The ventilated capsule technique is widely used to measure time‐dependent changes in sweating in humans. However, evaluations of its reliability (consistency) have been restricted to the forearm, despite extensive regional heterogeneity in the sweating response. Given the importance of such information for experimental design, statistical analysis and interpretation, we determined the reliability of local sweat rate at nine sites during whole‐body passive (resting) heating. On three separate occasions, a water‐perfused suit was used to increase and clamp oesophageal temperature 0.6, 1.2 and 1.8°C above baseline in 14 young men [24 (SD 5) years of age], while sweat rate was measured at the forehead, chest, abdomen, biceps, forearm, hand, quadriceps, calf and foot using ventilated capsules (3.8 cm2). Absolute and relative reliability were determined via the coefficient of variation (CV) and intraclass correlation coefficient (ICC), respectively. At low heat strain (0.6°C), almost all sites had acceptable relative reliability (ICC ≥ 0.70) and moderate absolute reliability (CV < 25%). At moderate heat strain (1.2°C), only the abdomen, hand, quadriceps and foot had acceptable relative reliability, whereas the forehead, abdomen, forearm, hand and quadriceps had moderate absolute reliability. At high heat strain (1.8°C), relative reliability was acceptable at the abdomen, quadriceps, calf and foot, whereas the chest, abdomen, forearm, hand, quadriceps, calf and foot had moderate absolute reliability. Our findings indicate that the measurement site and level of heat strain impact the consistency of local sweat rate measured via the ventilated capsule technique, and we demonstrate the possible implications for research design and data interpretation.

Laser‐Doppler flowmetry (LDF) is commonly used to assess cutaneous vasodilatation responses, but its reliability (i.e. consistency) during whole‐body passive heating is unknown. We therefore assessed the reliability of LDF‐derived indices of cutaneous vasodilatation during incremental whole‐body heating. Fourteen young men (age: 24 (SD 5) years) completed three identical trials, each separated by 1 week. During each trial, a water‐perfused suit was used to raise and clamp oesophageal temperature at 0.6°C (low‐heat strain; LHS) and 1.2°C (moderate‐heat strain; MHS) above baseline. LDF‐derived skin blood flow (SkBF) was measured at three dorsal mid‐forearm sites, with local skin temperature clamped at 34°C. Data were expressed as absolute cutaneous vascular conductance (CVCabs; SkBF/mean arterial pressure) and normalised to maximal conductance (%CVCmax) achieved via simultaneous local skin heating to 44°C and increasing oesophageal temperature to 1.8°C above baseline. Between‐day reliability was characterised as measurement consistency across trials, while within‐day reliability was characterised as measurement consistency across adjacent skin sites during each trial. Between‐ and within‐day absolute reliability (coefficient of variation) generally improved with increasing heat strain, changing from poor (>25%) at baseline, poor‐to‐moderate (15–34%) at LHS, and moderate (10–25%) at MHS. Generally, these estimates were more consistent when expressed as %CVCmax. Conversely, relative reliability was mostly acceptable (intraclass correlation coefficient ≥0.70) during LHS and when data were expressed as CVCabs. These findings indicate that the consistency of LDF‐derived CVC estimates during heat stress depends on the level of heat strain and method of data expression, which should be considered when designing and interpreting experiments.

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Heat shock protein 90 (HSP90) modulates exercise‐induced cutaneous vasodilation in young men via nitric oxide synthase (NOS), but only when core temperature is elevated ~1.0°C. While less is known about modulation of this heat loss response in women during exercise, sex differences may exist. Further, the mechanisms regulating cutaneous vasodilation can differ between exercise‐ and passive‐heat stress. Therefore, in 11 young women (23 ± 3 years), we evaluated whether HSP90 contributes to NOS‐dependent cutaneous vasodilation during exercise (Protocol 1) and passive heating (Protocol 2) and directly compared responses between end‐exercise and a matched core temperature elevation during passive heating. Cutaneous vascular conductance (CVC%max) was measured at four forearm skin sites continuously treated with (a) lactated Ringers solution (control), (b) 178 μM Geldanamycin (HSP90 inhibitor), (c) 10 mM L‐NAME (NOS inhibitor), or (d) combined 178 μM Geldanamycin and 10 mM L‐NAME. Participants completed both protocols during the early follicular (low hormone) phase of the menstrual cycle (0–7 days). Protocol 1: participants rested in the heat (35°C) for 70 min and then performed 50 min of moderate‐intensity cycling (~55% VO2peak) followed by 30 min of recovery. Protocol 2: participants were passively heated to increase rectal temperature by 1.0°C, comparable to end‐exercise. HSP90 inhibition attenuated CVC%max relative to control at end‐exercise (p < .05), but not during passive heating. While NOS inhibition and combined HSP90 + NOS inhibition attenuated CVC%max relative to control for both protocols (all p < .05), they did not differ from each other. We show that HSP90 modulates cutaneous vasodilation NOS‐dependently during exercise in young women, with no effect during passive heating, despite a similar NOS contribution.

New Findings What is the central question of this study?Nitric oxide modulates cutaneous vasodilatation and sweating during exercise‐induced heat stress in young men. However, it remains uncertain whether these effects are reduced in black‐African descendants, who commonly demonstrate reduced nitric oxide bioavailability. Therefore, we assessed whether black‐African descendants display reduced nitric oxide‐dependent cutaneous vasodilatation and sweating compared with Caucasians in these conditions. What is the main finding and its importance?Nitric oxide‐dependent cutaneous vasodilatation and sweating were similar between groups, indicating that reduced nitric oxide bioavailability in black‐African descendants does not attenuate these heat‐loss responses during an exercise‐induced heat stress. Abstract Men of black‐African descent are at an increased risk of heat‐related illness relative to their Caucasian counterparts. This might be attributable, in part, to reduced cutaneous nitric oxide (NO) bioavailability in this population, which might alter local cutaneous vasodilatation and sweating. To evaluate this, we compared these heat‐loss responses in young men (18–30 years of age) of black‐African (n = 10) and Caucasian (n = 10) descent during rest, exercise and recovery in the heat. Participants were matched for physical characteristics and fitness, and they were all born and raised in the same temperate environment (i.e. Canada; second generation and higher). Both groups rested for 10 min and then performed 50 min of moderate‐intensity exercise at 200 W m−2, followed by 30 min of recovery in hot, dry heat (35°C, 20% relative humidity). Local cutaneous vascular conductance (CVC%max) and sweat rate (SR) were measured at two forearm skin sites treated with either lactated Ringer solution (control) or 10 mm NG‐nitro‐l‐arginine methyl ester (l‐NAME, a nitric oxide (NO) synthase inhibitor). l‐NAME significantly reduced CVC%max throughout rest, exercise and recovery in both groups (both P < 0.001). However, there were no significant main effects for the contribution of NO to CVC%max between groups (all P > 0.500). l‐NAME significantly reduced local SR in both groups (both P < 0.050). The contribution of NO to SR was similar between groups such that l‐NAME reduced SR relative to control at 40 and 50 min into exercise (both P < 0.05). We demonstrate that ethnicity per se does not influence NO‐dependent cutaneous vasodilatation and sweating in healthy young men of black‐African and Caucasian descent during exercise in dry heat.