Exercise intensity- and body region-specific differences in sweating in middle-aged to older men with and without type 2 diabetes.

Type 2 diabetes (T2D) is associated with reduced whole body sweating during exercise-heat stress. However, it is unclear if this impairment is related to exercise intensity and whether it occurs uniformly across body regions. We evaluated whole body (direct calorimetry) and local (ventilated-capsule technique; chest, back, forearm, thigh) sweat rates in physically active men with type 2 diabetes [T2D; aged 59 (7) yr; V̇o2peak 32.3 (7.6) mL·kg-1·min-1; n = 26; HbA1c 5.1%-9.1%] and without diabetes [Control; aged 61 (5) yr; V̇o2peak 37.5 (5.4) mL·kg-1·min-1; n = 26] during light- (∼40% V̇o2peak), moderate- (∼50% V̇o2peak), and vigorous- (∼65% V̇o2peak) intensity exercise (elicited by fixing metabolic heat production at ∼150, 200, 250 W·m-2, respectively) in 40°C, ∼17% relative humidity. Whole body sweating was ∼11% (T2D: Control mean difference [95% confidence interval]: -37 [-63, -12] g·m-2·h-1) and ∼13% (-50 [-76, -25] g·m-2·h-1) lower in the T2D compared with the Control group during moderate- and vigorous- (P ≤ 0.001) but not light-intensity exercise (-21 [-47, 4] g·m-2·h-1; P = 0.128). Consequently, the diabetes-related reductions in whole body sweat rate were 2.3 [1.6, 3.1] times greater during vigorous relative to light exercise (P < 0.001). Furthermore, these diabetes-related impairments in local sweating were region-specific during vigorous-intensity exercise (group × region interaction: P = 0.024), such that the diabetes-related reduction in local sweat rate at the trunk (chest, back) was 2.4 [1.2, 3.7] times greater than that at the limbs (thigh, arm). In summary, when assessed under hot, dry conditions, diabetes-related impairments in sweating are exercise intensity-dependent and greater at the trunk compared with the limbs.NEW & NOTEWORTHY This study evaluates the influence of exercise intensity on decrements in whole body sweating associated with type 2 diabetes. Furthermore, it investigates whether diabetes-related sweating impairments were exhibited uniformly or heterogeneously across body regions. We found that whole body sweating was attenuated in the type 2 diabetes group relative to control participants during moderate- and vigorous-intensity exercise but not light-intensity exercise; impairments were largely mediated by reduced sweating at the trunk rather than the limbs.

Greater hyperthermia in men with type 2 diabetes does not lead to higher serum levels of cellular stress biomarkers following exercise-heat stress.

Type 2 diabetes (T2D) is associated with worsening age-related impairments in heat loss, causing higher core temperature during exercise. We evaluated whether these thermoregulatory impairments occur with altered serum protein responses to heat stress by measuring cytoprotection, inflammation, and tissue damage biomarkers in middle-aged-to-older men (50-74 years) with (n = 16) and without (n = 14) T2D following exercise in 40°C. There were no changes in irisin, klotho, HSP70, sCD14, TNF-α, and IL-6, whereas NGAL (+539 pg/mL, p = 0.002) and iFABP (+250 pg/mL, p < 0.001) increased similarly across groups. These similar response patterns occurred despite elevated core temperature in individuals with T2D, suggesting greater heat vulnerability.

Physiological responses to 9 hours of heat exposure in young and older adults. Part III: Association with self-reported symptoms and mood state.

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.

Body Core Temperature After Foot Immersion and Neck Cooling in Older Adults Exposed to Extreme Heat.

This randomized study evaluates the hypothesis that foot immersion in cool water alone or with supplemental neck cooling mitigates increases in core temperature in older adults exposed to environmental conditions simulating deadly heat waves in North America.

Cardiac autonomic modulation in individuals with controlled and uncomplicated hypertension during exercise-heat stress.

TAKE-HOME MESSAGE: During short bouts of light-to-vigorous exercise in the heat, controlled and uncomplicated hypertension did not significantly modulate HRV in physically active individuals. These findings can be used to refine guidance on use of exercise for hypertension management in the heat.

Physiological responses to 9 hours of heat exposure in young and older adults. Part II: Autophagy and the acute cellular stress response.

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 (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 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 (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.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.

Physiological responses to 9 hours of heat exposure in young and older adults. Part I: Body temperature and hemodynamic regulation.

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.

Serum klotho concentrations in older men with hypertension or type 2 diabetes during prolonged exercise in temperate and hot conditions.

PURPOSE: Klotho is a cytoprotective protein that increases during acute physiological stressors (e.g., exercise heat stress), although age-related declines in klotho may underlie cellular vulnerability to heat stress. The present study aimed to compare serum klotho in healthy older men and men with type 2 diabetes (T2D) or hypertension (HTN) during prolonged exercise in temperate or hot conditions. METHODS: We evaluated serum klotho in 12 healthy older men (mean [SD]; 59 years [4]), 10 men with HTN (60 years [4]), and 9 men with T2D (60 years [5]) before and after 180 min of moderate-intensity (fixed metabolic rate of 200 W/m2; ~ 3.4 METs) exercise and 60 min of recovery in temperate (wet-bulb globe temperature (WBGT) 16 °C) and hot (WBGT 32 °C) environments. Core temperature (rectal), heart rate (HR), and heart rate reserve (HRR) were measured continuously while klotho was measured at the end of baseline, exercise, and recovery. RESULTS: Total exercise duration was reduced during the hot condition in older men with HTN and T2D than healthy older men (both p ≤ 0.049), despite similar core temperatures, HR, and HRR. Klotho was higher than rest following exercise in the heat in healthy older men (+ 191 pg/mL [189]; p < 0.001) and responses were greater (p = 0.036) than men with HTN (+ 118 pg/mL [49]; p = 0.030), although klotho did not increase in men with T2D (+ 4 pg/mL [71]; p ≥ 0.638). CONCLUSION: Given klotho's role in cytoprotection, older men with HTN and especially T2D may be at increased cellular vulnerability to prolonged exercise or physically demanding exercise in the heat.

Association between haemoglobin A1c and whole-body heat loss during exercise-heat stress in physically active men with type 2 diabetes.

NEW FINDINGS: What is the central question of this study? Is the impairment in heat dissipation during exercise observed in men with type 2 diabetes related to glycaemic control (indexed by glycated haemoglobin; haemoglobin A1c )? What is the main finding and its importance? No association was found between haemoglobin A1c (range: 5.1-9.1%) and whole-body heat loss in men with type 2 diabetes during exercise in the heat. However, individuals with elevated haemoglobin A1c exhibited higher body core temperature and heart rate responses. Thus, while haemoglobin A1c is not associated with heat loss per se, it may still have important implications for physiological strain during exercise. ABSTRACT: Type 2 diabetes is associated with a reduced capacity to dissipate heat. It is unknown whether this impairment is related to glycaemic control (indexed by glycated haemoglobin; haemoglobin A1c ) is unknown. We evaluated the association between haemoglobin A1c and whole-body heat loss (via direct calorimetry), body core temperature, and heart rate in 26 physically active men with type 2 diabetes (43-73 years; HbA1c 5.1-9.1%) during exercise at increasing rates of metabolic heat production (∼150, 200, 250 W m-2 ) in the heat (40°C, ∼17% relative humidity). Haemoglobin A1c was not associated with whole-body heat loss (P = 0.617), nor the increase in core temperature from pre-exercise (P = 0.347). However, absolute core temperature and heart rate were elevated ∼0.2°C (P = 0.014) and ∼6 beats min-1 (P = 0.049), respectively, with every percentage point increase in haemoglobin A1c . Thus, while haemoglobin A1c does not appear to modify diabetes-related reductions in capacity for heat dissipation, it may still have important implications for physiological strain during exercise-heat stress.

The serum irisin response to prolonged physical activity in temperate and hot environments in older men with hypertension or type 2 diabetes.

Current labor demographics are changing, with the number of older adults increasingly engaged in physically demanding occupations expected to continually rise, which are often performed in the heat. Given an age-related decline in whole-body heat loss, older adults are at an elevated risk of developing heat injuries that may be exacerbated by hypertension (HTN) and type 2 diabetes (T2D). Elevated irisin production may play a role in mitigating the excess oxidative stress and acute inflammation associated with physically demanding work in the heat. However, the effects of HTN and T2D on this response remain unclear. Therefore, we evaluated serum irisin before and after 3-h of moderate intensity exercise (metabolic rate: 200 W/m2) and at the end of 60-min of post-exercise recovery in a temperate (wet-bulb globe temperature (WBGT) 16 °C) and high-heat stress (WBGT 32 °C) environment in 12 healthy older men (mean ± SD; 59 ± 4 years), 10 men with HTN (60 ± 4 years), and 9 men with T2D (60 ± 5 years). Core temperature (Tco) was measured continuously. In the heat, total exercise duration was significantly lower in older men with HTN and T2D (both, p ≤ 0.049). Despite Tco not being different between groups, Tco was higher in the hot compared to the temperate condition for all groups (p < 0.001). Similarly, serum irisin concentrations did not differ between groups under either condition but were elevated relative to the temperate condition during post-exercise and end-recovery in the heat (+93.9 pg/mL SEM 26 and + 70.5 pg/mL SEM 38 respectively; both p ≤ 0.014). Thus, our findings indicate similar irisin responses in HTN and T2D compared to healthy, age-matched controls, despite reduced exercise tolerance during prolonged exercise in the heat. Therefore, older workers with HTN and T2D may exhibit greater cellular stress during prolonged exercise in the heat, underlying greater vulnerability to heat-induced cellular injury.

The effect of acute intradermal administration of ascorbate on heat loss responses in older adults with uncomplicated controlled hypertension.

NEW FINDINGS: What is the central question of this study? Does acute intradermal administration of the antioxidant ascorbate augment local forearm cutaneous vasodilatation and sweating via nitric oxide synthase (NOS)-dependent mechanisms during exercise-heat stress in older adults with uncomplicated controlled hypertension? What is the main finding and its importance? Relative to the control site, ascorbate had no effect on forearm cutaneous vascular conductance (CVC) and sweat rate, although CVC was reduced with NOS inhibition in older adults with hypertension. Acute local administration of ascorbate to forearm skin does not modulate heat loss responses during exercise-heat stress in older adults with hypertension. ABSTRACT: 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 adults who 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-l-arginine 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.

Exercise in the heat induces similar elevations in serum irisin in young and older men despite lower resting irisin concentrations in older adults.

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/m2) and 60-min post-exercise recovery in temperate (wet-bulb globe temperature (WBGT) 16 °C) and hot (WBGT 32 °C) environments. Core temperature (Tco) was measured continuously. Post-exercise Tco was similarly higher in the hot compared to the temperate condition for both groups (p < 0.001), although Tco 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.

Does aging alter skin vascular function in humans when spatial variation is considered?

OBJECTIVE: Reports evaluating age-related impairments in cutaneous vascular function assessed by either the venoarteriolar reflex (VAR) induced by venous congestion, or post-occlusive reactive hyperemia (PORH) activated by arterial occlusion, have yielded mixed findings. This may be due to region-specific variability that occurs when assessing local cutaneous vascular responses. We evaluated the hypothesis that aging attenuates VAR and PORH responses in forearm skin assessed across four adjacent sites, each separated by ~4 cm to account for inter-site variability. METHODS: In twenty young (24 ± 4 years, 10 females) and twenty older (60 ± 7 years, 9 females) adults, VAR and PORH were achieved by a 3-min venous occlusion and 5-min arterial occlusion, each induced by inflating a pressure cuff to 45 and 240 mmHg, respectively. Cutaneous blood flow at all skin sites was measured by laser-Doppler flowmetry with the average response from all sites used for between-group comparisons. RESULTS: VAR and PORH responses were similar between groups with the exception that the time required to achieve peak PORH was delayed in older adults (mean difference of 5.5 ± 4.4 s, p = 0.003, Cohen's d = 0.812). CONCLUSIONS: We showed that aging had a negligible influence on VAR and PORH responses in forearm skin even when controlling for region-specific variability.

Heat Tolerance and Occupational Heat Exposure Limits in Older Men with and without Type 2 Diabetes or Hypertension.

PURPOSE: To mitigate rises in core temperature >1°C, the American Conference of Governmental Industrial Hygienists (ACGIH) recommends upper limits for heat stress (action limit values [ALV]), defined by wet-bulb globe temperature (WBGT) and a worker's metabolic rate. However, these limits are based on data from young men and are assumed to be suitable for all workers, irrespective of age or health status. We therefore explored the effect of aging, type 2 diabetes (T2D), and hypertension (HTN) on tolerance to prolonged, moderate-intensity work above and below these limits. METHODS: Core temperature and heart rate were assessed in healthy, heat unacclimatized young (18-30 yr, n = 13) and older (50-70 yr) men (n = 14) and heat unacclimatized older men with T2D (n = 10) or HTN (n = 13) during moderate-intensity (metabolic rate: 200 W·m-2) walking for 180 min (or until termination) in environments above (28°C and 32°C WBGT) and below (16°C and 24°C WBGT) the ALV for continuous work at this intensity (25°C WBGT). RESULTS: Work tolerance in the 32°C WBGT was shorter in men with T2D (median [IQR]; 109 [91-173] min; P = 0.041) and HTN (120 [65-170] min; P = 0.010) compared with healthy older men (180 [133-180] min). However, aging, T2D, and HTN did not significantly influence (i) core temperature or heart rate reserve, irrespective of WBGT; (ii) the probability that core temperature exceeded recommended limits (>1°C) under the ALV; and (iii) work duration before core temperature exceeded recommended limits (>1°C) above the ALV. CONCLUSION: These findings demonstrate that T2D and HTN attenuate tolerance to uncompensable heat stress (32°C WBGT); however, these chronic diseases do not significantly impact thermal and cardiovascular strain, or the validity of ACIGH recommendations during moderate-intensity work.

Effects of short-term heat acclimation on whole-body heat exchange and local nitric oxide synthase- and cyclooxygenase-dependent heat loss responses in exercising older men.

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/m2 , 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.

Impact of uncomplicated controlled hypertension on thermoregulation during exercise-heat stress.

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.

Effect of exercise-heat acclimation on cardiac autonomic modulation in type 2 diabetes: a pilot study.

The effects of exercise-heat acclimation on heart rate variability (HRV) in individuals with type 2 diabetes (T2D) remains unclear. We assessed electrocardiogram recordings during exercise-heat stress in middle-aged-to-older individuals (50-70 years) with (n = 6) and without (control; n = 8;) T2D, before and after 7 days of exercise-heat acclimation. Exercising heart rate was reduced (control, -9 ± 5 bpm; T2D, -14 ± 9 bpm) yet HRV was not significantly different. Given the negative correlations between diminished HRV and cardiac risk observed in the scientific literature, further research is warranted. Novelty: Our observations indicate that 7 days exercise-heat acclimation may not effectively attenuate the deviation toward reduced overall HRV and unfavourable cardiac autonomic modulation in individuals with T2D.

Type 2 diabetes does not exacerbate body heat storage in older adults during brief, extreme passive heat exposure.

Aging exacerbates hyperthermia and cardiovascular strain during passive heat exposure, but it remains unclear whether those effects worsen in older adults with type 2 diabetes (T2D). We examined these responses in unacclimatized, physically active, older individuals with (n = 13, mean ± SD age: 60 ± 8 years, HbA1c: 7.0 ± 1.0%) and without (Control, n = 30, 62 ± 6 years) well-controlled T2D during a brief, 3-h passive exposure to extreme heat (44°C, 30% relative humidity). Metabolic heat production, dry heat gain, total heat gain (metabolic heat production + dry heat gain), evaporative heat loss, body heat storage (summation of heat gain/loss), rectal and mean skin temperatures as well as heart rate were measured continuously. No between-group differences were observed for metabolic heat production (T2D vs. Control; 53 ± 5 vs. 55 ± 7 W/m2), dry heat gain (48 ± 9 vs. 47 ± 11 W/m2), total heat gain (101 ± 10 vs. 102 ± 14 W/m2) and evaporative heat loss (83 ± 10 vs. 85 ± 12 W/m2) over the 3 h (all P > 0.05). Consequently, the changes in body heat storage (380 ± 93 vs. 358 ± 172 kJ, P = 0.67) were similar between groups. Moreover, no between-group differences in rectal and mean skin temperatures or heart rate were measured. We conclude that unacclimatized, physically active, older adults with well-controlled T2D do not experience greater hyperthermia and cardiovascular strain compared to their healthy counterparts while resting in extreme heat for a brief, 3-h period.

Ageing attenuates the effect of extracellular hyperosmolality on whole-body heat exchange during exercise-heat stress.

KEY POINTS: In humans, hypohydration attenuates sweat secretion and attenuates whole-body heat loss, probably to mitigate further fluid losses and thereby support blood pressure regulation. Recently, however, we demonstrated that the hypohydration-mediated reduction in net whole-body heat exchange (evaporative heat loss - dry heat gain) was blunted in middle-aged compared to younger men during moderate exercise in dry heat; albeit, the underpinning mechanisms could not be determined. Here we evaluated the hypothesis that those findings stemmed from a diminished influence of extracellular hyperosmolality on net whole-body heat exchange in middle-aged-to-older compared to young men. Consistent with that hypothesis, extracellular hyperosmolality induced by an intravenous infusion of hypertonic saline (3% NaCl) reduced net heat exchange and augmented rectal temperature to a greater extent in the young compared to middle-aged-to-older men. Thus, age-related differences in the influence of hypohydration on thermoregulatory function appear to be due to blunted sensitivity to hyperosmolality with ageing. ABSTRACT: We recently demonstrated that sweating-induced hypohydration attenuated whole-body heat dissipation to a greater extent in young compared to middle-aged men during exercise-heat stress. Here, we evaluated whether this divergent response stemmed from an attenuated influence of extracellular hyperosmolality on heat exchange with ageing. To achieve this, ten young (mean (SD): 25 (5) years) and ten middle-aged-to-older (61 (5) years) men completed two trials involving a 90-min intravenous infusion of isosmotic saline (0.9% NaCl; ISO) or hyperosmotic saline (3.0% NaCl; HYP) followed by 60 min of cycling at a fixed metabolic heat production of 250 W/m2 (∼50% peak aerobic power) in dry heat (40°C, ∼17% relative humidity). Whole-body net heat exchange (evaporative heat loss - dry heat gain) was measured via direct calorimetry. Rectal temperature was monitored continuously. Heat exchange was attenuated in HYP compared to ISO in the young (233 (20) vs. 251 (17) W/m2 ; P = 0.002) but not older group (229 (16) vs. 227 (20) W/m2 ; P = 0.621). Further, heat exchange was lower in the middle-aged-to-older vs. young men in ISO (P = 0.034) but not in HYP (P = 0.623). Similarly, end-exercise rectal temperature was greater in HYP relative to ISO in the young (38.3 (0.4)°C vs. 37.9 (0.3)°C; P = 0.015) but not the middle-aged-to-older men (38.3 (0.3)°C vs. 38.2 (0.2)°C; P = 0.652). Compared to the young, rectal temperature was greater in the middle-aged-to-older during ISO (P = 0.035) whereas no between-group difference was observed in HYP (P = 0.746). Our findings indicate that ageing blunts the effect of extracellular hyperosmolality on thermoregulatory function during exercise-heat stress.