Background In hot weather, electric fans can potentially provide effective cooling for people, with lower greenhouse gas emissions and cost than air conditioning. However, international public health organisations regularly discourage fan use in temperatures higher than 35°C, despite little evidence. We aimed to determine humidity-dependent temperature thresholds at which electric fans would become detrimental in different age groups.Methods We used biophysical modelling to determine the upper humidity-dependent temperature thresholds at which fan use would become detrimental (ie, worsen heat stress) for healthy young adults (aged 18-40 years), healthy older adults (aged ≥65 years), and older adults taking anticholinergic medication. We also obtained hourly environmental data for the period Jan 1, 2007, to Dec 31, 2019, for 108 populous cities to determine the number of days fan use would be effective for cooling, standardised to a 31-day hot weather month. We established simplified temperature thresholds for future fan use recommendations on the basis of temperatures below which fan use would never have been detrimental between Jan 1, 2007, and Dec 31, 2019, across all prevailing levels of ambient humidity. FindingsAccording to our model, fan use would have been beneficial on 30•0 (96•6%) of 31 hot weather days for healthy young adults and 29•4 (94•9%) of 31 hot weather days for both older adults and older adults taking anticholinergic medication between Jan 1, 2007, and Dec 31, 2019. Adherence to the current WHO recommendation of fan use below temperatures of 35°C only, fan use would have been recommended on 27•2 days (87•7%) of 31 hot weather days. According to our simplified thresholds for fan use (at temperatures <39•0°C for healthy young adults, <38•0°C for healthy older adults, and <37•0°C for older adults taking anticholinergic medication), fan use would have been recommended on 29•6 (95•5%) of 31 hot weather days in healthy young adults, 29•4 (94•8%) days in healthy older adults, and 28•8 (93•0%) days in older adults taking anticholinergic medication between Jan 1, 2007, and Dec 31, 2019. Interpretation Electric fan use, particularly for healthy young adults, would not have worsened heat stress on the majority of study days between 2007 and 2019. Our newly proposed thresholds for fan use provide simple guidelines that improve future heatwave fan use recommendations.

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.

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During heat stress, the skin vasculature can greatly increase conductance secondary to vasodilation. The subsequent increase in skin blood flow allows for convective heat transfer from the core to the skin and between the skin surface and the surrounding environment. Measurement of skin blood flow, therefore, provides valuable information regarding heat exchange between the body and the environment. In addition, assessment of skin blood flow can be used to study vascular control mechanisms. Most often, skin blood flow is measured by venous occlusion plethysmography, Doppler ultrasound, laser-Doppler flowmetry, and, more recently, optical coherence tomography. However, important delimitations to each of these methods, which may be dependent on the research question, must be considered when responses from these approaches are interpreted. In this brief review, we discuss these methods of skin blood flow measurement and highlight potential sources of error and limitations. We also provide recommendations to guide the interpretation of skin blood flow data.

Key points With the advent of more frequent extreme heat events, adaptability to hot environments will be crucial for the survival of many species, including humans. However, the mechanisms that mediate human heat adaptation have remained elusive. We tested the hypothesis that heat acclimation improves the neural control of body temperature. Skin sympathetic nerve activity, comprising the efferent neural signal that activates heat loss thermoeffectors, was measured in healthy adults exposed to passive heat stress before and after a 7 day heat acclimation protocol. Heat acclimation reduced the activation threshold for skin sympathetic nerve activity, leading to an earlier activation of cutaneous vasodilatation and sweat production. These findings demonstrate that heat acclimation improves the neural control of body temperature in humans. Abstract Heat acclimation improves autonomic temperature regulation in humans. However, the mechanisms that mediate human heat adaptation remain poorly understood. The present study tested the hypothesis that heat acclimation improves the neural control of body temperature. Body temperatures, skin sympathetic nerve activity, cutaneous vasodilatation, and sweat production were measured in 14 healthy adults (nine men and five women, aged 27 ± 5 years) during passive heat stress performed before and after a 7 day heat acclimation protocol. Heat acclimation increased whole‐body sweat rate [+0.54 L h–1 (0.32, 0.75), P < 0.01] and reduced resting core temperature [–0.29°C (–0.40, –0.18), P < 0.01]. During passive heat stress, the change in mean body temperature required to activate skin sympathetic nerve activity was reduced [–0.21°C (–0.34, –0.08), P < 0.01] following heat acclimation. The earlier activation of skin sympathetic nerve activity resulted in lower activation thresholds for cutaneous vasodilatation [–0.18°C (–0.35, –0.01), P = 0.04] and local sweat rate [–0.13°C (–0.24, –0.01), P = 0.03]. These results demonstrate that heat acclimation leads to an earlier activation of the neural efferent outflow that activates the heat loss thermoeffectors of cutaneous vasodilatation and sweating.

Cold water ingestion enhanced exercise tolerance of MS participants in the heat by ∼30% despite no differences in Tre, Tsk or HR. These findings support the use of a simple cooling strategy for mitigating heat intolerance with MS and lend insight into the potential role of cold-afferent thermoreceptors that reside in the abdomen and oral cavity in the modulation of exercise tolerance with MS in the heat.

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.

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−1) 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−2·min−1·°C−1; CON, 0.86 ± 0.30 mg·cm−2·min−1·°C−1; 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.