Whole-body Heat Research Articles

Whole‐Body Heat Stress Alters the Exercise Pressor Reflex in Humans

The effects of whole-body heat stress on sympathetic and cardiovascular responses to stimulation of muscle metaboreceptors and mechanoreceptors remain unclear. We examined the muscle sympathetic nerve activity (MSNA), renal blood velocity, blood pressure and heart rate in 14 young healthy subjects during fatiguing isometric handgrip exercise, post exercise circulatory occlusion (PECO), and passive muscle stretch during PECO. The protocol was performed under normothermic and whole-body heat stress (increase internal temperature ~0.6 °C via a heating suit) conditions. Heat stress increased the resting MSNA and heart rate. Heat stress did not alter the responses to the fatiguing exercise in mean blood pressure (MAP), heart rate and MSNA, but augmented the response in renal vascular resistance (Δ45± 6 to Δ60±8 %, P=0.04). During PECO, the increase in MAP was lower during heat stress condition than during normothemic condition (Δ20±2 vs. Δ12±1 mmHg, P<0.001), while the increases in MSNA were not different between the thermal conditions (Δ16.4±2.8 vs. Δ17.3±3.8 bursts/min, P=0.74). Under normothermic conditions, the passive stretch during PECO evoked significant increases in MAP and MSNA, while these intervention did not alter MSNA or MAP in the presence of heat stress. These data show that the pressor response to metaboreceptor stimulation is attenuated, and the MSNA response to mechanoreceptor stimulation is also attenuated in heat stress condition. These observations suggest that whole body heat stress alters exercise pressor reflex in humans.

Acetylsalicylic acid does not alter thermo-effector responses during mild whole-body passive heat stress in young men

Acetylsalicylic acid (ASA), aspirin, exerts potent systemic effects that may interfere with normal thermo-effector responses. We investigated the influence of commonly ingested ASA doses on measures of skin blood flow (SkBF) and local sweat rate (SR) during whole-body, passive heat stress. Seven male participants completed counter-balanced trials to compare ASA treatments (single dose 325 mg or 4 consecutive days 81 mg (4-d 81 mg)) to control (no ASA). Laser-Doppler flowmetry provided an index of SkBF. A ventilated capsule measured local sweat rate via capacitance hygrometry. Mean body temperature () was increased by 1 °C above baseline using a water-perfused suit. was similar at the onset of cutaneous vasodilation among trials. Cutaneous vascular conductance, expressed as a percentage change from baseline, was not different among trials. Additionally, at the onset of local SR and SR sensitivity did not differ among trials. While ASA has previously been shown to influence SkBF during heat stress, it is possible our cohort’s relatively young age may have contributed to our dissimilar results.

Whole-body heat exchange during heat acclimation and its decay.

The purpose of this study was to quantify how much whole-body heat loss increases during heat acclimation and the decay in these improvements after heat acclimation. Ten males underwent a 14-d heat acclimation protocol that consisted of 90 min of cycling in the heat (40°C, 20% relative humidity) at approximately 50% of maximum oxygen consumption. Before (day 0), during (day 7), and at the end (day 14) of the heat acclimation protocol as well as 7 and 14 d after heat acclimation (days 21 and 28), whole-body heat exchange (evaporative and dry) was measured using direct calorimetry during three bouts of 30-min exercise at 300 (Ex1), 350 (Ex2), and 400 W·m (Ex3), each separated by 10 and 20 min of recovery, respectively, at 35°C and 16% relative humidity. Concurrent measurements of metabolic heat production (indirect calorimetry) allowed for the direct calculation of change in body heat content (ΔHb). After accounting for an increase in net dry heat gain, increases in whole-body evaporative heat loss were evident for Ex2 and Ex3 on day 7 (Ex2, 4.9 ± 5.6%; Ex3, 9.0 ± 6.0%; both P ≤ 0.05) and all heat loads on day 14 (Ex1, 7.6 ± 8.3%; Ex2, 7.7 ± 5.5%; Ex3, 11.2 ± 4.6%; all P ≤ 0.05) relative to day 0 (Ex1, 494 ± 27 W; Ex2, 583 ± 21 W; Ex3, 622 ± 36 W). As a result, a lower cumulative ΔHb was measured on day 7 (-18 ± 8%, P ≤ 0.001) and day 14 (-26 ± 10%, P ≤ 0.001) compared with that measured on day 0 (1062 ± 123 kJ). Most of these improvements were retained after 2 wk of nonexposure to the heat. This is the first study to quantify how much 14 d of heat acclimation can increase whole-body evaporative heat loss, which can improve by as much as approximately 11%.

Finite Element Analysis of the Displacement Adjustment Scheme for Column Bases of a 10000 m3 Spherical Tank During Whole-body Heat Treatment

The stress of spherical tank and displacement of column bases were calculated by finite element method, considering the uneven gravity loads on support columns which was caused by manufacturing and setting errors. The preliminary displacement adjustment scheme for column bases was made, according to the safety range of column bases displacement which was determined by the maximum stress restricted by allowable stress at the set heat treatment temperatures. The final scheme was made after checking the preliminary scheme. The method of making adjustment scheme of column bases for a 10000m3 spherical tank during the whole-body heat treatment may provide a reference for other large spherical tank.

Fever-range whole-body heat treatment stimulates antigen-specific T-cell responses in humans

Increase in body temperature has been thought to play an important role in the regulation of immune responses, although its precise mechanisms are still under investigation. Here, we examined the effects of physiologically relevant thermal stress on the cytokine production from human peripheral T cells. Volunteers were heated using a whole-body hyperthermia device, the rectal temperature was maintained above 38.5°C for more than 60min, and peripheral blood mononuclear cells (PBMCs) were obtained before and after the treatment. When T cells were stimulated with anti-CD3/CD28 antibodies, marked increases in the production of interferon-γ (IFN-γ) and interleukin-2 were observed in PBMCs prepared immediately after and 24h after the treatment. Similarly, enhanced production of IFN-γ in response to the tuberculin purified protein derivative or antigenic viral peptides was also observed immediately after and 24h after the treatment. Fluorescence photo-bleaching analyses showed heat-induced increase of membrane fluidity in T cells, which probably enables them to induce rapid and efficient cluster formation of molecules involved in antigen recognition and signal transduction for T-cell stimulation. We concluded that physiologically relevant thermal stress could efficiently modify T-cell responsiveness to various stimuli, including enhanced responses to specific antigens.

Effects of whole-body heat on male germ cell development and sperm motility in the laboratory mouse.

This study investigated the effects of high temperatures on male germ cell development and epididymal sperm motility of laboratory mice. In Experiment 1, adult males (n=16) were exposed to whole-body heat of 37-38°C for 8h day(-1) for 3 consecutive days, whereas controls (n=4) were left at 23-24°C. In Experiment 2, adult mice (n=6) were exposed to 37-38°C for a single 8-h period with controls (n=6) left at 23-24°C. Experiment 2 was conducted as a continuation of previous study that showed changes in spermatozoa 16h after exposure to heat of 37-38°C for 8h day(-1) for 3 consecutive days. In the present study, in Experiment 1, high temperature reduced testes weights 16h and 14 days after exposure, whereas by Day 21 testes weights were similar to those in the control group (P=0.18). At 16h, 7 and 14 days after exposure, an increase in germ cell apoptosis was noticeable in early and late stages (I-VI and XI-XII) of the cycle of the seminiferous epithelium. However, apoptosis in intermediate stages (VII-X) was evident 16h after heat exposure (P<0.05), without any change at other time periods. By 21 days, there were no significant differences between heat-treated groups and controls. Considerably more caspase-3-positive germ cells occurred in heat-treated mice 16h after heat exposure compared with the control group (P<0.0001), whereas 8h after heat in Experiment 2, sperm motility was reduced with a higher percentage of spermatozoa showing membrane damage. In conclusion, the present study shows that whole-body heat of 37-38°C induces stage-specific germ cell apoptosis and membrane changes in spermatozoa; this may result in reduced fertility at particular times of exposure after heating.

Sex-related differences in local and whole-body heat loss responses: Physical or physiological?

The current thesis examined whether sex differences in local and whole-body heat loss are evident after accounting for confounding differences in physical characteristics and rate of metabolic heat production. Three experimental studies were performed: the first examined whole-body heat loss in males and females matched for body mass and surface area during exercise at a fixed rate of metabolic heat production; the second examined local and whole-body heat loss responses between sexes during exercise at increasing requirements for heat loss; the third examined sex-differences in local sweating and cutaneous vasodilation to given doses of pharmacological agonists, as well as during passive heating. The first study demonstrated that females exhibit a lower whole-body sudomotor thermosensitivity (553 ± 77 vs. 795 ± 85 W·°C−1, p = 0.05) during exercise performed at a fixed rate of metabolic heat production. The second study showed that whole-body sudomotor thermosensitivity is similar between sexes at a requirement for heat loss of 250 W·m−2 (496 ± 139 vs. 483 ± 185 W·m−2·°C−1, p = 0.91) and 300 W·m−2 (283 ± 70 vs. 211 ± 66 W·m−2·°C−1, p = 0.17), only becoming greater in males at a requirement for heat loss of 350 W·m−2 (197 ± 61 vs. 82 ± 27 W·m−2·°C−1, p = 0.007). In the third study, a lower sweat rate to the highest concentration of acetylcholine (0.27 ± 0.08 vs. 0.48 ± 0.13 mg·min−1·cm−2, p = 0.02) and methacholine (0.41 ± 0.09 vs. 0.57 ± 0.11 mg·min−1·cm−2, p = 0.04) employed was evidenced in females, with no differences in cholinergic sensitivity. Taken together, the results of the current thesis show that sex itself can modulate sudomotor activity, specifically the thermosensitivity of the response, during both exercise and passive heat stress. Furthermore, the results of the third study point towards a peripheral modulation of the sweat gland as a mechanism responsible for the lower sudomotor thermosensitivity in females.

Sex-related differences in local and whole-body heat loss responses: Physical or physiological?

The current thesis examined whether sex differences in local and whole-body heat loss are evident after accounting for confounding differences in physical characteristics and rate of metabolic heat production. Three experimental studies were performed: the first examined whole-body heat loss in males and females matched for body mass and surface area during exercise at a fixed rate of metabolic heat production; the second examined local and whole-body heat loss responses between sexes during exercise at increasing requirements for heat loss; the third examined sex-differences in local sweating and cutaneous vasodilation to given doses of pharmacological agonists, as well as during passive heating. The first study demonstrated that females exhibit a lower whole-body sudomotor thermosensitivity (553 ± 77 vs. 795 ± 85 W·°C⁻¹, p = 0.05) during exercise performed at a fixed rate of metabolic heat production. The second study showed that whole-body sudomotor thermosensitivity is similar between sexes at a requirement for heat loss of 250 W·m⁻² (496 ± 139 vs. 483 ± 185 W·m⁻²·°C⁻¹, p = 0.91) and 300 W·m⁻² (283 ± 70 vs. 211 ± 66 W·m⁻²·°C⁻¹, p = 0.17), only becoming greater in males at a requirement for heat loss of 350 W·m⁻² (197 ± 61 vs. 82 ± 27 W·m⁻²·°C⁻¹, p = 0.007). In the third study, a lower sweat rate to the highest concentration of acetylcholine (0.27 ± 0.08 vs. 0.48 ± 0.13 mg·min⁻¹·cm⁻², p = 0.02) and methacholine (0.41 ± 0.09 vs. 0.57 ± 0.11 mg·min⁻¹·cm⁻², p = 0.04) employed was evidenced in females, with no differences in cholinergic sensitivity. Taken together, the results of the current thesis show that sex itself can modulate sudomotor activity, specifically the thermosensitivity of the response, during both exercise and passive heat stress. Furthermore, the results of the third study point towards a peripheral modulation of the sweat gland as a mechanism responsible for the lower sudomotor thermosensitivity in females.

Local Sweat Rates do not Accurately Represent Whole-Body Evaporative Heat Loss following 14-day Dry-Heat Acclimation

Local Sweat Rates do not Accurately Represent Whole-Body Evaporative Heat Loss following 14-day Dry-Heat Acclimation

At What Level Of Heat Stress Are Age-related Impairments In Whole-body Heat Loss Evident?

At What Level Of Heat Stress Are Age-related Impairments In Whole-body Heat Loss Evident?

Cerebral vasoreactivity: impact of heat stress and lower body negative pressure

Cerebrovascular reactivity represents the capacity of the cerebral circulation to raise blood flow in the face of increased demand, and may be reduced in some clinical and physiological conditions. We tested the hypothesis that the hypercapnia-induced increase in cerebral perfusion is attenuated during heat stress (HS) compared to normothermia (NT), and this response is further reduced during the combined challenges of HS and lower body negative pressure (LBNP). Ten healthy individuals (9 men) undertook rebreathing-induced hypercapnia during NT, HS, and HS+20mmHg LBNP (HSLBNP), while cerebral perfusion was indexed from middle cerebral artery blood velocity (MCA V mean). Cerebrovascular responses were calculated from the slope of the change in MCA V mean and cerebral vascular conductance (CVCi) relative to the increase in end tidal carbon dioxide ([Formula: see text]) during rebreathing. MCA V mean was similar in HS (55±19cms(-1)) and HSLBNP (52±16cms(-1)), and both values were reduced relative to NT (66±20cms(-1)), yet the rise in MCA V mean per Torr increase in [Formula: see text] during rebreathing was similar in each condition (NT: 2.5±0.6cms(-1)Torr(-1); HS: 2.4±0.8cms(-1)Torr(-1); HSLBNP: 2.1±1.1cms(-1)Torr(-1)). Likewise, the rate of increase in CVCi was not different between conditions (NT: 2.1±0.65cms(-1)mmHg(-1)100Torr(-1); HS: 2.4±0.8cms(-1)mmHg(-1)100Torr(-1); HSLBNP: 2.0±1.0cms(-1)mmHg(-1)100Torr(-1)). These data indicate that cerebrovascular reactivity is not compromised during whole-body heat stress alone or when combined with mild orthostatic stress relative to normothermic conditions.

Applicability of whole-body heat balance models for evaluating thermal sensation under non-uniform air movement in warm environments

In ASHRAE Standard 55-2010, the comfort effects of elevated air movement are evaluated using the SET index as computed by the Gagge 2-Node model of whole-body heat balance. Air movement in reality has many forms, which might create heat flows and thermal sensations that cannot be accurately predicted by a simple whole-body model. This paper addresses two of such potential inaccuracies: 1) indoor airflows may affect only a portion of the body surface (e.g., above desktop), and the affected body surface might be variably nude (e.g., face) or clothed, 2) the turbulence intensity (TI) in some typical airstreams (e.g., those created by fans) might have a different impact on heat transfer than the TI implicit in 2-Node's single convective heat transfer coefficient. For both these issues, can a whole-body index like SET represent such a wide range of possible exposures to airflow?Measurements of thermal sensation were obtained from human subjects using face-level fans in warm environments. Previous laboratory studies of a range of airstream sources were also analyzed. The effects of turbulence intensity were examined with manikin tests.The results show that indices derived from the 2-Node model of whole-body heat balance are effective at predicting thermal sensation under most non-uniform air movement. In contrast, the PMV index underestimates cooling in warm conditions. Turbulence increases the cooling effect of air movement, but by amounts that might be neglected for most design purposes.

Higher sweating rate and skin blood flow during the luteal phase of the menstrual cycle.

Evaporation by sweating is the most effective way to remove heat from the body. Sweat rates increase under both local and whole-body heat stress. Men and women differ in how they respond to heat, because sexual steroids alter resting body core temperature and the threshold for sweating and skin blood flow (SBF) during heating. The purpose of the present study was to compare local sweat rates and cutaneous vasodilatation during heat exposure in women with a regular menstrual cycle. The cutaneous vasodilatation was judged by measuring the SBF. Eight female and nine male subjects participated in this study, and their age range was 24-29 years. Female subjects were tested twice throughout one full menstrual cycle: once during the middle follicular phases and once during the luteal phase. Subjects remained in a temperature-regulated room at 41°C and 21% of relative humidity for 40 minutes. Sweat rate was recorded from the forehead, forearm, and thigh, and skin temperature and SBF were measured on the thigh and forehead. We found that the sweating rate and SBF were greater in the luteal phase compared to follicular phase (p<0.05). Since both SBF and sweating were controlled by the sympathetic nerve system, the sympathetic outflow was greater during whole body heat exposure in the luteal phase. In contrast, for men, there was no significant difference in sweating and SBF over the same calendar period (p>0.05). We propose the enhanced sympathetic activity in the luteal phase with a regular menstrual cycle.

Do Older Females Store More Heat than Younger Females during Exercise in the Heat?

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. 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. 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. 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). 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.

Neither Short-term Sprint nor Endurance Training Enhances Thermal Response to Exercise in a Hot Environment

Improvements in fitness from a brief period of physical training may elicit sufficient physiological adaptations to decrease thermal strain during exercise in the heat. This study tested heat adaptation from short-term endurance (ET) and sprint-interval (SIT) training in moderately fit individuals. The ET group (n = 8) cycled at 65% for 8 sessions (4 sessions each at 60 and 90 min, respectively) over two weeks, while the SIT group (n = 8) performed repeated 30-s Wingate sprints (resistance 7.5% body mass; 4 sessions each of 4 and 5 sprints, respectively). and heat stress testing (HST; 60 min cycling at 65% at 35ºC, 40% relative humidity) were performed pre- and post-training. increased by 11% (p = 0.025) and 14% (p = 0.020) for the ET and SIT groups post-training, respectively. Thermal stress was similar pre- and post-training, with no significant difference in the rate of whole-body metabolic heat production (p = 0.106) for either group post-training. Cardiovascular improvement was evident with both ET and SIT, with a significant mean decrease (p = 0.014) in HR for both groups (ET: 146 ± 15 beats·min−1pre vs. 142 ± 12 beats·min−1post; SIT: 149 ± 15 beats·min−1pre vs. 146 ± 12 beats·min−1post) during the HST post-training. However, mean sweat loss (p = 0.248) and the rise in core temperature (p = 0. 260) did not change significantly comparing pre- and post-training HST. While short-term ET and SIT both induced significant improvements in aerobic fitness and decreased cardiovascular strain, neither elicited improved thermal responses during exercise in the heat and do not replace heat acclimatization.

Whole-body heat treatment stimulates antigen-specific T cell responses in human system

Meeting abstracts Previous studies in mice have showed that fever-range thermal stress (approx. 38.5-40.5 degrees C) stimulates a variety of T cell functions ex vivo and in vivo. The aim of this study is to examine the effects of increase in core body temperature in human system on the function of

Older Adults with Type 2 Diabetes Store More Heat during Exercise

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. This study aimed to examine the effects of T2D on whole-body heat exchange during exercise in the heat. 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. 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). 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.

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.

Whole-Body Heat Loss during Exercise in the Heat Is Not Impaired in Type 1 Diabetes

The objective of this study is to determine whether individuals with type 1 diabetes exhibit impairments in local and whole-body heat loss responses that could affect core temperature regulation during exercise in the heat compared with matched, nondiabetic individuals. Twelve otherwise healthy individuals with type 1 diabetes (HbA1c = 7.7% ± 0.3%) and 12 controls matched for age, sex, body surface area, and physical fitness cycled continuously for 60 min at a set rate of metabolic heat production (approximately 400 W) in a whole-body direct calorimeter (35°C and 20% relative humidity). Local sweat rate (ventilated capsule) was measured on the back and skin blood flow (laser Doppler velocimetry) on the forearm. Core (rectal and esophageal) and mean skin temperatures and heart rate were measured continuously. Whole-body heat exchange and change in body heat content were measured using simultaneous direct whole-body and indirect calorimetry. The change (mean ± SE) in body heat content was similar between groups during exercise (diabetes, 409 ± 27 kJ; control, 386 ± 33 kJ; P = 0.584) and recovery (diabetes, -115 ± 16 kJ; control, -93 ± 24 kJ; P = 0.457). Local heat loss responses of sweating (P = 0.783) and skin blood flow (P = 0.078) as well as rectal temperature (diabetes, 37.87°C ± 0.10°C; control, 37.85°C; ± 0.13°C; P = 0.977) and heart rate (diabetes, 130 ± 9 beats·min, vs control, 126 ± 8 beats·min, P = 0.326) were comparable at the end of the exercise period. During light-to-moderate-intensity exercise performed under conditions permitting full sweat evaporation, otherwise healthy type 1 diabetic individuals did not show impaired heat loss responses during heat exposure when compared with matched individuals without diabetes.

Topical ibuprofen inhibits blushing during embarrassment and facial flushing during aerobic exercise in people with a fear of blushing

The flush that develops during whole-body heat stress depends partly on prostaglandins production in the skin. Variations in the strength of this local mechanism may contribute to individual differences in susceptibility to blushing and associated anxiety. To investigate this in the present study, the anti-inflammatory agent ibuprofen (which blocks prostaglandins formation) was applied topically to a small area of the cheek in 16 participants with a fear of blushing and in another 14 without this fear. Changes in skin blood flow were monitored at the ibuprofen-treated site and at a mirror image control site while participants sang (to induce embarrassment and blushing) and during aerobic exercise (to induce flushing). The topical ibuprofen treatment inhibited increases in cheek blood flow in both groups during both of these tasks. However, increases in cheek blood flow were greater in participants with high than low fear of blushing immediately after exercise. These findings suggest that prostaglandins contribute to dilatation of facial blood vessels both during emotional arousal (embarrassment) and aerobic exercise. Furthermore, fear of blushing may be associated with mechanisms that delay the resumption of normal vascular tone after a period of vasodilatation. Whether topical ibuprofen gel is suitable for intermittent or long-term use as an aid for blushing control requires further investigation.