Jill M. Stapleton

Ice Cooling Vest on Tolerance for Exercise under Uncompensable Heat Stress

This study was conducted to evaluate the effectiveness of a commercial, personal ice cooling vest on tolerance for exercise in hot (35°C), wet (65% relative humidity) conditions with a nuclear biological chemical suit (NBC). On three separate occasions, 10 male volunteers walked on a treadmill at 3 miles per hour and 2% incline while (a) seminude (denoted CON), (b) dressed with a nuclear, biological, chemical (NBC) suit with an ice vest (V) worn under the suit (denoted NBCwV); or (c) dressed with an NBC suit but without an ice vest (V) (denoted NBCwoV). Participants exercised for 120 min or until volitional fatigue, or esophageal temperature reached 39.5°C. Esophageal temperature (Tes), heart rate (HR), thermal sensation, and ratings of perceived exertion were measured. Exercise time was significantly greater in CON compared with both NBCwoV and NBCwV (p < 0.05), whereas Tes, thermal sensation, heart rate, and rate of perceived exertion were lower (p < 0.05). Wearing the ice vest increased exercise time (NBCwoV, 103.6 ± 7.0 min; NBCwV, 115.9 ± 4.1 min) and reduced the level of thermal strain, as evidenced by a lower Tes at end-exercise (NBCwoV, 39.03 ± 0.13°C; NBCwV, 38.74 ± 0.13°C) and reduced thermal sensation (NBCwoV, 6.4 ± 0.4; NBCwV, 4.8 ± 0.6). This was paralleled by a decrease in rate of perceived exertion (NBCwoV, 14.7 ± 1.6; NBCwV, 12.4 ± 1.6) (p < 0.05) and heat rate (NBCwoV, 169 ± 6; NBCwV, 159 ± 7) (p < 0.05). We show that a commercially available cooling vest can significantly reduce the level of thermal strain during work performed in hot environments.

Whole-body heat loss is reduced in older males during short bouts of intermittent exercise

Studies in young adults show that a greater proportion of heat is gained shortly following the start of exercise and that temporal changes in whole body heat loss during intermittent exercise have a pronounced effect on body heat storage. The consequences of short-duration intermittent exercise on heat storage with aging are unclear. We compared evaporative heat loss (HE) and changes in body heat content (ΔHb) between young (20-30 yr), middle-aged (40-45 yr), and older males (60-70 yr) of similar body mass and surface area, during successive exercise (4 × 15 min) and recovery periods (4 × 15 min) at a fixed rate of heat production (400 W) and under fixed environmental conditions (35 °C/20% relative humidity). HE was lower in older males vs. young males during each exercise (Ex1: 283 ± 10 vs. 332 ± 11 kJ, Ex2: 334 ± 10 vs. 379 ± 5 kJ, Ex3: 347 ± 11 vs. 392 ± 5 kJ, and Ex4: 347 ± 10 vs. 387 ± 5 kJ, all P < 0.02), whereas HE in middle-aged males was intermediate to that measured in young and older adults (Ex1: 314 ± 13, Ex2: 355 ± 13, Ex3: 371 ± 13, and Ex4: 365 ± 8 kJ). HE was not significantly different between groups during the recovery periods. The net effect over 2 h was a greater ΔHb in older (267 ± 33 kJ; P = 0.016) and middle-aged adults (245 ± 16 kJ; P = 0.073) relative to younger counterparts (164 ± 20 kJ). As a result of a reduced capacity to dissipate heat during exercise, which was not compensated by a sufficiently greater rate of heat loss during recovery, both older and middle-aged males had a progressively greater rate of heat storage compared with young males over 2 h of intermittent exercise.

Older adults with type 2 diabetes store more heat during exercise.

INTRODUCTION It is unknown if diabetes-related reductions in local skin blood flow (SkBF) and sweating (LSR) measured during passive heat stress translate into greater heat storage during exercise in the heat in individuals with type 2 diabetes (T2D) compared with nondiabetic control (CON) subjects. PURPOSE This study aimed to examine the effects of T2D on whole-body heat exchange during exercise in the heat. METHODS Ten adults (6 males and 4 females) with T2D and 10 adults (6 males and 4 females) without diabetes matched for age, sex, body surface area, and body surface area and aerobic fitness cycled continuously for 60 min at a fixed rate of metabolic heat production (∼370 W) in a whole-body direct calorimeter (30°C and 20% relative humidity). Upper back LSR, forearm SkBF, rectal temperature, and heart rate were measured continuously. Whole-body heat loss and changes in body heat content (ΔHb) were determined using simultaneous direct whole-body and indirect calorimetry. RESULTS Whole-body heat loss was significantly attenuated from 15 min throughout the remaining exercise with the differences becoming more pronounced over time for T2D relative to CON (P = 0.004). This resulted in a significantly greater ΔHb in T2D (367 ± 35; CON, 238 ± 25 kJ, P = 0.002). No differences were measured during recovery (T2D, -79 ± 23; CON, -132 ± 23 kJ, P = 0.083). By the end of the 60-min recovery, the T2D group lost only 21% (79 kJ) of the total heat gained during exercise, whereas their nondiabetic counterparts lost in excess of 55% (131 kJ). No difference were observed in LSR, SkBF, rectal temperature or heart rate during exercise. Similarly, no differences were measured during recovery with the exception that heart rate was elevated in the T2D group relative to CON (p=0.004). CONCLUSION Older adults with T2D have a reduced capacity to dissipate heat during exercise, resulting in a greater heat storage and therefore level of thermal strain.

Evidence for cyclooxygenase‐dependent sweating in young males during intermittent exercise in the heat

Previous studies implicate nitric oxide (NO) in the control of sweating during exercise in the heat; however, it is unclear whether cyclooxygenase (COX) is also involved. We demonstrated that exercise‐induced sweating at a moderate heat production (400 W, ∼40% V̇O2 max ) was similarly reduced when COX and NO synthase were inhibited separately and in combination. Alternatively, inhibiting COX and/or NO synthase did not influence exercise‐induced sweating at a high heat production (700 W, ∼70% V̇O2 max ). We show that both COX and NO are involved in sweating during exercise at moderate heat production and that the effects may not be independent. However, roles for COX and NO are less evident when heat production is elevated. The results lead to better understanding of the mechanisms of sweating and indicate that COX inhibitors (e.g. aspirin) may impair core body temperature regulation and thereby increase the risk of heat‐related illness.

Diminished nitric oxide-dependent sweating in older males during intermittent exercise in the heat.

What is the central question of this study? Sweating during exercise in the heat is, in part, mediated through nitric oxide‐dependent mechanisms. It is unclear whether ageing reduces nitric oxide‐dependent sweating during exercise in the heat. What is the main finding and its importance? Nitric oxide‐dependent sweating during short bouts of exercise in the heat was observed in young men, but not in older adults. These findings show that age‐related impairment in sweating may be associated with age‐related reductions in nitric oxide‐mediated sweating.

Aging impairs heat loss, but when does it matter?

Aging is associated with an attenuated physiological ability to dissipate heat. However, it remains unclear if age-related impairments in heat dissipation only occur above a certain level of heat stress and whether this response is altered by aerobic fitness. Therefore, we examined changes in whole body evaporative heat loss (HE) as determined using whole body direct calorimetry in young (n = 10; 21 ± 1 yr), untrained middle-aged (n = 10; 48 ± 5 yr), and older (n = 10; 65 ± 3 yr) males matched for body surface area. We also studied a group of trained middle-aged males (n = 10; 49 ± 5 yr) matched for body surface area with all groups and for aerobic fitness with the young group. Participants performed intermittent aerobic exercise (30-min exercise bouts separated by 15-min rest) in the heat (40°C and 15% relative humidity) at progressively greater fixed rates of heat production equal to 300 (Ex1), 400 (Ex2), and 500 (Ex3) W. Results showed that HE was significantly lower in middle-aged untrained (Ex2: 426 ± 34; and Ex3: 497 ± 17 W) and older (Ex2: 424 ± 38; and Ex3: 485 ± 44 W) compared with young (Ex2: 472 ± 42; and Ex3: 558 ± 51 W) and middle-aged trained (474 ± 21; Ex3: 552 ± 23 W) males at the end of Ex2 and Ex3 (P < 0.05). No differences among groups were observed during recovery. We conclude that impairments in HE in older and middle-aged untrained males occur at exercise-induced heat loads of ≥400 W when performed in a hot environment. These impairments in untrained middle-aged males can be minimized through regular aerobic exercise training.

Cyclooxygenase inhibition does not alter methacholine-induced sweating

Cholinergic agents (e.g., methacholine) induce cutaneous vasodilation and sweating. Reports indicate that either nitric oxide (NO), cyclooxygenase (COX), or both can contribute to cholinergic cutaneous vasodilation. Also, NO is reportedly involved in cholinergic sweating; however, whether COX contributes to cholinergic sweating is unclear. Forearm sweat rate (ventilated capsule) and cutaneous vascular conductance (CVC, laser-Doppler perfusion units/mean arterial pressure) were evaluated in 10 healthy young (24 ± 4 yr) adults (7 men, 3 women) at four skin sites that were continuously perfused via intradermal microdialysis with 1) lactated Ringer (control), 2) 10 mM ketorolac (a nonselective COX inhibitor), 3) 10 mM N(G)-nitro-l-arginine methyl ester (l-NAME, a nonselective NO synthase inhibitor), or 4) a combination of 10 mM ketorolac + 10 mM l-NAME. At the four skin sites, methacholine was simultaneously infused in a dose-dependent manner (1, 10, 100, 1,000, 2,000 mM). Relative to the control site, forearm CVC was not influenced by ketorolac throughout the protocol (all P > 0.05), whereas l-NAME and ketorolac + l-NAME reduced forearm CVC at and above 10 mM methacholine (all P < 0.05). Conversely, there was no main effect of treatment site (P = 0.488) and no interaction of methacholine dose and treatment site (P = 0.711) on forearm sweating. Thus forearm sweating (in mg·min(-1)·cm(-2)) from baseline up to the maximal dose of methacholine was not different between the four sites (at 2,000 mM, control 0.50 ± 0.23, ketorolac 0.44 ± 0.23, l-NAME 0.51 ± 0.22, and ketorolac + l-NAME 0.51 ± 0.23). We show that both NO synthase and COX inhibition do not influence cholinergic sweating induced by 1-2,000 mM methacholine.

Age-related differences in postsynaptic increases in sweating and skin blood flow postexercise

The influence of peripheral factors on the control of heat loss responses (i.e., sweating and skin blood flow) in the postexercise period remains unknown in young and older adults. Therefore, in eight young (22 ± 3 years) and eight older (65 ± 3 years) males, we examined dose‐dependent responses to the administration of acetylcholine (ACh) and methacholine (MCh) for sweating (ventilated capsule), as well as to ACh and sodium nitroprusside (SNP) for cutaneous vascular conductance (CVC, laser‐Doppler flowmetry, % of max). In order to assess if peripheral factors are involved in the modulation of thermoeffector activity postexercise, pharmacological agonists were perfused via intradermal microdialysis on two separate days: (1) at rest (DOSE) and (2) following a 30‐min bout of exercise (Ex+DOSE). No differences in sweat rate between the DOSE and Ex+DOSE conditions at either ACh or MCh were observed for the young (ACh: P = 0.992 and MCh: P = 0.710) or older (ACh: P = 0.775 and MCh: P = 0.738) adults. Similarly, CVC was not different between the DOSE and Ex+DOSE conditions for the young (ACh: P = 0.123 and SNP: P = 0.893) or older (ACh: P = 0.113 and SNP: P = 0.068) adults. Older adults had a lower sweating response for both the DOSE (ACh: P = 0.049 and MCh: P = 0.006) and Ex+DOSE (ACh: P = 0.050 and MCh: P = 0.029) conditions compared to their younger counterparts. These findings suggest that peripheral factors do not modulate postexercise sweating and skin blood flow in both young and older adults. Additionally, sweat gland function is impaired in older adults, albeit the impairments were not exacerbated during postexercise recovery.

Do Heat Events Pose a Greater Health Risk for Individuals with Type 2 Diabetes

Chronic medical conditions such as type 2 diabetes may alter the bodys normal response to heat. Evidence suggests that the local heat loss response of skin blood flow (SkBF) is affected by diabetes-related impairments in both endothelium-dependent and non-endothelium-dependent mechanisms, resulting in lower elevations in SkBF in response to a heat or pharmacological stimulus. Thermoregulatory sweating may also be diminished by type 2 diabetes, impairing the bodys ability to transfer heat from its core to the environment. Diabetes-associated co-morbidities and the medications (particularly those affecting fluid balance) required to treat these conditions may exacerbate the risk of heat-related illness by decreasing SkBF and sweating further. Unfortunately, the majority of studies measure local heat loss responses in the hands and feet and lack measures of core temperature. Therefore, the impact of these impairments on whole-body heat loss remains unknown. This review addresses heat-related vulnerability in individuals with type 2 diabetes by examining the literature related to heat loss responses in this population. Type 2 diabetes, its associated co-morbidities, and the medications required in their treatment may cause dehydration, lower SkBF, and reduced sweating, which could consequently impair thermoregulation. This effect is most evident in individuals with poor blood glucose control. Although type 2 diabetes can be associated with impairments in SkBF and sweating, more physically active individuals requiring fewer medications and having good blood glucose control may be able to tolerate heat as well as those of similar age and body composition.

Do older adults experience greater thermal strain during heat waves

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.