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This article describes the development and validation of accurate whole body sweat rate prediction equations for individuals performing indoor cycle ergometer and treadmill exercise, where power output can be measured or derived from simple inputs. For cycle ergometry, 112 trials (67 participants) were used for model development and another 56 trials (42 participants) for model validation. For treadmill exercise, 171 trials (67 participants) were used for model development and another 95 trials (63 participants) for model validation. Trials were conducted over a range of dry-bulb temperature (20°C to 40°C), relative humidity (14% to 60%), and exercise intensity (∼40% to 85% of peak aerobic power) conditions, which were matched between model development and model validation. Whole body sweat rates were measured, and proprietary prediction models were developed (accounting for all relevant biophysical factors) and then validated. For model validation, mean absolute error for predicted sweating rate was 0.01 and 0.02 L·h -1 for cycle and treadmill trials, respectively. The 95% confidence intervals were modest for cycle ergometer (+0.25 and -0.22 L·h -1 ) and treadmill exercise (+0.33 and -0.29 L·h -1 ). The accounted for variance between predicted and measured values was 92% and 78% for cycle and treadmill exercise, respectively. Bland-Altman analysis indicated that zero and one predicted value exceeded the a priori acceptable level of agreement (equivalent to ±2% of total body mass in 3 h) for cycle and treadmill exercise, respectively. There were fewer trials with female subjects, but their values did not differ from those expected for males. This is the foremost study to develop and validate whole body sweat rate prediction equations for indoor treadmill and cycle ergometer exercise of moderate to high intensity. These prediction equations are publicly available for use (https://sweatratecalculator.com). NEW & NOTEWORTHY This study presents the development of new proprietary whole body sweat rate prediction models for people exercising indoors on a cycle ergometer or treadmill using simple input parameters and delivered through a publicly available online calculator: https://sweatratecalculator.com. In an independent validation group, the predictive models for both indoor cycling and treadmill exercise were accurate across moderate to high exercise intensities in temperate to hot conditions. These equations will enable individualized hydration management during physical training and exercise physiology experiments.

The purpose of this study was to investigate the influence of biological sex, independent of differences in aerobic fitness and body fatness, on the change in gastrointestinal temperature (ΔT gi ) and whole body sweat rate (WBSR) of children exercising under uncompensable heat stress. Seventeen boys (means ± SD; 13.7 ± 1.3 yr) and 18 girls (13.7 ± 1.4 yr) walked for 45 min at a fixed rate of metabolic heat production per kg body mass (8 W·kg -1 ) in 40°C and 30% relative humidity. Sex and peak oxygen consumption (V̇o 2peak ) were entered into a Bayesian hierarchical general additive model (HGAM) for T gi . Sex, V̇o 2peak , and the evaporative requirement for heat balance (E req ) were entered into a Bayesian hierarchical linear regression for WBSR. For 26 (12 M and 14 F) of the 35 children with measured body composition, body fat percentage was entered in a separate HGAM and hierarchical linear regression for T gi and WBSR, respectively. Conditional on sex-specific mean V̇o 2peak , ΔT gi was 1.00°C [90% credible intervals (Crl): 0.84, 1.16] for boys and 1.17°C [1.01, 1.33] for girls, with a difference of 0.17°C [-0.39, 0.06]. When sex differences in V̇o 2peak were accounted for, the difference in ΔT gi between boys and girls was 0.01°C [-0.25, 0.22]. The difference in WBSR between boys and girls was 0.03 L·h -1 [-0.02, 0.07], when isolated from differences in E req . The difference in ΔT gi between boys and girls was -0.10°C [-0.38, 0.17] when sex differences in body fat (%) were accounted for. Biological sex did not independently influence the ΔT gi and WBSR of children exercising under uncompensable heat stress. NEW & NOTEWORTHY Limited studies have investigated the thermoregulatory responses of boys and girls exercising under uncompensable heat stress. Boys and girls often differ in physiological characteristics other than biological sex, such as aerobic fitness and body fat percentage, which may confound interpretations. We investigated the influence of biological sex on exercise thermoregulation in children, independent of differences in aerobic fitness and body fatness.

Purpose: This study aimed to investigate the associations of biological sex and aerobic fitness (i.e., V̇O 2peak ) on the change in gastrointestinal temperature (∆ Tgi ) and whole-body sweat rate (WBSR) of children exercising in warm conditions., Methods: Thirty-eight children (17 boys, mean ± SD = 13.7 ± 1.2 yr; 21 girls, 13.6 ± 1.8 yr) walked for 45 min at a fixed rate of metabolic heat production (8 W·kg -1 ) in 30°C and 40% relative humidity. Biological sex and relative V̇O 2peak were entered as predictors into a Bayesian hierarchical generalized additive model for Tgi . For a subsample of 13 girls with measured body composition, body fat percent was entered into a separate hierarchical generalized additive model for Tgi . Sex, V̇O 2peak , and the evaporative requirement for heat balance ( Ereq ) were entered into a Bayesian hierarchical linear regression for WBSR., Results: The mean ∆ Tgi for boys was 0.71°C (90% credible interval = 0.60-0.82) and for girls 0.78°C (0.68-0.88). A predicted 20 mL·kg -1 ·min -1 higher V̇O 2peak resulted in a 0.19°C (-0.03 to 0.43) and 0.24°C (0.07-0.40) lower ∆ Tgi in boys and girls, respectively. A predicted ~13% lower body fat in the subsample of girls resulted in a 0.15°C (-0.12 to 0.45) lower ∆ Tgi . When Ereq was standardized to the grand mean, the difference in WBSR between boys and girls was -0.00 L·h -1 (-0.06 to 0.06), and a 20-mL·kg -1 ·min -1 higher predicted V̇O 2peak resulted in a mean difference in WBSR of -0.07 L·h -1 (-0.15 to 0.00)., Conclusions: Biological sex did not independently influence ∆ Tgi and WBSR in children. However, a higher predicted V̇O 2peak resulted in a lower ∆ Tgi of children, which was not associated with a greater WBSR, but may be related to differences in body fat percent between high and low fitness individuals., (Copyright © 2023 by the American College of Sports Medicine.)

Purpose: This study aimed to determine the effect of different air velocities on heat exchange and performance during prolonged self-paced exercise in the heat., Methods: Twelve male cyclists performed a 700-kJ time trial in four different air velocity conditions (still air, 16, 30, and 44 km·h -1 ) in 32°C and 40% relative humidity. Performance, thermal, cardiovascular, and perceptual responses were measured, and heat balance parameters were estimated using partitional calorimetry, including the maximum potential for sweat evaporation ( Emax )., Results: Mean power output was lower in still air (232 ± 42 W) than 16 (247 ± 30 W), 30 (250 ± 32 W), and 44 km·h -1 (248 ± 32 W; all P < 0.001), but similar between the 16-, 30-, and 44-km·h -1 air velocity conditions ( P ≥ 0.275). Emax was lower in still air (160 ± 13 W·m -2 ) than 16 (298 ± 25 W·m -2 ), 30 (313 ± 23 W·m -2 ), and 44 km·h -1 (324 ± 31 W·m -2 ) and lower in 16 than 44 km·h -1 (all P < 0.001). Peak core temperature was higher in still air (39.4°C ± 0.7°C) than 16 (39.0°C ± 0.45°C), 30 (38.8°C ± 0.3°C), and 44 km·h -1 (38.8°C ± 0.5°C; all P ≤ 0.002). Mean skin temperature was lower with greater airflow ( P < 0.001) but similar in 30 and 40 km·h -1 ( P = 1.00). Mean heart rate was ~2 bpm higher in still air than 44 km·h -1 ( P = 0.035). RPE was greater in still air than 44 km·h -1 ( P = 0.017)., Conclusions: Self-paced cycling in still air was associated with a lower Emax and subsequently higher thermal strain, along with a similar or greater cardiovascular strain, despite work rate being lower than in conditions with airflow. The similarity in performance between the 16-, 30-, and 44-km·h -1 air velocity conditions suggests that airflow ≥16 km·h -1 does not further benefit self-paced exercise performance in the heat because of modest improvements in evaporative efficiency., (Copyright © 2023 by the American College of Sports Medicine.)

Objectives: Determine the extent and underlying causes of post-exercise hyperthermia in athletes with a spinal cord injury following exercise., Design: Observational., Methods: Thirty-one males (8 with tetraplegia [TP; C5-C8], 7 with high paraplegia [HP; T1-T5], 8 with low paraplegia [LP; T6-L1] and 8 able-bodied [AB]), recovered in 35°C/50%RH for 45min after 30-min of exercise at a metabolic heat production (H prod ) of 4.0W/kg (AB vs TP) or 6.0W/kg (AB vs HP vs LP). Esophageal (T es ), gastrointestinal (T gi ) and skin temperatures, H prod , local sweat rate (LSR) and mean arterial pressure were measured., Results: TP maintained a higher T es (38.05°C [95% CI: 37.83°C, 38.28°C], AB: 36.77°C [36.56°C, 36.98°C], p<0.001) and T gi (TP: 38.36°C [38.15°C, 38.58°C], AB: 37.26°C [37.04°C, 37.47°C], p<0.001), with peak values observed 45min post-exercise. Core temperatures all declined in HP, LP and AB, but HP maintained a higher T es than AB (p=0.030), and higher T gi than LP and AB (p=0.019). No differences in post-exercise H prod were observed between TP and AB (p=0.264), or HP, LP and AB (p=0.124). Evaporative heat loss was estimated to be zero in TP, while back LSR was greater in HP than LP (p=0.009). Minimal dry heat loss occurred in SCI groups (TP: 9W/m 2 [6, 12], HP: 4W/m 2 [1, 6], LP: 2W/m 2 [0, 5])., Conclusions: Substantial post-exercise hyperthermia is evident in TP (∼1.4°C hotter than AB after 45min of post-exercise recovery) due to minimal evaporation. HP have delayed post-exercise thermoregulatory recovery whereas LP respond similarly to AB., (Copyright © 2021. Published by Elsevier Ltd.)

Although it is well established that dehydration has a negative impact on thermoregulation during exercise in the heat, it is unclear whether this effect of dehydration is different between men and women, or across the phases of the menstrual cycle (MC). Twelve men and seven women (men: 20 ± 2 years, 70.13 ± 10.5 kg, 173.4 ± 6.0 cm, 54.2 ± 8.6 ml kg -1  min -1 ; women: 20 ± 2 years, 57.21 ± 7.58 kg, 161 ± 5 cm, 40.39 ± 3.26 ml kg -1  min -1 ) completed trials either euhydrated (urine specific gravity, USG ≤ 1.020, Euhy) or dehydrated (USG > 1.020, Dehy). Trial order was randomized and counterbalanced; men completed two trials (MEuhy and MDehy) and women completed four over two MC phases (late follicular: days 10-13, FDehy, FEuhy; midluteal: days 18-22, LDehy, LEuhy). Each trial consisted of 1.5 h, split into two 30 min blocks of exercise (B1 and B2, 15 min at 11 W/kg & 15 min at 7 W/kg) separated by 15 min rest in between and after. Rectal temperature (T re ) was measured continuously and estimated sweat loss was calculated from the body mass measured before and after each block of exercise. When dehydrated, the rate of rise in T re was greater in women in the first block of exercise compared to men, independently of the MC phase (MDehy: 0.03 ± 0.03°C/min, FDehy: 0.06 ± 0.02, LDehy: 0.06 ± 0.02, p = 0.03). Estimated sweat loss was lower in all groups in B1 compared to B2 when dehydrated (p < 0.05), with no difference between sexes for either hydration condition. These data suggest that women may be more sensitive to the negative thermoregulatory effects of dehydration during the early stages of exercise in the heat., (© 2021 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.)

Introduction: Exercise thermoregulation studies typically control for time of day. The present study assessed whether circadian rhythm independently alters time-dependent changes in core temperature and sweating during exercise at a fixed rate of metabolic heat production (Hprod) during the wake period., Methods: Ten men (26 ± 2 yr, 76.6 ± 6.3 kg, 1.95 ± 0.10 m2) cycled for 60 min in three combinations of ambient temperature and Hprod (23°C-7.5 W·kg-1, 33°C-5.5 W·kg-1, and 33°C-7.5 W·kg-1) at two times of day (a.m.: 0800 h, p.m.: 1600 h). Rectal temperature (Tre), local sweat rate, and whole-body sweat losses were measured., Results: Absolute Tre was lower at baseline in a.m. versus p.m. for all three conditions (a.m.: 36.8°C ± 0.2°C, p.m.: 37.0°C ± 0.2°C, P < 0.01). The ΔTre was not altered by time of day (P > 0.22) and not different at 60 min between a.m. and p.m. for 23°C-7.5 W·kg-1 (a.m.: 0.83°C ± 0.14°C, p.m.: 0.75°C ± 0.20°C; P = 0.20), 33°C-5.5 W·kg-1 (a.m.: 0.51°C ± 0.14°C, p.m.: 0.47°C ± 0.14°C; P = 0.22), and 33°C-7.5 W·kg-1 (a.m.: 0.77°C ± 0.20°C, p.m.: 0.73°C ± 0.21°C; P = 0.80). The change in local sweat rate was unaffected by time of day (P > 0.16) and not different at 60 min in 23°C-7.5 W·kg-1 (a.m.: 0.67 ± 0.20 mg·cm-2·min-1, p.m.: 0.62 ± 0.21 mg·cm-2·min-1; P = 0.55), 33°C-5.5 W·kg-1 (a.m.: 0.59 ± 0.13 mg·cm-2·min-1, p.m.: 0.57 ± 0.12 mg·cm-2·min-1; P = 0.65), and 33°C-7.5 W·kg-1 (a.m.: 0.91 ± 0.19 mg·cm-2·min-1, p.m.: 0.84 ± 0.15 mg·cm-2·min-1; P = 0.33). Whole-body sweat loss was not different between a.m. and p.m. for 23°C-7.5 W·kg-1 (a.m.: 579 ± 72 g, p.m.: 579 ± 96 g; P = 0.99), 33°C-5.5 W·kg-1 (a.m.: 558 ± 48 g, p.m.: 555 ± 83 g; P = 0.89), and 33°C-7.5 W·kg-1 (a.m.: 796 ± 72 g, p.m.: 783 ± 75 g; P = 0.31)., Conclusions: The change in core temperature and sweating throughout a 60-min exercise bout in 23°C and 33°C were unaffected by circadian rhythm during the wake period when exercise intensity was prescribed to elicit comparable rates of Hprod, suggesting that scheduling thermoregulatory exercise trials for the same time of day is unnecessary., (Copyright © 2020 by the American College of Sports Medicine.)

The purpose of this study is to determine whether thermoregulatory capacity is altered by multiple sclerosis (MS) during exercise in the heat. Sixteen MS participants (EDSS: 2.9 ± 0.9; 47 ± 8 yr; 77.6 ± 14.0 kg) and 14 healthy control (CON) participants (43 ± 11 yr; 78.6 ± 17.0 kg) cycled at a heat production of 4 W·kg -1 for 60 min at 30°C, 30% relative humidity (RH) (Warm). A subset of eight MS (EDSS: 2.6 ± 0.5; 44 ± 8 yr; 82.3 ± 18.2 kg) and 8 CON (44 ± 12 yr; 81.2 ± 21.1 kg) also exercised at 35°C, 30% RH (Hot). Rectal temperature (T re ), mean skin (T sk ) temperature, and local sweat rate (LSR) on the upper back (LSR back ) and forearm (LSR arm ) were measured. All CON, and only 9 of 16 and 7 of 8 MS participants completed 60 min of exercise in Warm and Hot trials, respectively. All MS participants who were unable to complete exercise stopped with a ΔT re between 0.2 and 0.5°C. The time to reach a ΔT re of 0.2°C was similar (MS: 28 ± 15 min, CON: 32 ± 18 min; P = 0.51). For MS participants, completing 60-min of exercise in Warm, ΔT re ( P = 0.13), ΔT sk ( P = 0.45), LSR back ( P = 0.69), and LSR arm ( P = 0.54) was similar to CON, but ΔT b (body temperature) (MS: 0.16 ± 0.13°C, CON: 0.07 ± 0.06°C; P = 0.02) and onset time (MS: 16 ± 10 min, CON: 8 ± 5 min; P = 0.02) for sweating were greater in MS. Similarly, in Hot, ΔT re ( P = 0.52), ΔT sk ( P = 0.06), LSR back ( P = 0.59), and LSR arm ( P = 0.08) were similar, but ΔT b (MS: 0.19 ± 0.16°C, CON: 0.06 ± 0.04°C; P = 0.04) and onset time (MS: 13 ± 7 min, CON: 6 ± 3 min; P = 0.02) for sweating were greater in MS. Even at 35°C, a delayed sweating onset did not alter heat loss to sufficiently affect exercise-induced rises in core temperature. Heat intolerance with MS does not seem attributable to thermoregulatory impairments.

New Findings: What is the central question of this study? Are fitness-related improvements in thermoregulatory responses during uncompensable heat stress mediated by aerobic capacity V ̇ O 2 max or is it the partial heat acclimation associated with training? What is the main finding and its importance? During uncompensable heat stress, individuals with high and low V ̇ O 2 max displayed similar sweating and core temperature responses whereas exercise training in previously untrained individuals resulted in a greater sweat rate and a smaller rise in core temperature. These observations suggest that it is training, not V ̇ O 2 max per se, that mediates thermoregulatory improvements during uncompensable heat stress., Abstract: It remains unclear whether aerobic fitness, as defined by the maximum rate of oxygen consumption V ̇ O 2 max , independently improves heat dissipation in uncompensable environments, or whether the thermoregulatory adaptations associated with heat acclimation are due to repeated bouts of exercise-induced heat stress during regular aerobic training. The present analysis sought to determine if V ̇ O 2 max independently influences thermoregulatory sweating, maximum skin wettedness (ω max ) and the change in rectal temperature (ΔT re ) during 60 min of exercise in an uncompensable environment (37.0 ± 0.8°C, 4.0 ± 0.2 kPa, 64 ± 3% relative humidity) at a fixed rate of heat production per unit mass (6 W kg -1 ). Retrospective analyses were performed on 22 participants (3 groups), aerobically unfit (UF; n = 7; V ̇ O 2 max : 41.7 ± 9.4 ml kg -1  min -1 ), aerobically fit (F; n = 7; V ̇ O 2 max : 55.6 ± 4.3 ml kg -1  min -1 ; P < 0.01) and aerobically unfit (n = 8) individuals, before (pre; V ̇ O 2 max : 45.8 ± 11.6 ml kg -1  min -1 ) and after (post; V ̇ O 2 max : 52.0 ± 11.1 ml kg -1  min -1 ; P < 0.001) an 8-week training intervention. ω max was similar between UF (0.74 ± 0.09) and F (0.78 ± 0.08, P = 0.22). However, ω max was greater post- (0.84 ± 0.08) compared to pre- (0.72 ± 0.06, P = 0.02) training. During exercise, mean local sweat rate (forearm and upper-back) was greater post- (1.24 ± 0.20 mg cm -2  min -1 ) compared to pre- (1.04 ± 0.25 mg cm -2  min -1 , P < 0.01) training, but similar between UF (0.94 ± 0.31 mg cm -2  min -1 , P = 0.90) and F (1.02 ± 0.30 mg cm -2  min -1 ). The ΔT re at 60 min of exercise was greater pre- (1.13 ± 0.16°C, P < 0.01) compared to post- (0.96 ± 0.14°C) training, but similar between UF (0.85 ± 0.29°C, P = 0.22) and F (0.95 ± 0.22°C). Taken together, aerobic training, not V ̇ O 2 max per se, confers an increased ω max , greater sweat rate, and smaller rise in core temperature during uncompensable heat stress in fit individuals., (© 2020 The Authors. Experimental Physiology © 2020 The Physiological Society.)

New Findings: What is the central question of this study? Hypoxia reportedly does not impair thermoregulation during exercise in compensable heat stress conditions: does it have an impact on maximal heat dissipation and therefore the critical environmental limit for the physiological compensability of core temperature? What is the main finding and its importance? Although skin blood flow was higher in hypoxia, no differences in sweat rates or the critical environmental limit for the physiological compensability of core temperature - an indicator of maximal heat loss - were found compared to exercise in normoxia, indicating no influence of normobaric hypoxia on thermoregulatory capacity in warm conditions., Abstract: Altered control of skin blood flow (SkBF) in hypoxia does not impair thermoregulation during exercise in compensable conditions, but its impact on maximal heat dissipation is unknown. This study therefore sought to determine whether maximum heat loss is altered by hypoxia during exercise in warm conditions. On separate days, eight males exercised for 90 min at a fixed heat production of ∼500 W in normoxia (NORM) or normobaric hypoxia (HYP, F I O 2  = 0.13) in a 34°C environment. Ambient vapour pressure was maintained at 2.13 kPa for 45 min, after which it was raised 0.11 kPa every 7.5 min. The critical ambient vapour pressure at which oesophageal temperature inflected upward (P crit ) indicated that maximum heat dissipation had been reached. Neither local sweat rates on the upper arm, back and forehead (average NORM: 1.46 (0.15) vs. HYP: 1.41 (0.16) mg cm -2  min -1 ; P = 0.59) nor whole-body sweat losses (NORM: 1029 (137) g vs. HYP: 1025 (150) g; P = 0.95) were different between trials. Laser-Doppler flux values (LDF; arbitrary units), an index of SkBF, were not different between NORM and HYP on the forearm (P = 0.23) or back (P = 0.73); however, when normalized as a percentage of maximum, LDF values tended to be higher in HYP compared to NORM at the forearm (condition effect, P = 0.05) but not back (P = 0.19). Despite potentially greater SkBF in hypoxia, there was no difference in P crit between conditions (NORM: 3.67 (0.35) kPa; HYP: 3.46 (0.39) kPa; P = 0.22). These findings suggest that hypoxia does not independently alter thermoregulatory capacity during exercise in warm conditions., (© 2020 The Authors. Experimental Physiology © 2020 The Physiological Society.)

Objective: To determine whether coating prosthesis liners with a 5% aluminium zirconium tetrachlorohydrate antiperspirant solution (AZCH) reduces local sweating on the thigh., Design: Double-blinded counter-balanced crossover design METHODS: Fourteen able-bodied participants (age: 28±5 y; body mass: 73.9±7.9kg, height: 1.73±0.09m; peak oxygen consumption [VO 2peak ]: 50.7±9.1 mlO 2 ⋅kg -1 ⋅min -1 ) simultaneously wore a prosthesis liner on each leg, one treated with AZCH and one untreated, for four days prior to running at 50% of VO 2peak for 60min in a temperate (23.7±0.7°C and 42.2±2.6% relative humidity) or hot (34.0±1.6°C and 40.8±6.1% relative humidity) environment. Rectal temperature (T re ) and whole-body sweat rates (WBSR) were measured to characterize thermal strain. Local sweat rate (LSR) was measured bilaterally underneath the liners, continuously, and heat-activated-sweat gland density (HASGD) was measured bilaterally every 15min., Results: In temperate condition, the mean change in T re was 1.2±0.4°C and WBSR was 723±129g⋅h -1 , whereas in the hot condition, change in T re was 1.2±0.5°C and WBSR was 911±231g⋅h -1 . In the temperate condition, AZCH treatment did not alter LSR (treated: 0.50±0.17 mg·cm -2 min -1 , untreated: 0.50±0.17 mg·cm -2 min -1 ; P=0.87) or HASGD (treated: 54±14 glands·cm -2 , untreated 55±14 glands·cm -2 ; P=0.38). In the hot condition, AZCH treatment paradoxically increased LSR (treated: 0.88±0.38 mg·cm -2 min -1 , untreated: 0.74±0.28 mg·cm -2 min -1 ; P=0.04) but not HASGD (treated: 52±17 glands·cm -2 , untreated: 48±19 glands·cm -2 ; P=0.77)., Conclusion: These results indicate coating prosthesis liners with 5% AZCH is ineffective at reducing local sweating., (Copyright © 2020 Sports Medicine Australia. Published by Elsevier Ltd. All rights reserved.)

Purpose: It is often assumed that a person with a higher mean skin temperature (Tsk) will sweat more during exercise. However, it has not yet been demonstrated whether Tsk describes any individual variability in whole-body sweat rate (WBSR) independently of the evaporative requirement for heat balance (Ereq)., Methods: One hundred forty bouts of 2-h treadmill walking completed by a pool of 21 participants (23 ± 4 yr, 174 ± 8 cm, 76 ± 11 kg, 1.9 ± 0.2 m) under up to nine conditions were analyzed. Trials employed varying rates of metabolic heat production (Hprod; 197-813 W), and environmental conditions (15°C, 20°C, 25°C, 30°C; all 50% relative humidity), yielding a wide range of Ereq (86-684 W) and Tsk values (26.9°C-34.4°C)., Results: The individual variation observed in WBSR was best described using Ereq (in watts; R = 0.784) as a sole descriptor, relative to Ereq (in watts per meter squared; R = 0.735), Hprod (in watts; R = 0.639), Hprod (in watts per meter squared; R = 0.584), ambient air temperature (Ta) (R = 0.263), and Tsk (R = 0.077; all, P < 0.001). A multiple stepwise linear regression included only Ereq (in watts; adjusted R = 0.784), with Tsk not significantly correlating with the residual variance (P = 0.285), independently of Ereq (in watts). Hprod (in watts) had similar predictive strength to Ereq (in watts) at a fixed air temperature, explaining only 5.2% at 30°C, 4.9% at 25°C, 2.7% at 20°C, and 0.5% at 15°C (all, P < 0.001) less variance in WBSR compared with Ereq. However, when data from all ambient temperatures were pooled, Hprod alone was a markedly worse predictor of WBSR than Ereq (R = 0.639 vs 0.784; P < 0.001)., Conclusions: Ereq (in watts) explained approximately four-fifths of the individual variation in WBSR over a range of ambient temperatures and exercise intensities, whereas Tsk did not explain any residual variance independently of Ereq.

Objectives: This study aimed to identify factors important to quality in exercise performance studies, specifically in the domains of aerobic, anaerobic and strength exercise. Factors related to diet and body composition were also targeted as these often influence or change with exercise., Design: Cross-sectional study employing focus groups and a modified Delphi method., Methods: Academic staff and research students within the discipline of exercise science in a research-intensive university participated in focus groups to generate discipline-specific factors important to study quality. These factors were subsequently presented in a modified Delphi survey to a panel of international researchers with expertise in at least one of the domains. Item consensus was defined as >70% agreement on importance. The initial round contained all items generated from the focus groups. Subsequent rounds only presented items where consensus was not achieved, and additional items suggested by participants., Results: The academic staff (n = 10) and research students (n = 9) generated 22 items generic to all exercise performance studies and 71 domain-specific items. Over two Delphi survey rounds involving 18 international researchers, consensus on importance was achieved for 19 generic items. Identified factors addressed exercise testing and prescription protocols, equipment and compliance to interventions. Consensus on 66 specific items was achieved but was limited by small domain-specific participant numbers (4-8)., Conclusions: Numerous discipline-specific factors were identified as important to study quality. These factors can subsequently be used to inform the development of a tool to evaluate study quality in exercise performance research or inform best clinical practice., (Copyright © 2020. Published by Elsevier Ltd.)

It is the position of Sports Dietitians Australia (SDA) that exercise in hot and/or humid environments, or with significant clothing and/or equipment that prevents body heat loss (i.e., exertional heat stress), provides significant challenges to an athlete's nutritional status, health, and performance. Exertional heat stress, especially when prolonged, can perturb thermoregulatory, cardiovascular, and gastrointestinal systems. Heat acclimation or acclimatization provides beneficial adaptations and should be undertaken where possible. Athletes should aim to begin exercise euhydrated. Furthermore, preexercise hyperhydration may be desirable in some scenarios and can be achieved through acute sodium or glycerol loading protocols. The assessment of fluid balance during exercise, together with gastrointestinal tolerance to fluid intake, and the appropriateness of thirst responses provide valuable information to inform fluid replacement strategies that should be integrated with event fuel requirements. Such strategies should also consider fluid availability and opportunities to drink, to prevent significant under- or overconsumption during exercise. Postexercise beverage choices can be influenced by the required timeframe for return to euhydration and co-ingestion of meals and snacks. Ingested beverage temperature can influence core temperature, with cold/icy beverages of potential use before and during exertional heat stress, while use of menthol can alter thermal sensation. Practical challenges in supporting athletes in teams and traveling for competition require careful planning. Finally, specific athletic population groups have unique nutritional needs in the context of exertional heat stress (i.e., youth, endurance/ultra-endurance athletes, and para-sport athletes), and specific adjustments to nutrition strategies should be made for these population groups.

Purpose: This study aimed to establish the true influence of spinal cord injury (SCI) level on core temperature and sweating during exercise in the heat independently of biophysical factors., Methods: A total of 31 trained males (8 with tetraplegia [TP; C5-C8], 7 with high paraplegia [HP; T1-T5], 8 with low paraplegia [LP; T6-L1], and 8 able bodied [AB]) performed 3 × 10 min of arm ergometry with 3-min rest at a metabolic heat production of (a) 4.0 W·kg (AB vs TP) or (b) 6.0 W·kg (AB vs HP vs LP), in 35°C, 50% relative humidity. Esophageal (Tes) and local skin temperatures and local sweat rate (LSR) on the forehead and upper back were measured throughout., Results: Change in Tes was greatest in TP (1.86°C ± 0.32°C vs 0.29°C ± 0.07°C, P < 0.001) and greater in HP compared with LP and AB, reaching 1.20°C ± 0.50°C, 0.66°C ± 0.23°C, and 0.53°C ± 0.12°C, respectively (P < 0.001). Approximately half of the variability in end-trial ΔTes was described by SCI level in paraplegics (adjusted R = 0.490, P = 0.005). Esophageal temperature onset thresholds of sweating at the forehead and upper back were similar among HP, LP, and AB, whereas no sweating was observed in TP. Thermosensitivity (ΔTes vs ΔLSR) was also similar, except for LP demonstrating lower thermosensitivity than AB at the upper back (0.78 ± 0.26 vs 1.59 ± 0.89 mg·cm·min, P = 0.039). Change in skin temperature was greatest in denervated regions, most notably at the calf in all SCI groups (TP, 2.07°C ± 0.93°C; HP, 2.73°C ± 0.68°C; LP, 2.92°C ± 1.48°C)., Conclusion: This study is the first to show the relationship between ΔTes and SCI level in athletes with paraplegia after removing variability arising from differences in metabolic heat production and mass. Individual variability in ΔTes is further reduced among athletes with TP because of minimal evaporative heat loss secondary to an absence of sweating.

Objective: Pregnant women are advised to avoid heat stress (eg, excessive exercise and/or heat exposure) due to the risk of teratogenicity associated with maternal hyperthermia; defined as a core temperature (T core ) ≥39.0°C. However, guidelines are ambiguous in terms of critical combinations of climate and activity to avoid and may therefore unnecessarily discourage physical activity during pregnancy. Thus, the primary aim was to assess T core elevations with different characteristics defining exercise and passive heat stress (intensity, mode, ambient conditions, duration) during pregnancy relative to the critical maternal T core of ≥39.0°C., Design: Systematic review with best evidence synthesis., Data Sources: EMBASE, MEDLINE, SCOPUS, CINAHL and Web of Science were searched from inception to 12 July 2017., Study Eligibility Criteria: Studies reporting the T core response of pregnant women, at any period of gestation, to exercise or passive heat stress, were included., Results: 12 studies satisfied our inclusion criteria (n=347). No woman exceeded a T core of 39.0°C. The highest T core was 38.9°C, reported during land-based exercise. The highest mean end-trial T core was 38.3°C (95% CI 37.7°C to 38.9°C) for land-based exercise, 37.5°C (95% CI 37.3°C to 37.7°C) for water immersion exercise, 36.9°C (95% CI 36.8°C to 37.0°C) for hot water bathing and 37.6°C (95% CI 37.5°C to 37.7°C) for sauna exposure., Conclusion: The highest individual core temperature reported was 38.9°C. Immediately after exercise (either land based or water immersion), the highest mean core temperature was 38.3°C; 0.7°C below the proposed teratogenic threshold. Pregnant women can safely engage in: (1) exercise for up to 35 min at 80%-90% of their maximum heart rate in 25°C and 45% relative humidity (RH); (2) water immersion (≤33.4°C) exercise for up to 45 min; and (3) sitting in hot baths (40°C) or hot/dry saunas (70°C; 15% RH) for up to 20 min, irrespective of pregnancy stage, without reaching a core temperature exceeding the teratogenic threshold., Competing Interests: Competing interests: None declared., (© Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2019. All rights reserved. No commercial use is permitted unless otherwise expressly granted.)

Introduction: Impairments in sudomotor function during passive whole-body heating have been reported in multiple sclerosis (MS), a demyelinating disease of the CNS that disrupts autonomic function. However, the capability of the thermoregulatory system to control body temperature during exercise has never been assessed in MS. Thus, the aim of the present study was to test the hypothesis that thermoregulatory function is impaired in MS patients compared with healthy controls (CON) exercising at similar rates of metabolic heat production., Methods: Sweating and skin blood flow responses were compared between 12 individuals diagnosed with relapsing-remitting MS (9 females, 3 males) and 12 sex-, age-, mass-, and BSA-matched CON during a single bout of cycling exercise (rate of metabolic heat production: ∼4.5 W·kg) for 60 min in a climate-controlled room (25°C, 30% RH)., Results: Individuals with MS exhibited an attenuated increase in cumulative whole-body sweat loss after 30 min (MS, 72 ± 51 g; CON, 104 ± 37 g; P = 0.04) and 60 min (MS, 209 ± 94 g; CON, 285 ± 62 g; P = 0.02), as well as lower sweating thermosensitivity (MS, 0.49 ± 0.26 mg·cm·min·°C; CON, 0.86 ± 0.30 mg·cm·min·°C; P = 0.049). Despite evidence for thermoregulatory dysfunction, there were no differences between MS and CON in esophageal or rectal temperatures at 30- or 60-min time points (P > 0.05). Cutaneous vasculature responses were also not different in MS compared with CON (P > 0.05)., Conclusion: Taken together, MS blunts sweating responses during exercise while cutaneous vasculature responses are preserved. Altered mechanisms of body temperature regulation in persons with MS may lead to temporary worsening of disease symptoms and limit exercise tolerance under more thermally challenging conditions.

Objectives: To investigate whether the exercise performance benefits with neck cooling in the heat are attributable to neck-specific cooling, general body cooling, a cooler site-specific thermal perception or a combination of the above., Design: Counter-balanced crossover design., Methods: Twelve healthy participants cycled in the heat (34°C, 30% relative humidity), at a power output (PO) self-selected to maintain a fixed rating of perceived exertion (RPE) of 16. Each participant underwent four experimental trials: no cooling (CON), neck cooling (NEC), abdominal cooling (ABD), or neck cooling with menthol (MEN). Participants cycled for 90min or until their workload reduced by <70% of their initial PO. Changes in PO, rectal temperature (T re ), mean skin temperature (T sk ), whole-body thermal sensation (TS wb ) and thermal sensation of the neck (TS neck ) were recorded throughout., Results: The mean reduction in PO throughout exercise was similar (p=0.431) for CON (175±10W), NEC (176 ±12W), ABD (172±13W) and MEN (174±12W). The ΔT re at the end of exercise was similar (p=0.874) for CON (0.83±0.5°C), NEC (0.85±0.5°C), ABD (0.82±0.5°C) and MEN (0.81±0.5°C). TS wb was cooler (p<0.013) in MEN (125±8mm) compared to CON (146±19mm), NEC (135±11mm) and ABD (141±16mm)., Conclusions: No differences in exercise performance or thermal strain were observed in any of the cooling trials compared to the CON trial, despite significantly cooler TS wb values in the MEN and NEC trials compared to the CON trial. These findings differ from previous observations and highlight that the benefit of neck cooling may be situation dependent., (Copyright © 2018 Sports Medicine Australia. Published by Elsevier Ltd. All rights reserved.)

Objectives: This study investigated indirect measures of post-exercise parasympathetic reactivation (using heart-rate-variability, HRV) and sympathetic withdrawal (using systolic-time-intervals, STI) following upper- and lower-body exercise., Design: Randomized, counter-balanced, crossover., Methods: 13 males (age 26.4±4.7years) performed maximal arm-cranking (MAX-ARM) and leg-cycling (MAX-LEG). Subsequently, participants undertook separate 8-min bouts of submaximal HR-matched exercise of each mode (ARM and LEG). HRV (including natural-logarithm of root-mean-square-of-successive-differences, Ln-RMSSD) and STI (including pre-ejection-period, PEP) were assessed throughout 10-min seated recovery., Results: Peak-HR was higher (p=0.001) during MAX-LEG (182±7beatsmin -1 ) compared with MAX-ARM (171±12beatsmin -1 ), while HR (p<0.001) and Ln-RMSSD (p=0.010) recovered more rapidly following MAX-ARM. PEP recovery was similar between maximal bouts (p=0.106). HR during submaximal exercise was 146±7 (LEG) and 144±8beatsmin -1 (LEG) (p=0.139). Recovery of HR and Ln-RMSSD was also similar between submaximal modalities, remaining below baseline throughout recovery (p<0.001). PEP was similar during submaximal exercise (LEG 70±6ms; ARM 72±9ms; p=0.471) although recovery was slower following ARM (p=0.021), with differences apparent from 1- to 10-min recovery (p≤0.036). By 10-min post-exercise, PEP recovered to baseline (132±21ms) following LEG (130±21ms; p=0.143), but not ARM (121±17ms; p=0.001)., Conclusions: Compared with submaximal lower-body exercise, HR-matched upper-body exercise elicited a similar recovery of HR and HRV indices of parasympathetic reactivation, but delayed recovery of PEP (reflecting sympathetic withdrawal). Exercise modality appears to influence post-exercise parasympathetic reactivation and sympathetic withdrawal in an intensity-dependent manner. These results highlight the need for test standardization and may be relevant to multi-discipline athletes and in clinical applications with varying modes of exercise testing., (Copyright © 2018 Sports Medicine Australia. Published by Elsevier Ltd. All rights reserved.)

Heart failure (HF) patients are susceptible to heat strain during exercise, secondary to blunted skin blood flow (SkBF) responses, which may be explained by impaired nitric oxide (NO)-dependent vasodilation. Folic acid improves vascular endothelial function and SkBF through NO-dependent mechanisms in healthy older individuals and patients with cardiovascular disease. We examined the effect of folic acid supplementation (5 mg/day for 6 wk) on vascular function [brachial artery flow-mediated dilation (FMD)] and SkBF responses [cutaneous vascular conductance (CVC)] during 60 min of exercise at a fixed metabolic heat production (300 Ẇ Hprod ) in a 30°C environment in 10 patients with HF (New York Heart Association Class I-II) and 10 healthy controls (CON). Serum folic acid concentration increased in HF [preintervention (pre): 1.4 ± 0.2; postintervention (post): 8.9 ± 6.7 ng/ml, P = 0.01] and CON (pre: 1.3 ± 0.6; post: 5.2 ± 4.9 ng/ml, P = 0.03). FMD improved by 2.1 ± 1.3% in HF ( P < 0.01), but no change was observed in CON postintervention ( P = 0.20). During exercise, the external workload performed on the cycle ergometer to attain the fixed level of heat production for exercise was similar between groups (HF: 60 ± 13; CON: 65 ± 20 external workload, P = 0.52). Increases in CVC during exercise were similar in HF (pre: 0.89 ± 0.43; post: 0.83 ± 0.45 au/mmHg, P = 0.80) and CON (pre: 2.01 ± 0.79; post: 2.03 ± 0.72 au/mmHg, P = 0.73), although the values were consistently lower in HF for both pre- and postintervention measurement intervals ( P < 0.05). These findings demonstrate that folic acid improves vascular endothelial function in patients with HF but does not enhance SkBF during exercise at a fixed metabolic heat production in a warm environment.

Purpose: Heart failure (HF) patients seem to exhibit altered thermoregulatory responses during exercise in the heat. However, the extent to which these responses are altered due to physiological impairments independently of biophysical factors associated with differences in metabolic heat production (Hprod), evaporative heat balance requirements (Ereq), and/or body size is presently unclear. Therefore, we examined thermoregulatory responses in 10 HF patients and 10 age-matched controls (CON) similar in body size during exercise at a fixed rate of Hprod and therefore Ereq in a 30°C environment., Methods: Rectal temperature, local sweat rate, and cutaneous vascular conductance were measured throughout 60 min of cycle ergometry. Whole-body sweat rate was estimated from pre-post nude body weight corrected for fluid intake., Results: Despite exercising at the same rate of Hprod (HF, 338 ± 43 W; CON, 323 ± 31 W; P = 0.25), the rise in rectal temperature was greater (P < 0.01) in HF (0.81°C ± 0.16°C) than in CON (0.49°C ± 0.27°C). In keeping with a similar Ereq (HF, 285 ± 40 W; CON, 274 ± 28 W; P = 0.35), no differences in whole-body sweat rate (HF, 0.45 ± 0.11 L·h; CON, 0.41 ± 0.07 L·h; P = 0.38) or local sweat rate (HF, 0.96 ± 0.17 mg·cm·min; CON, 0.79 ± 0.15 mg·cm·min; P = 0.50) were observed between groups. However, the rise in cutaneous vascular conductance was lower in HF than in CON (HF, 0.83 ± 0.42 au·mm Hg; CON, 2.10 ± 0.79 au·mm Hg; P < 0.01). In addition, the cumulative body heat storage estimated from partitional calorimetry was similar between groups (HF, 154 ± 106 kJ; CON, 196 ± 174 kJ; P = 0.44)., Conclusions: Collectively, these findings demonstrate that HF patients exhibit a blunted skin blood flow response, but no differences in sweating. Given that HF patients had similar body heat storage to that of CON at the same Hprod, their greater rise in core temperature can be attributed to a less uniform internal distribution of heat between the body core and periphery.

Cold water or ice slurry ingestion during exercise seems to be an effective and practical means to improve endurance exercise performance in the heat. However, transient reductions in sweating appear to decrease the potential for evaporative heat loss from the skin by a magnitude that at least negates the additional internal heat loss as a cold ingested fluid warms up to equilibrate with body temperature; thus explaining equivalent core temperatures during exercise at a fixed heat production irrespective of the ingested fluid temperature. Internal heat transfer with cold fluid/ice is always 100% efficient; therefore, when a decrement occurs in the efficiency that sweat evaporates from the skin surface (i.e. sweating efficiency), a net cooling effect should begin to develop. Using established relationships between activity, climate and sweating efficiency, the boundary conditions beyond which cold ingested fluids are beneficial in terms of increasing net heat loss can be calculated. These conditions are warmer and more humid for cycling relative to running by virtue of the greater skin surface airflow, which promotes evaporation, for a given metabolic heat production and thus sweat rate. Within these boundary conditions, athletes should ingest fluids at the temperature they find most palatable, which likely varies from athlete to athlete, and therefore best maintain hydration status. The cooling benefits of cold fluid/ice ingestion during exercise are likely disproportionately greater for athletes with physiological disruptions to sweating, such as those with a spinal cord injury or burn injuries, as their capacity for skin surface evaporative heat loss is much lower; however, more research examining these groups is needed.

Purpose: To quantify how maximum skin wettedness (ωmax); that is, the determinant of the boundary between compensable and uncompensable heat stress, is altered by aerobic training in previously unfit individuals and further augmented by heat acclimation., Methods: Eight untrained individuals completed an 8-wk aerobic training program immediately followed by 8 d of hot/humid (38°C, 65%RH) heat acclimation. Participants completed a humidity ramp protocol pretraining (PRE-TRN), posttraining (POST-TRN), and after heat acclimation (POST-HA), involving treadmill marching at a heat production of 450 W for 105 min in 37.5°C, 2.0 kPa (35%RH). After attaining a steady-state esophageal temperature (Tes), humidity increased 0.04 kPa·min. An upward inflection in Tes indicated the upper limit of physiological compensability (Pcrit), which was then used to quantify ωmax. Local sweat rate, activated sweat gland density, and sweat gland output on the back and arm were simultaneously measured throughout., Results: Peak aerobic capacity increased POST-TRN by approximately 14% (PRE-TRN: 45.8 ± 11.8 mL·kg·min; POST-TRN: 52.0 ± 11.1 mL·kg·min, P < 0.001). ωmax values became progressively greater from PRE-TRN (0.72 ± 0.06) to POST-TRN (0.84 ± 0.08; P = 0.02), to POST-HA (0.95 ± 0.05; P = 0.03). These shifts in ωmax were facilitated by a progressively greater local sweat rate and activated sweat gland density from PRE-TRN (0.84 ± 0.21 mg·cm·min; 67 ± 20 glands per square centimeter) to POST-TRN (0.96 ± 0.21 mg·cm·min, P = 0.03; 86 ± 27 glands per square centimeter; P = 0.009), to POST-HA (1.15 ± 0.21 mg·cm·min; P < 0.001; 98 ± 35 glands per square centimeter; P < 0.001). No differences in sweat gland output were observed., Conclusions: A greater ωmax occurred after 8 wk of aerobic training, but ωmax was further augmented with heat acclimation, indicating only a partially increased heat loss capacity with training. These ωmax values may assist future predictions of heat stress risk in untrained/trained unacclimated individuals and trained heat-acclimated individuals.

New Findings: What is the central question of this study? Between 60 and 80% of multiple sclerosis (MS) patients experience transient worsening of symptoms with increased body temperature (heat sensitivity). As sensory abnormalities are common in MS, we asked whether afferent thermosensory function is altered in MS following exercise-induced increases in body temperature. What is the main finding and its importance? Increases in body temperature of as little as ∼0.4°C were sufficient to decrease cold, but not warm, skin thermosensitivity (∼10%) in MS, across a wider temperature range than in age-matched healthy individuals. These findings provide new evidence on the impact of heat sensitivity on afferent function in MS, which could be useful for clinical evaluation of this neurological disease. In multiple sclerosis (MS), increases in body temperature result in transient worsening of clinical symptoms (heat sensitivity or Uhthoff's phenomenon). Although the impact of heat sensitivity on efferent physiological function has been investigated, the effects of heat stress on afferent sensory function in MS are unknown. Hence, we quantified afferent thermosensory function in MS following exercise-induced increases in body temperature with a new quantitative sensory test. Eight relapsing-remitting MS patients (three men and five women; 51.4 ± 9.1 years of age; Expanded Disability Status Scale score 2.8 ± 1.1) and eight age-matched control (CTR) subjects (five men and three women; 47.4 ± 9.1 years of age) rated the perceived magnitude of two cold (26 and 22°C) and two warm stimuli (34 and 38°C) applied to the dorsum of the hand before and after 30 min cycling in the heat (30°C air; 30% relative humidity). Exercise produced similar increases in mean body temperature in MS [+0.39°C (95% CI: +0.21, +0.53) P = 0.001] and CTR subjects [+0.41°C (95% CI: +0.25, +0.58) P = 0.001]. These changes were sufficient to decrease thermosensitivity significantly to all cold [26°C stimulus, -9.1% (95% CI: -17.0, -1.5), P = 0.006; 22°C stimulus, -10.6% (95% CI: -17.3, -3.7), P = 0.027], but not warm, stimuli in MS. Contrariwise, CTR subjects showed sensitivity reductions to colder stimuli only [22°C stimulus, -9.7% (95% CI: -16.4, -3.1), P = 0.011]. The observation that reductions in thermal sensitivity in MS were confined to the myelinated cold-sensitive pathway and extended across a wider (including milder and colder) temperature range than what is observed in CTR subjects provides new evidence on the impact of rising body temperature on afferent neural function in MS. Also, our findings support the use of our new approach to investigate afferent sensory function in MS during heat stress., (© 2017 The Authors. Experimental Physiology © 2017 The Physiological Society.)

This study sought to assess the within-subject influence of acute hypoxia on exercise-induced changes in core temperature and sweating. Eight participants [1.75 (0.06) m, 70.2 (6.8) kg, 25 (4) yr, 54 (8) ml·kg -1 ·min -1 ] completed 45 min of cycling, once in normoxia (NORM; [Formula: see text] = 0.21) and twice in hypoxia (HYP1/HYP2; [Formula: see text]= 0.13) at 34.4(0.2)°C, 46(3)% RH. These trials were designed to elicit 1 ) two distinctly different %V̇o 2peak [NORM: 45 (8)% and HYP1: 62 (7)%] at the same heat production (H prod ) [NORM: 6.7 (0.6) W/kg and HYP1: 7.0 (0.5) W/kg]; and 2 ) the same %V̇o 2peak [NORM: 45 (8)% and HYP2: 48 (5)%] with different H prod [NORM: 6.7 (0.6) W/kg and HYP2: 5.5 (0.6) W/kg]. At a fixed %V̇o 2peak , changes in rectal temperature (ΔT re ) and changes in esophageal temperature (ΔT es ) were greater at end-exercise in NORM [ΔT re : 0.76 (0.19)°C; ΔT es : 0.64 (0.22)°C] compared with HYP2 [ΔT re : 0.56 (0.22)°C, P < 0.01; ΔT es : 0.42 (0.21)°C, P < 0.01]. As a result of a greater H prod ( P < 0.01) in normoxia, and therefore evaporative heat balance requirements, to maintain a similar %V̇o 2peak compared with hypoxia, mean local sweat rates (LSR) from the forearm, upper back, and forehead were greater (all P < 0.01) in NORM [1.10 (0.20) mg·cm -2 ·min -1 ] compared with HYP2 [0.71 (0.19) mg·cm -2 ·min -1 ]. However, at a fixed H prod , ΔT re [0.75 (0.24)°C; P = 0.77] and ΔT es [0.63 (0.29)°C; P = 0.69] were not different in HYP1, compared with NORM. Likewise, mean LSR [1.11 (0.20) mg·cm -2 ·min -1 ] was not different ( P = 0.84) in HYP1 compared with NORM. These data demonstrate, using a within-subjects design, that hypoxia does not independently influence thermoregulatory responses. Additionally, further evidence is provided to support that metabolic heat production, irrespective of %V̇o 2peak , determines changes in core temperature and sweating during exercise. NEW & NOTEWORTHY Using a within-subject design, hypoxia does not independently alter core temperature and sweating during exercise at a fixed rate of heat production. These findings also further contribute to the development of a methodological framework for assessing differences in thermoregulatory responses to exercise between various populations and individuals. Using the combined environmental stressors of heat and hypoxia we conclusively demonstrate that exercise intensity relative to aerobic capacity (i.e., %V̇o 2max ) does not influence changes in thermoregulatory responses., (Copyright © 2017 the American Physiological Society.)

We sought to identify the appropriate exercise intensity for unbiased comparisons of changes in rectal temperature (ΔT re ) and local sweat rates (LSR) between groups unmatched for body size during uncompensable heat stress. Sixteen males vastly different in body morphology were separated into two equal groups [small (SM): 65.8 ± 6.2 kg, 1.8 ± 0.1 m 2 ; large (LG): 100.0 ± 13.1 kg, 2.3 ± 0.1 m 2 ], but matched for sudomotor thermosensitivity (SM: 1.3 ± 0.6; LG: 1.1 ± 0.4 mg·cm -2 ·min -1 ·°C -1 ). The maximum potential for evaporation (E max ) for each participant was assessed using an incremental humidity protocol. On separate occasions, participants then completed 60 min of cycling in a 35°C and 70% RH environment at (1) 50% of VO 2max , (2) a heat production (H prod ) of 520 W, (3) H prod relative to mass (6 W·kg -1 ), and (4) H prod relative to mass above E max (3 W·kg -1 >E max ). E max was similar between LG (347 ± 39 W, 154 ± 15 W·m -2 ) and SM (313 ± 63 W, 176 ± 34 W·m -2 , P  >   0.12). ΔT re was greater in SM compared to LG at 520 W (SM: 1.5 ± 0.5; LG 0.8 ± 0.3°C, P  <   0.001) and at 50% of VO 2max (SM: 1.4 ± 0.5; LG 0.9 ± 0.3°C, P  <   0.001). However, ΔT re was similar between groups when H prod was either 6 W·kg -1 (SM: 0.9 ± 0.3; LG 0.9 ± 0.2°C, P  =   0.98) and 3 W·kg -1 >E max (SM: 1.4 ± 0.5; LG 1.3 ± 0.4°C, P  =   0.99). LSR was similar between LG and SM irrespective of condition, suggesting maximum LSR was attained (SM: 1.10 ± 0.23; LG: 1.07 ± 0.35 mg·cm -2 ·min -1 , P  =   0.50). In conclusion, systematic differences in ΔT re and LSR between groups unmatched for body size during uncompensable heat stress can be avoided by a fixed H prod in W·kg -1 or W·kg -1 >E max ., (© 2017 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.)

Heart failure (HF) patients appear to exhibit impaired thermoregulatory capacity during passive heating, as evidenced by diminished vascular conductance. Although some preliminary studies have described the thermoregulatory response to passive heating in HF, responses during exercise in the heat remain to be described. Therefore, the aim of this study was to compare thermoregulatory responses in HF and controls (CON) during exercise in the heat. Ten HF (NYHA classes I-II) and eight CON were included. Core temperature (T c ), skin temperature (T sk ), and cutaneous vascular conductance (CVC) were assessed at rest and during 1 h of exercise at 60% of maximal oxygen uptake. Metabolic heat production (H prod ) and the evaporative requirements for heat balance (E req ) were also calculated. Whole-body sweat rate was determined from pre-post nude body mass corrected for fluid intake. While H prod (HF: 3.9 ± 0.9; CON: 6.4 ± 1.5 W/kg) and E req (HF: 3.3 ± 0.9; CON: 5.6 ± 1.4 W/kg) were lower (P < 0.01) for HF compared to CON, both groups demonstrated a similar rise in T c (HF: 0.9 ± 0.4; CON: 1.0 ± 0.3°C). Despite this similar rise in T c , T sk (HF: 1.6 ± 0.7; CON: 2.7 ± 1.2°C), and the elevation in CVC (HF: 1.4 ± 1.0; CON: 3.0 ± 1.2 au/mmHg) was lower (P < 0.05) in HF compared to CON Additionally, whole-body sweat rate (HF: 0.36 ± 0.15; CON: 0.81 ± 0.39 L/h) was lower (P = 0.02) in HF compared to CON Patients with HF appear to be limited in their ability to manage a thermal load and distribute heat content to the body surface (i.e., skin), secondary to impaired circulation to the periphery., (© 2016 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.)

Humans maintain a relatively constant core temperature through the dynamic balance between endogenous heat production and heat dissipation to the surrounding environment. In response to metabolic or environmental disturbances to heat balance, the autonomic nervous system initiates cutaneous vasodilation and eccrine sweating to facilitate higher rates of dry (primarily convection and radiation) and evaporative transfer from the body surface; however, absolute heat losses are ultimately governed by the properties of the skin and the environment. Over the duration of a heat exposure, the cumulative imbalance between heat production and heat dissipation leads to body heat storage, but the consequent change in core temperature, which has implications for health and safety in occupational and athletic settings particularly among certain clinical populations, involves a complex interaction between changes in body heat content and the body's morphological characteristics (mass, surface area, and tissue composition) that collectively determine the body's thermal inertia. The aim of this review is to highlight the biophysical aspects of human core temperature regulation by outlining the principles of human energy exchange and examining the influence of body morphology during exercise and environmental heat stress. An understanding of the biophysical factors influencing core temperature will enable researchers and practitioners to better identify and treat individuals/populations most vulnerable to heat illness and injury during exercise and extreme heat events. Further, appropriate guidelines may be developed to optimize health, safety, and work performance during heat stress., (Copyright © 2016 Elsevier B.V. All rights reserved.)

Purpose: This study investigated whether short-term heart rate variability (HRV) can be used to differentiate between the immediate recovery periods following three different intensities of preceding exercise., Methods: 12 males cycled for 8 min at three intensities: LOW (40-45 %), MOD (75-80 %) and HIGH (90-95 %) of heart rate (HR) reserve. HRV was assessed during exercise and throughout 10-min seated recovery., Results: 1-min HR recovery was reduced following greater exercise intensities when expressed as R-R interval (RRI, ms) (p < 0.001), but not b min(-1) (p = 0.217). During exercise, the natural logarithm of root mean square of successive differences (Ln-RMSSD) was higher during LOW (1.66 ± 0.47 ms) relative to MOD (1.14 ± 0.32 ms) and HIGH (1.30 ± 0.25 ms) (p ≤ 0.037). Similar results were observed for high-frequency spectra (Ln-HF-LOW: 2.9 ± 1.0; MOD: 1.6 ± 0.6; HIGH: 1.6 ± 0.3 ms(2), p < 0.001). By 1-min recovery, higher preceding exercise intensities resulted in lower HRV amongst all three intensities for Ln-RMSSD (LOW: 3.45 ± 0.58; MOD: 2.34 ± 0.81; HIGH: 1.66 ± 0.78 ms, p < 0.001) and Ln-HF (LOW: 6.0 ± 1.0; MOD: 4.3 ± 1.4; HIGH: 2.8 ± 1.4 ms(2), p < 0.001). Similarly, by 1-min recovery 'HR-corrected' HRV (Ln-RMSSD: RRI × 10(3)) was different amongst all three intensities (LOW: 3.64 ± 0.49; MOD: 2.90 ± 0.65; HIGH: 2.40 ± 0.67, p < 0.001). These differences were maintained throughout 10-min recovery (p ≤ 0.027)., Conclusion: Preceding exercise intensity has a graded effect on recovery HRV measures reflecting cardiac vagal activity, even after correcting for the underlying HR. The immediate recovery following exercise is a potentially useful period to investigate autonomic activity, as multiple levels of autonomic activity can be clearly differentiated between using HRV. When investigating post-exercise HRV it is critical to account for the relative exercise intensity.

We sought to determine 1) the influence of adiposity on thermoregulatory responses independently of the confounding biophysical factors of body mass and metabolic heat production (Hprod); and 2) whether differences in adiposity should be accounted for by prescribing an exercise intensity eliciting a fixed Hprod per kilogram of lean body mass (LBM). Nine low (LO-BF) and nine high (HI-BF) body fat males matched in pairs for total body mass (TBM; LO-BF: 88.7 ± 8.4 kg, HI-BF: 90.1 ± 7.9 kg; P = 0.72), but with distinctly different percentage body fat (%BF; LO-BF: 10.8 ± 3.6%; HI-BF: 32.0 ± 5.6%; P < 0.001), cycled for 60 min at 28.1 ± 0.2 °C, 26 ± 8% relative humidity (RH), at a target Hprod of 1) 550 W (FHP trial) and 2) 7.5 W/kg LBM (LBM trial). Changes in rectal temperature (ΔTre) and local sweat rate (LSR) were measured continuously while whole body sweat loss (WBSL) and net heat loss (Hloss) were estimated over 60 min. In the FHP trial, ΔTre (LO-BF: 0.66 ± 0.21 °C, HI-BF: 0.87 ± 0.18 °C; P = 0.02) was greater in HI-BF, whereas mean LSR (LO-BF 0.52 ± 0.19, HI-BF 0.43 ± 0.15 mg·cm(-2)·min(-1); P = 0.19), WBSL (LO-BF 586 ± 82 ml, HI-BF 559 ± 75 ml; P = 0.47) and Hloss (LO-BF 1,867 ± 208 kJ, HI-BF 1,826 ± 224 kJ; P = 0.69) were all similar. In the LBM trial, ΔTre (LO-BF 0.82 ± 0.18 °C, HI-BF 0.54 ± 0.19 °C; P < 0.001), mean LSR (LO-BF 0.59 ± 0.20, HI-BF 0.38 ± 0.12 mg·cm(-2)·min(-1); P = 0.04), WBSL (LO-BF 580 ± 106 ml, HI-BF 381 ± 68 ml; P < 0.001), and Hloss (LO-BF 1,884 ± 277 kJ, HI-BF 1,341 ± 184 kJ; P < 0.001) were all greater at end-exercise in LO-BF. In conclusion, high %BF individuals demonstrate a greater ΔTre independently of differences in mass and Hprod, possibly due to a lower mean specific heat capacity or impaired sudomotor control. However, thermoregulatory responses of groups with different adiposity levels should not be compared using a fixed Hprod in watts per kilogram lean body mass., (Copyright © 2016 the American Physiological Society.)

Purpose: To compare the reductions in evaporative heat loss from the skin (Esk) to internal heat loss (Hfluid) induced by ice slurry (ICE) ingestion relative to 37 °C fluid and the accompanying body temperature and local thermoeffector responses during exercise in warm, dry conditions (33.5 °C ± 1.4 °C; 23.7% ± 2.6% relative humidity [RH])., Methods: Nine men cycled at approximately 55% VO2peak for 75 min and ingested 3.2 mL · kg(-1) aliquots of 37 °C fluid or ICE after 15, 30, and 45 min of exercise. Metabolic heat production (M-W), rectal temperature (Tre), mean skin temperature (Tsk), whole-body sweat loss (WBSL), local sweat rate (LSR), and skin blood flow (SkBF) were measured throughout. Net heat loss (HLnet) and heat storage (S) were estimated using partitional calorimetry., Results: Relative to the 37 °C trial, M-W was similar (P = 0.81) with ICE ingestion; however, the 200 ± 20 kJ greater Hfluid (P < 0.001) with ICE ingestion was overcompensated by a 381 ± 199-kJ lower Esk (P < 0.001). Net heat loss (HLnet) was consequently 131 ± 120 kJ lower (P = 0.01) and S was greater (P = 0.05) with ICE ingestion compared with 37 °C fluid ingestion. Concurrently, LSR and WBSL were lower by 0.16 ± 0.14 mg · min(-1) · cm(-2) (P < 0.01) and 191 ± 122 g (P < 0.001), respectively, and SkBF tended to be lower (P = 0.06) by 5.4%maxAU ± 13.4%maxAU in the ICE trial. Changes in Tre and Tsk were similar throughout exercise with ICE compared to 37 °C fluid ingestion., Conclusions: Relative to 37 °C, ICE ingestion caused disproportionately greater reductions in Esk relative to Hfluid, resulting in a lower HLnet and greater S. Mechanistically, LSR and possibly SkBF were suppressed independently of Tre or Tsk, reaffirming the concept of human abdominal thermoreception. From a heat balance perspective, recommendations for ICE ingestion during exercise in warm, dry conditions should be reconsidered.

Individual variation in the thermoregulatory responses to exercise is notoriously large. Although aerobic fitness (V̇o2 max) and body fatness are traditionally considered important predictors of individual core temperature and sweating responses, recent evidence indicates potentially important and independent roles for biophysical factors. Using stepwise regression, we examined the proportion of individual variability in rectal temperature changes (ΔTre), whole body sweat loss (WBSL), and steady-state local sweat rate (LSRss) independently described by 1) biophysical factors associated with metabolic heat production (Hprod) and evaporative heat balance requirements (Ereq) relative to body size and 2) factors independently related to V̇o2 max and body fatness. In a total of 69 trials, 28 males of wide-ranging morphological traits and V̇o2 max values cycled at workloads corresponding to a range of absolute Hprod (410-898 W) and relative intensities (32.2-82.0% V̇o2 max) for 60 min in 24.8 ± 0.7°C and 33.4 ± 12.2% relative humidity. Hprod (in W/kg total body mass) alone described ∼50% of the variability in ΔTre (adjusted to r(2) = 0.496; P < 0.001), whereas surface area-to-mass ratio and body fat percentage (BF%) explained an additional 4.3 and 2.3% of variability, respectively. For WBSL, Ereq (in W) alone explained ∼71% of variance (adjusted to r(2) = 0.713, P < 0.001), and the inclusion of BF% explained an additional 1.3%. Similarly, Ereq (in W/m(2)) correlated significantly with LSRss (adjusted to r(2) = 0.603, P < 0.001), whereas %V̇o2 max described an additional ∼4% of total variance. In conclusion, biophysical parameters related to Hprod, Ereq, and body size explain 54-71% of the individual variability in ΔTre, WBSL, and LSRss, and only 1-4% of additional variance is explained by factors related to fitness or fatness., (Copyright © 2015 the American Physiological Society.)

Multiple sclerosis (MS), a progressive neurological disease, can result in autonomic dysfunction. Impairments in the autonomic control of cardiovascular and thermoregulatory function during exercise have been observed in MS. Attenuated elevations in blood pressure during exercise in MS patients can negatively impact blood flow to skeletal muscle. Diminished sweating during exercise may impair heat dissipation likely limiting the exercise intensity that can be performed before detrimental core temperatures are reached. Further understanding the physiologic mechanisms of autonomic dysfunction during exercise in MS may lead to the development of novel therapeutic strategies targeted at improving quality of life in individuals with this disease., (Copyright © 2014 Elsevier B.V. All rights reserved.)

Aim: To reevaluate the previous hypothesis that greater reductions in self-paced exercise intensity in the heat are mediated by early differences in the rate of body heat storage (S)., Methods: Eight trained volunteers cycled in 19 °C/1.8 kPa (COOL), 25 °C/1.2 kPa (NORM), and 34 °C/1.6 kPa (HOT), while maintaining an RPE of 16. Potential differences in S following the onset of exercise were assessed by comparing rates of esophageal temperature change (ΔT es/Δt); and estimated S values using a traditional two-compartment thermometric model (S therm) of changes in rectal (T re) and skin (T sk) temperature, and partitional calorimetry (S cal)., Results: After 15 min of exercise, workload decreased more in HOT vs. COOL (P = 0.03), resulting in a shorter time (HOT: 40.7 ± 14.9 min; COOL: 53.5 ± 18.7 min; P = 0.04) to 70 % of initial workload. However, there were no preceding differences in ΔT es/Δt between conditions (P = 0.18). S therm values were different between HOT and COOL during the first 5 min of exercise (P < 0.05), primarily due to negative S therm values (-32 ± 15 kJ min(-1)) in COOL, which according to partitional calorimetric measurements, required improbably high (~56 kJ min(-1)) rates of evaporation when no sweating on the back and thigh was observed until after 7.6 ± 1.5 min and 4.8 ± 1.7 min of exercise, respectively. S cal values in the first 5 min of exercise confirmed S was actually positive in COOL (+21 ± 8 kJ min(-1)) and not negative. Different S therm values following the onset of exercise at different environmental temperatures are simply due to transient differences in the rate of change in T sk., Conclusion: Reductions in self-paced exercise intensity in the heat are not mediated by early differences in S following the onset of exercise.

We assessed whether comparisons of thermoregulatory responses between groups unmatched for body mass and surface area (BSA) should be performed using a metabolic heat production (prod) in Watts or Watts per kilogram for changes in rectal temperature (ΔTre), and an evaporative heat balance requirement (Ereq) in Watts or Watts per square meter for local sweat rates (LSR). Two groups with vastly different mass and BSA [large (LG): 91.5 ± 6.8 kg, 2.12 ± 0.09 m(2), n = 8; small (SM): 67.6 ± 5.6 kg, 1.80 ± 0.09 m(2), n = 8; P < 0.001], but matched for heat acclimation status, sex, age, and with the same onset threshold esophageal temperatures (LG: +0.37 ± 0.12°C; SM: +0.41 ± 0.17°C; P = 0.364) and thermosensitivities (LG: 1.02 ± 0.54, SM: 1.00 ± 0.38 mg·cm(-2)·min(-1)·°C(-1); P = 0.918) for sweating, cycled for 60 min in 25°C at different levels of prod (500 W, 600 W, 6.5 W/kg, 9.0 W/kg) and Ereq (340 W, 400 W, 165 W/m(2), 190 W/m(2)). ΔTre was different between groups at a prod of 500 W (LG: 0.52 ± 0.15°C, SM: 0.92 ± 0.24°C; P < 0.001) and 600 W (LG: 0.78 ± 0.19°C, SM: 1.14 ± 0.24°C; P = 0.007), but similar at 6.5 W/kg (LG: 0.79 ± 0.21°C, SM: 0.85 ± 0.14°C; P = 0.433) and 9.0 W/kg (LG: 1.02 ± 0.22°C, SM: 1.14 ± 0.24°C; P = 0.303). Furthermore, ΔTre was the same at 9.0 W/kg in a 35°C environment (LG: 1.12 ± 0.30°C, SM: 1.14 ± 0.25°C) as at 25°C (P > 0.230). End-exercise LSR was different at Ereq of 400 W (LG: 0.41 ± 0.18, SM: 0.57 ± 0.13 mg·cm(-2)·min(-1); P = 0.043) with a trend toward higher LSR in SM at 340 W (LG: 0.28 ± 0.06, SM: 0.37 ± 0.15 mg·cm(-2)·min(-1); P = 0.057), but similar at 165 W/m(2) (LG: 0.28 ± 0.06, SM: 0.28 ± 0.12 mg·cm(-2)·min(-1); P = 0.988) and 190 W/m(2) (LG: 0.41 ± 0.18, SM: 0.37 ± 0.15 mg·cm(-2)·min(-1); P = 0.902). In conclusion, when comparing groups unmatched for mass and BSA, future experiments can avoid systematic differences in ΔTre and LSR by using a fixed prod in Watts per kilogram and Ereq in Watts per square meter, respectively.

Although the requirements for heat dissipation during exercise are determined by the necessity for heat balance, few studies have considered them when examining sweat production and its potential modulators. Rather, the majority of studies have used an experimental protocol based on a fixed percentage of maximum oxygen uptake (% ). Using multiple regression analysis, we examined the independent contribution of the evaporative requirement for heat balance (Ereq) and % to whole-body sweat rate (WBSR) during exercise. We hypothesised that WBSR would be determined by Ereq and not by % . A total of 23 males performed two separate experiments during which they exercised for 90 min at different rates of metabolic heat production (200, 350, 500 W) at a fixed air temperature (30°C, n = 8), or at a fixed rate of metabolic heat production (290 W) at different air temperatures (30, 35, 40°C, n = 15 and 45°C, n = 7). Whole-body evaporative heat loss was measured by direct calorimetry and used to calculate absolute WBSR in grams per minute. The conditions employed resulted in a wide range of Ereq (131-487 W) and % (15-55%). The individual variation in non-steady-state (0-30 min) and steady-state (30-90 min) WBSR correlated significantly with Ereq (P < 0.001). In contrast, % correlated negatively with the residual variation in WBSR not explained by Ereq, and marginally increased (∼2%) the amount of total variability in WBSR described by Ereq alone (non-steady state: R(2) = 0.885; steady state: R(2) = 0.930). These data provide clear evidence that absolute WBSR during exercise is determined by Ereq, not by % . Future studies should therefore use an experimental protocol which ensures a fixed Ereq when examining absolute WBSR between individuals, irrespective of potential differences in relative exercise intensity.

The present study investigated the influence of maximal oxygen uptake (V(O2 max)) on local steady-state sudomotor responses to exercise, independently of evaporative requirements for heat balance (E(req)). Eleven fit (F; (V(O2 max))61.9 ± 6.0 ml kg(-1) min(-1)) and 10 unfit men (UF; (V(O2 max)) 40.4 ± 3.8 ml kg(-1) min(-1)) cycled for 60 min at an air temperature of 24.5 ± 0.8°C and ambient humidity of 0.9 ± 0.3 kPa at a set metabolic heat production per unit surface area, producing the same E(req) in all participants (BAL trial) and, in a second trial, at 60% of (V(O2 max)). During the BAL trial, absolute power (F 107 ± 2 and UF 102 ± 2 W; P = 0.126), E(req) (F 175 ± 5 and UF 176 ± 9 W m(-2); P = 0.855), steady-state whole-body sweat rate (F 0.44 ± 0.02 and UF 0.47 ± 0.02 mg cm(-2) min(-1); P = 0.385) and local sweat rate on the arm (F 0.29 ± 0.03 and UF 0.35 ± 0.03 mg cm(-2) min(-1); P = 0.129) were not different between groups; however, local sweat rate on the forehead in UF (1.67 ± 0.20 mg cm(-2) min(-1)) was almost double (P = 0.002) that of F (0.87 ± 0.11 mg cm(-2) min(-1)). Heart rate, ratings of perceived exertion and relative exercise intensity were also significantly greater in UF (P < 0.05). There was a trend towards an elevated minute ventilation in UF (P = 0.052), while end-tidal P(CO2) was significantly lower in UF (P = 0.028). At 60% (V(O2 max)), absolute power (F 174 ± 6 and UF 110 ± 5 W; P < 0.001), E(req) (F 291 ± 14 and UF 190 ± 17 W m(-2); P < 0.001), steady-state whole-body sweat rate (F 0.84 ± 0.05 and UF 0.53 ± 0.03 mg cm(-2) min(-1); P < 0.001) and local sweat rate on the arm (F 0.75 ± 0.04 and UF 0.35 ± 0.03 mg cm(-2) min(-1); P < 0.001) and on the forehead (F 2.92 ± 0.42 and UF 1.68 ± 0.23 mg cm(-2) min(-1); P = 0.022) were all significantly greater in F compared with UF. Heart rate and ratings of perceived exertion were similar at all time points (P > 0.05). Significantly greater minute ventilation (P < 0.001) and end-tidal P (CO2) responses (P = 0.017) were found in F. In conclusion, aerobic fitness alters local sweating on the forehead, but not the forearm, independently of evaporative requirements for heat balance, and may be the result of differential control of sweating in these skin areas associated with the relative intensity of exercise.

The independent influence of peak oxygen uptake (Vo(₂ peak)) on changes in thermoregulatory responses during exercise in a neutral climate has not been previously isolated because of complex interactions between Vo(₂ peak), metabolic heat production (H(prod)), body mass, and body surface area (BSA). It was hypothesized that Vo(₂ peak) does not independently alter changes in core temperature and sweating during exercise. Fourteen males, 7 high (HI) Vo(₂ peak): 60.1 ± 4.5 ml·kg⁻¹·min⁻¹; 7 low (LO) Vo(₂ peak): 40.3 ± 2.9 ml·kg⁻¹·min⁻¹ matched for body mass (HI: 78.2 ± 6.1 kg; LO: 78.7 ± 7.1 kg) and BSA (HI: 1.97 ± 0.08 m²; LO: 1.94 ± 0.08 m²), cycled for 60-min at 1) a fixed heat production (FHP trial) and 2) a relative exercise intensity of 60% Vo(₂ peak) (REL trial) at 24.8 ± 0.6°C, 26 ± 10% RH. In the FHP trial, H(prod) was similar between the HI (542 ± 38 W, 7.0 ± 0.6 W/kg or 275 ± 25 W/m²) and LO (535 ± 39 W, 6.9 ± 0.9 W/kg or 277 ± 29 W/m²) groups, while changes in rectal (T(re): HI: 0.87 ± 0.15°C, LO: 0.87 ± 0.18°C, P = 1.00) and aural canal (T(au): HI: 0.70 ± 0.12°C, LO: 0.74 ± 0.21°C, P = 0.65) temperature, whole-body sweat loss (WBSL) (HI: 434 ± 80 ml, LO: 440 ± 41 ml; P = 0.86), and steady-state local sweating (LSR(back)) (P = 0.40) were all similar despite relative exercise intensity being different (HI: 39.7 ± 4.2%, LO: 57.6 ± 8.0% Vo(2 peak); P = 0.001). At 60% Vo(2 peak), H(prod) was greater in the HI (834 ± 77 W, 10.7 ± 1.3 W/kg or 423 ± 44 W/m²) compared with LO (600 ± 90 W, 7.7 ± 1.4 W/kg or 310 ± 50 W/m²) group (all P < 0.001), as were changes in T(re) (HI: 1.43 ± 0.28°C, LO: 0.89 ± 0.19°C; P = 0.001) and T(au) (HI: 1.11 ± 0.21°C, LO: 0.66 ± 0.14°C; P < 0.001), and WBSL between 0 and 15, 15 and 30, 30 and 45, and 45 and 60 min (all P < 0.01), and LSR(back) (P = 0.02). The absolute esophageal temperature (T(es)) onset for sudomotor activity was ∼0.3°C lower (P < 0.05) in the HI group, but the change in T(es) from preexercise values before sweating onset was similar between groups. Sudomotor thermosensitivity during exercise were similar in both FHP (P = 0.22) and REL (P = 0.77) trials. In conclusion, changes in core temperature and sweating during exercise in a neutral climate are determined by H(prod), mass, and BSA, not Vo(₂ peak).

It has been previously demonstrated that the individual variation in whole-body sweat rate is described by differences in each participant's heat balance status. It was hypothesized that the individual variation in local sweat rate of the forehead (LSR(head)) and forearm (LSR(arm)) would be similarly described using a whole-body heat balance approach, specifically the ratio of evaporation required for heat balance relative to the maximum evaporation possible (i.e. E (req):E (max)). Twelve males cycled at 60% [Formula: see text] for 60 min at 24.9 ± 0.5°C, 31 ± 14% relative humidity. Rectal (T (re)) and aural canal (T (au)) temperatures as well as mean skin temperature ([Formula: see text]), metabolic energy expenditure (M) and rate of external work (W) were measured throughout. In addition, whole-body sweat rate at steady state (WBSR(ss)) was estimated using the change in body mass over the last 15 min of exercise, with LSR(head) and LSR(arm) estimated using technical absorbent patches applied between the 50th and 55th minute. WBSR(ss) significantly correlated with M-W (r = 0.66, P = 0.021), E (req) (r = 0.69, P = 0.013) and E (req):E (max) (r = 0.87, P < 0.001); LSR(head) was significantly correlated with E (req):E (max) (r = 0.82, P = 0.001), but not M-W (r = 0.31, P = 0.328) or E (req) (r = 0.38, P = 0.227); and LSR(arm) significantly correlated with E (req) (r = 0.62, P = 0.031) and E (req):E (max) (r = 0.78, P = 0.003) but not M-W (r = 0.56, P = 0.059). None of WBSR(ss), LSR(head) or LSR(arm) significantly correlated with any variations in T (re), T (au) or [Formula: see text] (i.e. 0.8T (re) + 0.2[Formula: see text]). Secondary analyses also demonstrated that both LSR(head) (r = 0.79, P = 0.002) and LSR(arm) (r = 0.89, P < 0.001) correlated with WBSR(ss). In conclusion, the individual variation in WBSR(ss), LSR(head) and LSR(arm) is described by the ratio of E (req) relative to E (max).

On separate days, eight physically active younger (22 +/- 2 years) and eight highly trained middle-aged (45 +/- 4 years) men matched for physical fitness and body composition performed 90 min of semi-recumbent cycling at a constant rate of heat production (290 W) followed by 60 min of seated recovery in either a temperate (T, 30 degrees C), warm (W, 35 degrees C) or hot (H, 40 degrees C) ambient condition. Rectal temperature (T (re)) was measured continuously, while the rate of whole-body heat loss (H (L)), as well as changes in body heat content (H (b)) was measured simultaneously using direct whole-body and indirect calorimetry. No difference in H (L) was observed between age groups for all ambient conditions. Accordingly, the average H (b) during the 90-min exercise was similar for the younger (+193 +/- 52, 212 +/- 82 and +211 +/- 44 kJ for T, W and H, respectively) and middle-aged men (+192 +/- 119, +225 +/- 76 and +217 +/- 130 kJ for T, W and H, respectively). This was paralleled by a similar increase in T (re) of 0.40 +/- 0.20, 0.36 +/- 0.14 and 0.34 +/- 0.23 degrees C for T, W and H, respectively in the younger men and 0.37 +/- 0.23, 0.32 +/- 0.19 and 0.28 +/- 0.14 degrees C for T, W and H, respectively in the middle-aged men. After 60 min of recovery, H (b) was similar for the younger and the middle-aged men, respectively (-45 +/- 52 and -38 +/- 31 kJ for T; -57 +/- 78 and -40 +/- 25 kJ for W; and -32 +/- 71 and 11 +/- 96 kJ for H). End recovery T (re) remained elevated to similar levels in both the younger and middle-aged men, respectively, for each of the ambient conditions (0.24 +/- 019 and 0.18 +/- 0.18 degrees C for T; 0.25 +/- 0.11 and 0.24 +/- 0.14 degrees C for W and 0.33 +/- 0.21 and 0.33 +/- 0.13 degrees C for H). We conclude that highly trained middle-aged men demonstrate a similar capacity for heat dissipation when compared with physically active younger men.

Purpose: We evaluated differences between sexes in core cooling rates during cold water immersion after exercise-induced hyperthermia., Methods: Ten male (M) and nine female (F) participants, matched for body surface area-to-mass ratio (AD/M) (F: 268 +/- 19 vs M: 261 +/- 16 cm2 x kg(-1)), were recruited for the study. Participants exercised until rectal temperature reached 39.5 degrees C and were subsequently immersed in a 2.0 degrees C circulated water bath until rectal temperature decreased to 37.5 degrees C. Rectal and mean skin temperatures and the relative rate of nonevaporative heat loss (W x m(-2)) were measured continuously during the immersion period., Results: Males were heavier, had a lower body fat percentage, and had a greater amount of lean body mass compared with females (P < or = 0.05). Significant differences were found in the overall cooling rate for rectal temperature (F: 0.22 +/- 0.07 vs M: 0.12 +/- 0.03 degrees C x min(-1), P = 0.001) and in the overall immersion times (F: 10.89 +/- 4.49 vs M: 18.13 +/- 4.47 min, P = 0.003). Mean skin temperature was lower in females compared with that in males during the immersion period (P < 0.001), although there were no differences between sexes in the rate of nonevaporative heat loss (P = 0.180)., Conclusions: Although females had a similar AD/M and greater body adiposity, they had approximately 1.7-fold greater rectal cooling rate. Because AD/M and body adiposity do not seem to influence rectal cooling rates in previously hyperthermic individuals, the greater cooling rates in females may be attributed to physical differences in lean body mass.

We examined differences in dynamic heat balance between males and females during intermittent exercise. Six males (M) and six females (F) performed three 30-min bouts of exercise (Ex1, Ex2, Ex3) at a constant rate of metabolic heat production (M - W) of approximately 500 W separated by three 15-min periods of inactive recovery. Rate of total heat loss (M - W) was measured by direct calorimetry, while M - W was determined by indirect calorimetry. Esophageal (T (es)) was measured continuously. Exercise at a constant M - W of approximately 500 W, was paralleled by a similar HL between sexes at the end of Ex1 (M: 462 +/- 30 W, F: 442 +/- 9 W, p = 0.117), Ex2 (M: 468 +/- 28 W, F: 508 +/- 18 W, p = 0.343), and Ex3 (M: 469 +/- 17 W, F: 465 +/- 13 W, p = 0.657). Consequently, changes in body heat content were comparable after Ex1 (M: 218 +/- 21 kJ, F: 287 +/- 35 kJ, p = 0.134), Ex2 (M: 109 +/- 18 kJ, F: 158 +/- 29 kJ, p = 0.179), and Ex3 (M: 92 +/- 19 kJ, F: 156 +/- 35 kJ, p = 0.136). However, females had greater overall increases in T (es) at the end of Ex3 (M: 0.55 +/- 0.25 degrees C, F: 0.97 +/- 0.26 degrees C, p

We evaluated the hypothesis that different rates of metabolic heat production between sexes, during exercise at the same percentage of maximum oxygen consumption [VO2 max] give proportional differences in evaporative heat loss. Seven males and seven females, exercised at 41.3 +/- 2.7% VO2 Max for 60-min at 40 degrees C and 30% relative humidity. Whole-body direct air calorimetry measured rate of whole-body evaporative heat loss (H e) while metabolic heat production (M - W) was measured by indirect calorimetry. M -W was greater in males (243 +/- 18 W m(-2)) relative to females (201 +/- 4 W m(-2)) (P

It is unknown whether menstrual cycle or oral contraceptive (OC) use influences nonthermal control of postexercise heat loss responses. We evaluated the effect of menstrual cycle and OC use on the activation of heat loss responses during a passive heating protocol performed pre- and postexercise. Women without OC (n = 8) underwent pre- and postexercise passive heating during the early follicular phase (FP) and midluteal phase (LP). Women with OC (n = 8) underwent testing during the active pill consumption (high exogenous hormone phase, HH) and placebo (low exogenous hormone phase, LH) weeks. After a 60-min habituation at 26 degrees C, subjects donned a liquid conditioned suit. Mean skin temperature was clamped at approximately 32.5 degrees C for approximately 15 min and then gradually increased, and the absolute esophageal temperature at which the onset of forearm vasodilation (Th(vd)) and upper back sweating (Th(sw)) were noted. Subjects then cycled for 30 min at 75% Vo(2 peak) followed by a 15-min seated recovery. A second passive heating was then performed to establish postexercise values for Th(vd) and Th(sw). Between 2 and 15 min postexercise, mean arterial pressure (MAP) remained significantly below baseline (P < 0.05) by 10 +/- 1 and 11 +/- 1 mmHg for the FP/LH and LP/HH, respectively. MAP was not different between cycle phases. During LP/HH, Th(vd) was 0.16 +/- 0.24 degrees C greater than FP/LH preexercise (P = 0.020) and 0.15 +/- 0.23 degrees C greater than FP/LH postexercise (P = 0.017). During LP/HH, Th(sw) was 0.17 +/- 0.23 degrees C greater than FP/LH preexercise (P = 0.016) and 0.18 +/- 0.16 degrees C greater than FP/LH postexercise (P = 0.001). Postexercise thresholds were significantly greater (P < or = 0.001) than preexercise during both FP/LH (Th(vd), 0.22 +/- 0.03 degrees C; Th(sw), 0.13 +/- 0.03 degrees C) and LP/HH (Th(vd), 0.21 +/- 0.03 degrees C; Th(sw), 0.14 +/- 0.03 degrees C); however, the effect of exercise was similar between LP/HH and FP/LH. No effect of OC use was observed. We conclude that neither menstrual cycle nor OC use modifies the magnitude of the postexercise elevation in Th(vd) and Th(sw).

Purpose: Previous studies have shown a rapid reduction in postexercise local sweating and blood flow despite elevated core temperatures. However, local heat loss responses do not illustrate how much whole-body heat dissipation is reduced, and core temperature measurements do not accurately represent the magnitude of residual body heat storage. Whole-body evaporative (H(E)) and dry (H(D)) heat loss as well as changes in body heat content (DeltaH(b)) were measured using simultaneous direct whole-body and indirect calorimetry., Methods: Eight participants cycled for 60 min at an external work rate of 70 W followed by 60 min of recovery in a calorimeter at 30 degrees C and 30% relative humidity. Core temperature was measured in the esophagus (T(es)), rectum (T(re)), and aural canal (T(au)). Regional muscle temperature was measured in the vastus lateralis (T(vl)), triceps brachii (T(tb)), and upper trapezius (T(ut))., Results: After 60 min of exercise, average DeltaH(b) was +273 +/- 57 kJ, paralleled by increases in T(es), T(re), and T(au) of 0.84 +/- 0.49, 0.67 +/- 0.36, and 0.83 +/- 0.53 degrees C, respectively, and increases in T(vl), T(tb), and T(ut) of 2.43 +/- 0.60, 2.20 +/- 0.64, and 0.80 +/- 0.20 degrees C, respectively. After a 10-min recovery, metabolic heat production returned to pre-exercise levels, and H(E) was only 22.9 +/- 6.9% of the end-exercise value despite elevations in all core temperatures. After a 60-min recovery, DeltaH(b) was +129 +/- 58 kJ paralleled by elevations of T(es) = 0.19 +/- 0.13 degrees C, T(re) = 0.20 +/- 0.03 degrees C, T(au) = 0.18 +/- 0.04 degrees C, Tvl = 1.00 +/- 0.43 degrees C, T(tb) = 0.92 +/- 0.46 degrees C, and T(ut) = 0.31 +/- 0.27 degrees C. Despite this, H(E) returned to preexercise levels. Only minimal changes in H(D) occurred throughout., Conclusion: We confirm a rapid reduction in postexercise whole-body heat dissipation by evaporation despite elevated core temperatures. Consequently, only 53% of the heat stored during 60 min of exercise was dissipated after 60 min of recovery, with the majority of residual heat stored in muscle tissue.