Key points• A relative exercise intensity (%V O 2 max ) protocol is often used to compare absolute whole-body sweat rates (WBSRs) during exercise between participants of different aerobic capacity.• Under conditions permitting full evaporation, heat balance theory suggests that exercise intensity should be fixed to elicit the same rate of evaporation required for heat balance (E req ).• Whole-body direct calorimetry was employed to measure WBSRs throughout 90 min of exercise across a range of air temperatures and rates of metabolic heat production.• Irrespective of ambient temperature and metabolic heat production, E req alone described ∼90% of all variability in WBSR during steady-state and non-steady-state exercise, whereas <2% of variation was independently described by %V O 2 max .• To perform an unbiased comparison of WBSRs (but not necessarily core temperature) between different individuals/groups under conditions allowing full evaporation, future studies should consider using a fixed E req irrespective of the %V O 2 max incurred.Abstract 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 (%V O 2 max ). Using multiple regression analysis, we examined the independent contribution of the evaporative requirement for heat balance (E req ) and %V O 2 max to whole-body sweat rate (WBSR) during exercise. We hypothesised that WBSR would be determined by E req and not by %V O 2 max . 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 E req (131-487 W) and %V O 2 max (15-55%). The individual variation in non-steady-state (0-30 min) and steady-state (30-90 min) WBSR correlated significantly with E req (P < 0.001). In contrast, %V O 2 max correlated negatively with the residual variation in WBSR not explained by E req , and marginally increased (∼2%) the amount of total variability in WBSR described by E req 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 E req , not by %V O 2 max . Future studies should

To assess potential mechanisms responsible for the lower sudomotor thermosensitivity in women during exercise, we examined sex differences in sudomotor function and skin blood flow (SkBF) during exercise performed at progressive increases in the requirement for heat loss. Eight men and eight women cycled at rates of metabolic heat production of 200, 250, and 300 W/m(2) of body surface area, with each rate being performed sequentially for 30 min. The protocol was performed in a direct calorimeter to measure evaporative heat loss (EHL) and in a thermal chamber to measure local sweat rate (LSR) (ventilated capsule), SkBF (laser-Doppler), sweat gland activation (modified iodine-paper technique), and sweat gland output (SGO) on the back, chest, and forearm. Despite a similar requirement for heat loss between the sexes, significantly lower increases in EHL and LSR were observed in women (P ≤ 0.001). Sex differences in EHL and LSR were not consistently observed during the first and second exercise periods, whereas EHL (348 ± 13 vs. 307 ± 9 W/m(2)) and LSR on the back (1.61 ± 0.07 vs. 1.20 ± 0.09 mg · min(-1) · cm(-2)), chest (1.33 ± 0.06 vs. 1.08 ± 0.09 mg · min(-1) · cm(-2)), and forearm (1.53 ± 0.07 vs. 1.20 ± 0.06 mg · min(-1) · cm(-2), men vs. women) became significantly greater in men during the last exercise period (P < 0.05). At each site, differences in LSR were solely due to a greater SGO in men, as opposed to differences in sweat gland activation. In contrast, no sex differences in SkBF were observed throughout the exercise period. The present study demonstrates that sex differences in sudomotor function are only evidenced beyond a certain requirement for heat loss, solely through differences in SGO. In contrast, the lower EHL and LSR in women are not paralleled by a lower SkBF response.

We demonstrate that lower limb heating acutely improves macro- and microvascular dilator function within the atherosclerotic prone vasculature of the leg in aged adults. These findings provide evidence for a potential therapeutic use of chronic lower limb heating to improve vascular health in primary aging and various disease conditions.

The current study aimed to determine whether a peripheral modulation of sweating contributes to the lower sudomotor thermosensitivity previously observed in females during exercise. We examined dose-response relationships in 12 males and 12 females to incremental doses of acetylcholine (ACh) and methylcholine (MCh) for sweating (ventilated capsule), as well as to ACh and sodium nitroprusside (SNP) for cutaneous vasodilation (laser-Doppler). All drugs were infused using intradermal microdialysis. On a separate day, potential sex differences in the onset threshold and/or thermosensitivity of heat loss responses were assessed during progressive increases in mean body temperature elicited by passive heating. Increases in sweating as a function of increasing concentration of ACh (P = 0.008) and MCh (P = 0.046) significantly differed between males and females. Although the concentration eliciting 50% of the maximal sweating response did not differ between sexes for either agonist (P > 0.1), maximum values were lower in females in response to ACh (0.34 ± 0.12 vs. 0.59 ± 0.19 mg·min(-1)·cm(-2), P = 0.04) and MCh (0.48 ± 0.12 vs. 0.78 ± 0.26 mg·min(-1)·cm(-2), P = 0.05). This observation was paralleled by a lower thermosensitivity of sudomotor activity in females during passive heating (1.29 ± 0.34 vs. 1.83 ± 0.33 mg·min(-1)·cm(-2)·°C(-1), P = 0.03), with no significant differences in the change in mean body temperature at which onset of sweating occurred (0.85 ± 0.19 vs. 0.67 ± 0.13°C, P = 0.10). No sex differences in cutaneous vasodilation were observed in response to ACh and SNP, as well as during passive heating (all P > 0.1). These findings provide direct evidence for a peripheral modulation of sudomotor activity in females. In contrast, sex does not modulate cutaneous vasodilation.

Although a number of studies have examined potential differences in temperature regulation between males and females during heat stress, conclusions have remained limited as to whether reported differences are due to confounding physical characteristics or to actual differences in the physiological variables of temperature regulation. Recent observations suggest that sex differences in temperature regulation, particularly in sudomotor activity, go beyond those associated with physical characteristics. Females have recently been shown to have a lower sudomotor activity, as well as a lower thermosensitivity of the response compared to males during exercise performed at a fixed rate of metabolic heat production. Furthermore, sex differences in local and whole-body sudomotor activity are only evident above a certain combination of environmental conditions and rate of metabolic heat production. In contrast, both the onset threshold and thermosensitivity of cutaneous vasodilatation are similar between males and females. In theory, differences in the thermosensitivity of sudomotor activity could be related to either a central (neural activity/integration) and/or peripheral (effector organ) modulation of temperature regulation. Based on recent findings, sex differences in sudomotor activity appear to be mediated peripherally, although a central modulation has yet to be conclusively ruled out. Here we present a brief yet comprehensive review of the current state of knowledge pertaining to sex differences in temperature regulation during exercise in the heat.

Non-technical summary The human body controls its temperature through coordinated physiological processes. Prior to the current study, it remained unknown if differences between males and females existed in these processes. The results from the current study show that females have a lower whole-body sweat response during exercise in the heat compared to males, which results in a greater increase in body temperature. The physiological process responsible for the lower whole-body sweat rate was a lower thermosensitivity of the response, meaning a lower increase in sweat production for a given increase in body temperature. Knowledge of sex-related differences in the physiology of temperature regulation may lead to better improvements in heat exposure guidelines for industrial, military and athletic settings.Abstract It is unclear whether true physiological differences exist in temperature regulation between males and females during exercise, independently of differences in physical characteristics and metabolic heat production. Therefore, we examined differences in the onset threshold and thermosensitivity of whole-body sudomotor activity and cutaneous vascular conductance between males and females matched for body mass and surface area. Nine males and nine females performed 90 min of exercise at each of the following intensities in a warm/dry environment: 50% of maximum oxygen consumption (V O 2 max ) and at a fixed rate of metabolic heat production equal to 500 W. Evaporative heat loss (EHL, direct calorimetry) and cutaneous vascular conductance (CVC, laser-Doppler) were measured continuously. Mean body temperature was calculated from the measurements of oesophageal and mean skin temperatures. During exercise at 50%V O 2 max , a lower rate of sudomotor activity was observed in females (385 ± 12 vs. 512 ± 24 W, P < 0.001). However, irrespective of sex, individual EHL values were strongly associated with metabolic heat production (R 2 = 0.82, P < 0.001). Nonetheless, a lower rate of EHL was observed in females when exercise was performed at 500 W of metabolic heat production (419 ± 7 vs. 454 ± 11 W, P = 0.032). Furthermore, a lower increase in EHL per increase in mean body temperature was observed in females (553 ± 77 vs. 795 ± 85 W• C −1 , P = 0.051), with no differences in the onset threshold (36.77 ± 0.06 vs. 36.61 ± 0.11• C, P = 0.242). In contrast, no differences were observed in CVC. Collectively, these findings demonstrate that females have a lower thermosensitivity of the whole-body sudomotor response compared to males during exercise in the heat performed at a fixed rate of metabolic heat production.

Immersion for approximately 9 minutes to a rectal temperature cooling limit of 38.6°C negated any risk associated with overcooling hyperthermic individuals when they were immersed in 2°C water.

Plasma hyperosmolality and baroreceptor unloading have been shown to independently influence the heat loss responses of sweating and cutaneous vasodilation. However, their combined effects remain unresolved. On four separate occasions, eight males were passively heated with a liquid-conditioned suit to 1.0°C above baseline core temperature during a resting isosmotic state (infusion of 0.9% NaCl saline) with (LBNP) and without (CON) application of lower-body negative pressure (-40 cmH2O) and during a hyperosmotic state (infusion of 3.0% NaCl saline) with (LBNP + HYP) and without (HYP) application of lower-body negative pressure. Forearm sweat rate (ventilated capsule) and skin blood flow (laser-Doppler), as well as core (esophageal) and mean skin temperatures, were measured continuously. Plasma osmolality increased by ∼10 mosmol/kgH2O during HYP and HYP + LBNP conditions, whereas it remained unchanged during CON and LBNP (P ≤ 0.05). The change in mean body temperature (0.8 × core temperature + 0.2 × mean skin temperature) at the onset threshold for increases in cutaneous vascular conductance (CVC) was significantly greater during LBNP (0.56 ± 0.24°C) and HYP (0.69 ± 0.36°C) conditions compared with CON (0.28 ± 0.23°C, P ≤ 0.05). Additionally, the onset threshold for CVC during LBNP + HYP (0.88 ± 0.33°C) was significantly greater than CON and LBNP conditions (P ≤ 0.05). In contrast, onset thresholds for sweating were not different during LBNP (0.50 ± 0.18°C) compared with CON (0.46 ± 0.26°C, P = 0.950) but were elevated (P ≤ 0.05) similarly during HYP (0.91 ± 0.37°C) and LBNP + HYP (0.94 ± 0.40°C). Our findings show an additive effect of hyperosmolality and baroreceptor unloading on the onset threshold for increases in CVC during whole body heat stress. In contrast, the onset threshold for sweating during heat stress was only elevated by hyperosmolality with no effect of the baroreflex.