.

Irisin is thought to play a cytoprotective role during acute stressors, such as exercise, by reducing oxidative stress and inflammation. Relative to young adults, older individuals exhibit an impaired capacity to dissipate heat during exercise, which can exacerbate elevations in oxidative stress and the acute inflammatory response especially in the heat. In turn, this could induce a greater increase in circulating irisin. Thus, we evaluated age-related differences in irisin expression during prolonged exercise in a non-heat stress and high-heat stress environment. Specifically, we assessed serum irisin in 12 young (22 ± 3 years) and 12 older (59 ± 4 years) men before and after 3-h moderate-intensity exercise (metabolic rate: 200 W/m 2 ) and 60-min post-exercise recovery in temperate (wet-bulb globe temperature (WBGT) 16 °C) and hot (WBGT 32 °C) environments. Core temperature (T co ) was measured continuously. Post-exercise T co was similarly higher in the hot compared to the temperate condition for both groups (p < 0.001), although T co remained elevated at end-recovery in the heat in older but not young adults (p = 0.006). Absolute serum irisin concentrations were significantly higher (p ≤ 0.002) under all conditions in the young relative to older adults. Post-exercise and end-recovery irisin was elevated above baseline in both groups in the hot (+39.3 pg/mL SEM 8 and + 48.9 pg/mL SEM 10, respectively; both p ≤ 0.043) but not the temperate condition. When comparing between conditions, the change in irisin concentrations at post-exercise did not differ, although serum irisin was elevated in the hot (+48.9 pg/mL SEM 10) relative to the temperate (+0.88 pg/mL SEM 0.2) condition in both groups at end-recovery (p = 0.004). Our findings indicate that irisin concentrations were elevated after exercise compared to rest in hot, but not temperate conditions across groups. However, older adults may still have greater cellular vulnerability to heat stress given their blunted circulating irisin levels., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Exercise is promoted for management of hypertension and as a general healthy behavior, but environmental conditions are seldom considered in these recommendations. Hypertension may affect skin blood flow and sweating, two of the primary mechanisms which prevent continued elevations in core temperature by facilitating whole-body heat loss during exercise-heat stress. We show that during incremental exercise-heat stress (in hot-dry conditions), controlled and uncomplicated hypertension is unlikely to exert a meaningful effect on whole-body heat loss in individuals who are already physically active., (© 2020. Springer Nature Limited.)

New Findings: What is the central question of this study? Does short-term heat acclimation enhance whole-body evaporative heat loss and augment nitric oxide synthase (NOS)-dependent cutaneous vasodilatation and NOS- and cyclooxygenase (COX)-dependent sweating, in exercising older men? What is the main finding and its importance? Our preliminary data (n = 8) demonstrated that short-term heat acclimation improved whole-body evaporative heat loss, but it did not influence the effects of NOS and/or COX inhibition on cutaneous vasodilatation or sweating in older men during an exercise-heat stress. These outcomes might imply that although short-term heat acclimation enhances heat dissipation in older men, it does not modulate NOS- and COX-dependent control of cutaneous vasodilatation or sweating on the forearm., Abstract: Ageing is associated with decrements in whole-body heat loss (evaporative + dry heat exchange), which might stem from alterations in nitric oxide synthase (NOS)- and cyclooxygenase (COX)-dependent cutaneous vasodilatation and sweating. We evaluated whether short-term heat acclimation would (i) enhance whole-body heat loss primarily by increasing evaporative heat loss, and (ii) augment NOS-dependent cutaneous vasodilatation and NOS- and COX-dependent sweating, in exercising older men. Eight older men [mean (SD) age, 59 (8) years] completed a calorimetry and microdialysis trial before and after 7 days of exercise-heat acclimation. For the calorimetry trials, whole-body evaporative and dry heat exchange were assessed using direct calorimetry during 30 min bouts of cycling at light, moderate and vigorous metabolic heat productions (150, 200 and 250 W/m 2 , respectively) in dry heat (40°C, 20% relative humidity). For the microdialysis trials, local cutaneous vascular conductance and sweat rate were assessed during 60 min exercise in the heat (35°C, 20% relative humidity) at four dorsal forearm skin sites treated with lactated Ringer solution (control), NOS inhibitor, COX inhibitor or combined NOS and COX inhibitors, via microdialysis. Evaporative heat loss during moderate (P = 0.036) and vigorous (P = 0.021) exercise increased after acclimation. Inhibition of NOS alone reduced cutaneous vascular conductance to a similar extent before and after acclimation (P < 0.040), whereas separate and combined NOS and COX inhibition had no significant effects on sweating relative to the control site (P = 0.745). Our preliminary results might suggest that short-term heat acclimation improves evaporative heat loss, but does not significantly modulate the contributions of NOS or COX to cutaneous vasodilatation or sweating on the forearm in older men during an exercise-heat stress., (© 2020 The Authors. Experimental Physiology © 2020 The Physiological Society.)

New Findings: What is the central question of this study? Repeated heat exposure during the summer months can enhance heat loss in humans (seasonal heat acclimatisation), but does the magnitude of that enhancement differ between young and older adults when assessed during passive heat exposure? What is the main finding and its importance? While seasonal heat acclimatisation enhanced evaporative heat loss (i.e. sweating) in both young and older adults, those improvements led to a greater reduction in body heat storage in older adults. These outcomes indicate that heat acclimatisation may confer greater thermoregulatory benefits with increasing age., Abstract: Repeated heat exposure throughout summer can enhance heat loss in humans (seasonal heat acclimatisation), although the effect of ageing on those improvements remains unclear. We therefore sought to assess thermoregulatory function in young and older adults during environmental heat exposure prior to and following seasonal heat acclimatisation, hypothesizing that the magnitude of adaptation would be greater in older relative to young adults. To achieve this, 14 young (19-27 years) and 10 older adults (55-72 years), who resided in a temperate humid-continental climate, completed a 3 h resting heat exposure (44°C, ∼30% relative humidity) in the winter-spring months as part of a larger investigation (pre-acclimatisation), before being re-evaluated using the same heat stress test following the summer months (post-acclimatisation). Whole-body dry and evaporative heat exchange, and metabolic rate were measured throughout using direct and indirect calorimetry (respectively), and used to quantify body heat storage (metabolic rate + dry heat gain - evaporative heat loss). Evaporative heat loss increased in both groups following acclimatisation, but those improvements led to a decrease in body heat storage in older (mean difference (95% CI); 213 (295, 131) kJ; P < 0.001), but not young adults (-25 (-94, 44) kJ; P = 0.458). Thus, body heat storage was greater in older compared to young adults before (222 (123, 314) kJ; P < 0.001), but not following acclimatisation (34 (-55, 123) kJ; P = 0.433). Although there is a need for larger and more controlled confirmatory studies, our findings indicate that seasonal heat acclimatisation may induce greater thermoregulatory adaptation in older compared to young adults., (© 2020 The Authors. Experimental Physiology © 2020 The Physiological Society.)

Aim: Ageing and hypohydration independently attenuate heat dissipation during exercise; however, the interactive effects of these factors remain unclear. We assessed the hypothesis that ageing suppresses hypohydration-induced reductions in whole-body heat loss during exercise in the heat., Methods: On two occasions, eight young (mean [SD]: 24 [4] years) and eight middle-aged (59 [5] years) men performed 30-minute bouts of light (heat production of 175 W m -2 ) and moderate (275 W m -2 ) cycling (separated by 15-minute rest) in the heat (40°C, 15% relative humidity) when euhydrated and hypohydrated (~4% reduction in body mass). Heat production and whole-body net heat exchange (evaporative heat loss + dry heat gain) were measured via indirect and direct calorimetry (respectively) and heat storage was calculated via their temporal summation., Results: Net heat exchange was reduced, while heat storage was elevated, in the middle-aged men during moderate exercise when euhydrated (both P ≤ 0.01). In the young, evaporative heat loss was attenuated in the hypohydrated vs euhydrated condition during light (199 ± 6 vs 211 ± 10 W m -2 ; P ≤ 0.01) and moderate (287 ± 15 vs 307 ± 13 W m -2 ; P ≤ 0.01) exercise, but was similar in the middle-aged men, averaging 223 ± 6 and 299 ± 15 W m -2 , respectively, across conditions (both P ≥ 0.32). Heat storage was thereby exacerbated by hypohydration in the young (both P < 0.01) but not the middle-aged (both P ≥ 0.32) during both exercise bouts and, as a result, was similar between groups when hypohydrated (both P ≥ 0.50)., Conclusion: Hypohydration attenuates heat loss via sweating in young but not middle-aged men, indicating that ageing impairs one's ability to mitigate further sweat-induced fluid loss during hypohydration., (© 2018 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd.)

Purpose: This study was designed to determine whether age-related impairments in whole-body heat loss, which are known to exist in dry heat, also occur in humid heat in women., Methods: To evaluate this possibility, 10 young (25 ± 4 yr) and 10 older (51 ± 7 yr) women matched for body surface area (young, 1.69 ± 0.11; older, 1.76 ± 0.14 m, P = 0.21) and peak oxygen consumption (V˙O2peak) (young, 38.6 ± 4.6; older, 34.8 ± 6.6 mL·kg·min, P = 0.15) performed four 15-min bouts of cycling at a fixed metabolic heat production rate (300 W; equivalent to ~45% V˙O2peak), each separated by a 15-min recovery, in dry (35°C, 20% relative humidity) and humid heat (35°C, 60% relative humidity). Total heat loss (evaporative ± dry heat exchange) and metabolic heat production were measured using direct and indirect calorimetry, respectively. Body heat storage was measured as the temporal summation of heat production and loss., Results: Total heat loss was lower in humid conditions compared with dry conditions during all exercise bouts in both groups (all P < 0.05), resulting in 49% and 39% greater body heat storage in young and older women, respectively (both P < 0.01). Total heat loss was also lower in older women compared with young women during exercise bouts 1, 2 and 3 in dry heat (all P < 0.05) and bouts 1 and 2 in humid heat (both P < 0.05). Consequently, body heat storage was 29% and 16% greater in older women compared with young women in dry and humid conditions, respectively (both P < 0.05)., Conclusions: Increasing ambient humidity reduces heat loss capacity in young and older women. However, older women display impaired heat loss relative to young women in both dry and humid heat, and may therefore be at greater risk of heat-related injury during light-to-moderate activity.

Purpose: The American Conference of Governmental and Industrial Hygienists (ACGIH®) Threshold Limit Values (TLV® guidelines) for work in the heat consist of work-rest (WR) allocations designed to ensure a stable core temperature that does not exceed 38°C. However, the TLV® guidelines have not been validated in older workers. This is an important shortcoming given that adults as young as 40 years demonstrate impairments in their ability to dissipate heat. We therefore evaluated body temperature responses in older adults during work performed in accordance to the TLV® recommended guidelines., Methods: On three occasions, 9 healthy older (58 ± 5 years) males performed a 120-min work-simulated protocol in accordance with the TLV® guidelines for moderate-to-heavy intensity work (360 W fixed rate of heat production) in different wet-bulb globe temperatures (WBGT). The first was 120 min of continuous (CON) cycling at 28.0°C WBGT (CON[28°C]). The other two protocols were 15-min intermittent work bouts performed with different WR cycles and WBGT: (i) WR of 3:1 at 29.0°C (WR3:1[29°C]) and (ii) WR of 1:1 at 30.0°C (WR1:1[30°C]). Rectal temperature was measured continuously. The rate of change in mean body temperature was determined via thermometry (weighting coefficients: rectal, 0.9; mean skin temperature, 0.1) and direct calorimetry., Results: Rectal temperature exceeded 38°C in all participants in CON[28°C] and WR3:1[29°C] whereas a statistically similar proportion of workers exceeded 38°C in WR1:1[30°C] (χ 2 ; P = 0.32). The average time for rectal temperature to reach 38°C was: CON[28°C], 53 ± 7; WR3:1[29°C], 79 ± 11; and WR1:1[30°C], 100 ± 29 min. Finally, while a stable mean body temperature was not achieved in any work condition as measured by thermometry (i.e., >0°C·min -1 ; all P<0.01), heat balance as determined by direct calorimetry was achieved in WR3:1[29°C] and WR1:1[30°C] (both P ≥ 0.08)., Conclusion: Our findings indicate that the TLV® guidelines do not prevent body core temperature from exceeding 38°C in older workers. Furthermore, a stable core temperature was not achieved within safe limits (i.e., ≤38°C) indicating that the TLV® guidelines may not adequately protect all individuals during work in hot conditions.

Studies have reported that older females have impaired heat loss responses during work in the heat compared to young females. However, it remains unclear at what level of heat stress these differences occur. Therefore, we examined whole-body heat loss [evaporative (HE) and dry heat loss, via direct calorimetry] and changes in body heat storage (∆Hb, via direct and indirect calorimetry) in 10 young (23±4 years) and 10 older (58±5 years) females matched for body surface area and aerobic fitness (VO2peak) during three 30-min exercise bouts performed at incremental rates of metabolic heat production of 250 (Ex1), 325 (Ex2) and 400 (Ex3) W in the heat (40°C, 15% relative humidity). Exercise bouts were separated by 15 min of recovery. Since dry heat gain was similar between young and older females during exercise (p=0.52) and recovery (p=0.42), differences in whole-body heat loss were solely due to HE. Our results show that older females had a significantly lower HE at the end of Ex2 (young: 383±34 W; older: 343±39 W, p=0.04) and Ex3 (young: 437±36 W; older: 389±29 W, p=0.008), however no difference was measured at the end of Ex1 (p=0.24). Also, the magnitude of difference in the maximal level of HE achieved between the young and older females became greater with increasing heat loads (Ex1=10.2%, Ex2=11.6% and Ex3=12.4%). Furthermore, a significantly greater ∆Hb was measured for all heat loads for the older females (Ex1: 178±44 kJ; Ex2: 151±38 kJ; Ex3: 216±25 kJ, p=0.002) relative to the younger females (Ex1: 127±35 kJ; Ex2: 96±45 kJ; Ex3: 146±46 kJ). In contrast, no differences in HE or ∆Hb were observed during recovery (p>0.05). We show that older habitually active females have an impaired capacity to dissipate heat compared to young females during exercise-induced heat loads of ≥325 W when performed in the heat.

Unlabelled: Studies show that vasomotor and sudomotor activities are compromised in individuals with Type 1 diabetes mellitus (T1DM), which could lead to impaired skin blood flow (SkBF) and sweating during heat stress. However, recent work suggests the impairments may only be evidenced beyond a certain level of heat stress., Purpose: We examined T1DM-related differences in heat loss responses of SkBF and sweating during exercise performed at progressive increases in the requirement for heat loss., Methods: Sixteen adults (10 males and six females) with (T1DM, n = 8) and without T1DM (control, n = 8) matched for age, sex, body surface area, and fitness cycled at fixed rates of metabolic heat production of 200, 250, and 300 W·m in the heat (35°C and 20% relative humidity). Each rate was performed sequentially for 30 min. Local sweat rate (LSR, ventilated capsule), sweat gland activation (modified iodine paper technique), and sweat gland output were measured on the forearm, upper back, and chest, whereas SkBF (laser Doppler) was measured on the forearm and upper back., Results: Despite a similar requirement for heat loss, LSR was lower in T1DM on the forearm and chest relative to that in the control. Reductions were measured in the second (forearm: 0.68 ± 0.14 vs 0.85 ± 0.11 mg·min·cm, P = 0.004; chest: 0.58 ± 0.08 vs 0.82 ± 0.12 mg·min·cm, P = 0.046) and third exercise bouts (forearm: 0.75 ± 0.11 vs 0.98 ± 0.12 mg·min·cm, P = 0.005; chest: 0.66 ± 0.1 vs 1.02 ± 0.16 mg·min·cm, P = 0.032). Differences in forearm LSR were the result of a reduction in sweat gland output, whereas the decrease in chest LSR was due to lower sweat gland activation. SkBF did not differ between groups., Conclusions: We show that T1DM is associated with impairments in heat dissipation during exercise in the heat, as evidenced by attenuated LSR. However, these differences are only shown beyond a certain requirement for heat loss.

Purpose: Repeated strenuous work in the heat may predispose firefighters to augmented immune responses and inflammation. This study examined the immune responses in 12 older Firefighters (FF) and 12 older Non-Firefighters (Non-FF), and a group of 6 young FF and 6 young Non-FF, following intermittent exercise in the heat., Methods: The participants, matched for age, body surface area, body composition, and VO(2peak), cycled 4 × 15 min at moderate-to-high heat production (400 W), each followed by 15-min rest, in dry [10-20% relative humidity (RH)] and humid (60% RH) heat (35 °C). Rectal temperature (T(re)) and heart rate (HR) were measured continuously, and blood samples at baseline (PRE) and following 60-min recovery (POST) were analyzed for Interleukin (IL)-6, Tumor Necrosis Factor (TNF-α), C-reactive protein (CRP), platelet count (PLT), and mean platelet volume (MPV)., Results: No differences were observed for T(re), HR, TNF-α, CRP, or PLT between the FF and Non-FF in either condition. The Non-FF had greater changes in IL-6 (Warm/Dry = +1.10 ± 0.18, Warm/Humid = +2.94 ± 0.74 pg mL(-1)), compared to the FF (Warm/Dry = +0.67 ± 0.17, Warm/Humid = +0.70 ± 0.33 pg mL(-1)), and MPV at PRE/POST compared to the FF. Between the young and older FF and Non-FF, no differences in T(re), HR, PLT, or MPV were observed, however, elevated CRP (Warm/Dry) in the older FF, and IL-6 (Warm/Dry) and TNF-α (both conditions) in the older Non-FF, were observed., Conclusions: The elevated IL-6 in the Non-FF is potentially indicative of increased strain in the Non-FF and/or adaptive changes in the FF due to the occupational demands.

Heat waves are the cause of many preventable deaths around the world, especially among older adults and in countries with more temperate climates. In the present study, we examined the effects of age on whole-body heat loss and heat storage during passive exposure to environmental conditions representative of the upper temperature extremes experienced in Canada. Direct and indirect calorimetry measured whole-body evaporative heat loss and dry heat exchange, as well as the change in body heat content. Twelve younger (21 ± 3 years) and 12 older (65 ± 5 years) adults with similar body weight (younger: 72.0 ± 4.4 kg; older: 80.1 ± 4.2 kg) and body surface area (younger: 1.8 ± 0.1 m(2); older: 2.0 ± 0.1 m(2)) rested for 2 h in a hot-dry [36.5 °C, 20% relative humidity (RH)] or hot-humid (36.5 °C, 60% RH) environment. In both conditions, evaporative heat loss was not significantly different between groups (dry: p = 0.758; humid: p = 0.814). However, the rate of dry heat gain was significantly greater (by approx. 10 W) for older adults relative to younger adults during the hot-dry (p = 0.032) and hot-humid exposure (p = 0.019). Consequently, the cumulative change in body heat content after 2 h of rest was significantly greater in older adults in the hot-dry (older: 212 ± 25 kJ; younger: 131 ± 27 kJ, p = 0.018) as well as the hot-humid condition (older: 426 ± 37 kJ; younger: 317 ± 45 kJ, p = 0.037). These findings demonstrate that older individuals store more heat during short exposures to dry and humid heat, suggesting that they may experience increased levels of thermal strain in such conditions than people of younger age.

Introduction: Aging is associated with a reduction in the body's capacity to dissipate heat. To date, few studies have examined age-related changes in thermoregulatory function during short exercise periods in the heat in older females., Purpose: This study aimed to investigate the effects of age on whole-body heat loss during intermittent exercise in the heat in young and older females., Methods: Direct and indirect calorimetry was used to measure whole-body evaporative heat loss (EHL), change in body heat content, and metabolic heat production. Eleven young (Y) (mean ± SD age = 24 ± 4 yr) and 13 older (O) (51 ± 8 yr) females matched for body surface area (Y, 1.72 ± 0.15; O, 1.75 ± 0.12 m²) and fitness (V(˙)O(2max)) (Y, 36.7 ± 6.8 mL O₂·kg⁻¹·min⁻¹; O, 33.8 ± 8.0 mL O₂·kg⁻¹·min⁻¹) performed four bouts of 15-min cycling (Ex1, Ex2, Ex3, and Ex4) at a constant rate of heat production (300 W) at 35°C and 20% relative humidity. Each exercise bout was separated by 15 min of rest., Results: EHL was reduced in O compared with Y during Ex1 (O, 199 ± 6 W; Y, 240 ± 9 W; P = 0.001), Ex2 (O, 238 ± 4 W; Y, 261 ± 9 W, P = 0.023), and Ex3 (O, 249 ± 4 W; Y, 274 ± 11 W; P = 0.040). EHL was not different between groups during Ex4 or during the recovery periods. Older females had a greater change in body heat content compared with young females (O, 270 ± 20 kJ; Y, 166 ± 20 kJ; P = 0.001)., Conclusion: These findings suggest that older females have a lower capacity for whole-body EHL compared with younger females during short intermittent exercise in the heat performed at a fixed rate of metabolic heat production.

Unlabelled: During periods of extreme heat individuals with diabetes have greater rates of heat-related morbidity and mortality compared to their non-diabetic counterparts. The reason for this discrepancy is currently unknown. Furthermore, there is a lack of information about whether or not individuals with type 1 diabetes are at a thermoregulatory disadvantage during strenuous physical activity especially when performed in the heat., Purpose: This review discusses the current literature pertaining to thermoregulatory responses in individuals with type 1 diabetes., Methods: We included 14 reviews and 95 original research articles identified by searches of PubMed and Google Scholar and deemed relevant to our subject by three independent readers., Results: Individuals with poorly controlled type 1 diabetes may have impaired heat sensation, and a reduced capacity to dissipate heat due to lower skin blood flow and sweating responses and a greater tendency towards dehydration compared to individuals without diabetes. Impairments may be attenuated or absent in those with good blood glucose control. We found no published studies examining thermoregulatory responses to physical activity in the heat in individuals with type 1 diabetes., Conclusions: Type 1 diabetes may cause impairments in heat loss resulting in a greater level of thermal strain. Advancement in our understanding about the effects of type 1 diabetes on the heat stress response, especially during different challenges to human heat balance associated with changes in both environmental heat load and metabolic heat production (physical activity), will help us to determine where the risk of heat-illness/injury actually exists.

The hypothesis that exercise causes an increase in the postexercise esophageal temperature threshold for onset of cutaneous vasodilation through an alteration of active vasodilator activity was tested in nine subjects. Increases in forearm skin blood flow and arterial blood pressure were measured and used to calculate cutaneous vascular conductance at two superficial forearm sites: one with intact alpha-adrenergic vasoconstrictor activity (untreated) and one infused with bretylium tosylate (bretylium treated). Subjects remained seated resting for 15 min (no-exercise) or performed 15 min of treadmill running at either 55, 70, or 85% of peak oxygen consumption followed by 20 min of seated recovery. A liquid-conditioned suit was used to increase mean skin temperature ( approximately 4.0 degrees C/h), while local forearm temperature was clamped at 34 degrees C, until cutaneous vasodilation. No differences in the postexercise threshold for cutaneous vasodilation between untreated and bretylium-treated sites were observed for either the no-exercise or exercise trials. Exercise resulted in an increase in the postexercise threshold for cutaneous vasodilation of 0.19 +/- 0.01, 0.39 +/- 0.02, and 0.53 +/- 0.02 degrees C above those of the no-exercise resting values for the untreated site (P < 0.05). Similarly, there was an increase of 0.20 +/- 0.01, 0.37 +/- 0.02, and 0.53 +/- 0.02 degrees C for the treated site for the 55, 70, and 85% exercise trials, respectively (P < 0.05). It is concluded that reflex activity associated with the postexercise increase in the onset threshold for cutaneous vasodilation is more likely mediated through an alteration of active vasodilator activity rather than through adrenergic vasoconstrictor activity.