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Total sleep deprivation (TSD) alters local cold tolerance and could thus increase the risk of cold injury. We evaluated the impact of acute caffeine intake, the main countermeasure to TSD‐related deleterious effects, on local cold tolerance before and after TSD. Thirty‐six healthy subjects underwent two TSD protocols (i.e., continuous wakefulness), with randomized crossover intake of acute caffeine or placebo (2.5 mg/kg) administered twice during wakefulness. Before and after 33 h of TSD, finger (index and annular) temperature and skin blood flow were assessed during cold‐water immersion (CWI, 5°C, 20 min) followed by 20 min of rewarming in ambient air. We showed no significant effects of TSD on mean finger temperature during CWI in the placebo condition, but a significant reduction of the minimal temperature (8.86°C ± 0.35°C vs. 8.64°C ± 0.27°C, p = 0.02). During rewarming, we showed a reduction in temperature in the placebo condition (p = 0.02 for the mean temperature and p = 0.03 for the maximal) and an increase in the skin blood flow disparity between fingers at the four points of laser speckle rewarming measurements (p = 0.03). After TSD, acute caffeine intake (vs. placebo) increased mean (+2.11°C ± 0.21°C, p = 0.01) and minimal (+0.61°C ± 0.10°C, p = 0.02) finger temperatures during CWI, and improved rewarming after CWI (mean and maximal temperatures) (+2.28°C ± 0.08°C, p = 0.01, and +2.06°C ± 0.12°C, p = 0.02, respectively). Before TSD, acute caffeine intake significantly increased (vs. placebo) mean temperatures during CWI (p = 0.03) and reduced pain from the onset (p = 0.03) to the end of CWI (p = 0.02) and the first 2 min of rewarming (p = 0.04). There was also a significant main effect of habitual daily caffeine consumption on minimal finger temperatures during CWI, which decreased significantly between 0 and 600 mg consumption (R2 = −0.43, p = 0.01), independently of the effects of day (before and after TSD) and treatment (caffeine and placebo conditions). These findings suggest that acute caffeine intake could be a protective countermeasure to local cold tolerance, particularly during TSD. However, habitual daily caffeine consumption is a factor of individual variability that should be recorded during CWI protocols. Clinical trial NCT03859882. What is the central question of this study? What is the effect of acute caffeine intake on local (finger) cold tolerance before and after total sleep deprivation (TSD)? What is the main finding and its importance? We found that acute caffeine intake (compared with placebo): (1) increased TSD‐related reductions in finger temperature and skin blood flow during rewarming after cold‐water immersion (CWI); and (2) decreased pain during CWI before TSD only. We also evidenced a significant effect of habitual daily caffeine consumption on minimal temperatures during CWI, without an interaction with TSD or acute caffeine intake.

PurposeCold-induced vasodilation (CIVD) is an oscillatory rise in blood flow to glabrous skin that occurs in cold-exposed extremities. Dietary flavanols increase bioavailable nitric oxide, a proposed mediator of CIVD through active vasodilation and/or withdrawal of sympathetic vascular smooth muscle tone. However, no studies have examined the effects of flavanol intake on extremity skin perfusion during cold exposure. We tested the hypothesis that acute and 8-day flavanol supplementation would augment CIVD during single-digit cold water immersion (CWI).MethodsEleven healthy adults (24 ± 6 years; 10 M/1F) ingested cocoa flavanols (900 mg/day) or caffeine- and theobromine-matched placebo for 8 days in a double-blind, randomized, crossover design. On Days 1 and 8, CIVD was assessed 2 h post-treatment. Subjects immersed their 3rd finger in warm water (42 °C) for 15 min before CWI (4 °C) for 30 min, during which nail bed and finger pad skin temperature were measured.ResultsFlavanol ingestion had no effect on CIVD frequency (Day 1, Flavanol: 3 ± 2 vs. Placebo: 3 ± 2; Day 8, Flavanol: 3 ± 2 vs. Placebo: 3 ± 1) or amplitude (Day 1, Flavanol: 4.3 ± 1.7 vs. Placebo: 4.9 ± 2.6 °C; Day 8, Flavanol: 3.9 ± 1.9 vs. Placebo: 3.9 ± 2.0 °C) in the finger pad following acute or 8-day supplementation (P > 0.05). Furthermore, average, nadir, and apex finger pad temperatures during CWI were not different between treatments on Days 1 or 8 of supplementation (P > 0.05). Similarly, no differences in CIVD parameters were observed in the nail bed following supplementation (P > 0.05).ConclusionThese data suggest that cocoa flavanol ingestion does not alter finger CIVD.Clinical Trial Registration Clinicaltrials.gov Identifier: NCT04359082. April 24, 2020.

Thermal comfort is an essential environmental factor related to quality of life and work effectiveness. We assessed the feasibility of wrist skin temperature monitoring for estimating subjective thermal sensation. We invented a wrist band that simultaneously monitors skin temperatures from the wrist (i.e., the radial artery and ulnar artery regions, and upper wrist) and the fingertip. Skin temperatures from eight healthy subjects were acquired while thermal sensation varied. To develop a thermal sensation estimation model, the mean skin temperature, temperature gradient, time differential of the temperatures, and average power of frequency band were calculated. A thermal sensation estimation model using temperatures of the fingertip and wrist showed the highest accuracy (mean root mean square error [RMSE]: 1.26 ± 0.31). An estimation model based on the three wrist skin temperatures showed a slightly better result to the model that used a single fingertip skin temperature (mean RMSE: 1.39 ± 0.18). When a personalized thermal sensation estimation model based on three wrist skin temperatures was used, the mean RMSE was 1.06 ± 0.29, and the correlation coefficient was 0.89. Thermal sensation estimation technology based on wrist skin temperatures, and combined with wearable devices may facilitate intelligent control of one’s thermal environment.

The aim of this investigation was to elucidate the reductions in muscle, skin and core temperature following exposure to -110°C whole body cryotherapy (WBC), and compare these to 8°C cold water immersion (CWI). Twenty active male subjects were randomly assigned to a 4-min exposure of WBC or CWI. A minimum of 7 days later subjects were exposed to the other treatment. Muscle temperature in the right vastus lateralis (n=10); thigh skin (average, maximum and minimum) and rectal temperature (n=10) were recorded before and 60 min after treatment. The greatest reduction (P<0.05) in muscle (mean ± SD; 1 cm: WBC, 1.6 ± 1.2°C; CWI, 2.0 ± 1.0°C; 2 cm: WBC, 1.2 ± 0.7°C; CWI, 1.7 ± 0.9°C; 3 cm: WBC, 1.6 ± 0.6°C; CWI, 1.7 ± 0.5°C) and rectal temperature (WBC, 0.3 ± 0.2°C; CWI, 0.4 ± 0.2°C) were observed 60 min after treatment. The largest reductions in average (WBC, 12.1 ± 1.0°C; CWI, 8.4 ± 0.7°C), minimum (WBC, 13.2 ± 1.4°C; CWI, 8.7 ± 0.7°C) and maximum (WBC, 8.8 ± 2.0°C; CWI, 7.2 ± 1.9°C) skin temperature occurred immediately after both CWI and WBC (P<0.05). Skin temperature was significantly lower (P<0.05) immediately after WBC compared to CWI. The present study demonstrates that a single WBC exposure decreases muscle and core temperature to a similar level of those experienced after CWI. Although both treatments significantly reduced skin temperature, WBC elicited a greater decrease compared to CWI. These data may provide information to clinicians and researchers attempting to optimise WBC and CWI protocols in a clinical or sporting setting.

Cold-stimulated adaptive thermogenesis in brown adipose tissue (BAT) to increase energy expenditure is suggested as a possible therapeutic target for the treatment of obesity. We have recently shown high prevalence of BAT in adult humans, which was inversely related to body mass index (BMI) and body fat percentage (BF%), suggesting that obesity is associated with lower BAT activity. Here, we examined BAT activity in morbidly obese subjects and its role in cold-induced thermogenesis (CIT) after applying a personalized cooling protocol. We hypothesize that morbidly obese subjects show reduced BAT activity upon cold exposure. After applying a personalized cooling protocol for maximal non-shivering conditions, BAT activity was determined using positron-emission tomography and computed tomography (PET-CT). Cold-induced BAT activity was detected in three out of 15 morbidly obese subjects. Combined with results from lean to morbidly obese subjects (n = 39) from previous study, the collective data show a highly significant correlation between BAT activity and body composition (P<0.001), respectively explaining 64% and 60% of the variance in BMI (r = 0.8; P<0.001) and BF% (r = 0.75; P<0.001). Obese individuals demonstrate a blunted CIT combined with low BAT activity. Only in BAT-positive subjects (n = 26) mean energy expenditure was increased significantly upon cold exposure (51.5±6.7 J/s versus 44.0±5.1 J/s, P = 0.001), and the increase was significantly higher compared to BAT-negative subjects (+15.5±8.9% versus +3.6±8.9%, P = 0.001), indicating a role for BAT in CIT in humans. This study shows that in an extremely large range of body compositions, BAT activity is highly correlated with BMI and BF%. BAT-positive subjects showed higher CIT, indicating that BAT is also in humans involved in adaptive thermogenesis. Increasing BAT activity could be a therapeutic target in (morbid) obesity.

Regional variation in sweating over the body is widely recognised. However, most studies only measured a limited number of regions, with the use of differing thermal states across studies making a good meta-analysis to obtain a whole body map problematic. A study was therefore conducted to investigate regional sweat rates (RSR) and distributions over the whole body in male athletes. A modified absorbent technique was used to collect sweat at two exercise intensities [55% (I1) and 75% (I2) ] in moderately warm conditions (25°C, 50% rh, 2 m s −1 air velocity). At I1 and I2, highest sweat rates were observed on the central (upper and mid) and lower back, with values as high as 1,197, 1,148, and 856 g m −2  h −1 , respectively, at I2. Lowest values were observed on the fingers, thumbs, and palms, with values of 144, 254, and 119 g m −2  h −1 , respectively at I2. Sweat mapping of the head demonstrated high sweat rates on the forehead (1,710 g m −2  h −1 at I2) compared with low values on the chin (302 g m −2  h −1 at I2) and cheeks (279 g m −2  h −1 at I2). Sweat rate increased significantly in all regions from the low to high exercise intensity, with exception of the feet and ankles. No significant correlation was present between RSR and regional skin temperature ( T sk ), nor did RSR correspond to known patterns of regional sweat gland density. The present study has provided detailed regional sweat data over the whole body and has demonstrated large intra- and inter-segmental variation and the presence of consistent patterns of regional high versus low sweat rate areas in Caucasians male athletes. This data may have important applications for clothing design, thermophysiological modelling and thermal manikin design.

Afferent neural transmission of temperature sensation from skin thermoreceptors to the central thermoregulatory system is important for the defense of body temperature against environmental thermal challenges. Here, we report a thermosensory pathway that triggers physiological heat-defense responses to elevated environmental temperature. Using in vivo electrophysiological and anatomical approaches in the rat, we found that neurons in the dorsal part of the lateral parabrachial nucleus (LPBd) glutamatergically transmit cutaneous warm signals from spinal somatosensory neurons directly to the thermoregulatory command center, the preoptic area (POA). Intriguingly, these LPBd neurons are located adjacent to another group of neurons that mediate cutaneous cool signaling to the POA. Functional experiments revealed that this LPBd-POA warm sensory pathway is required to elicit autonomic heat-defense responses, such as cutaneous vasodilation, to skin-warming challenges. These findings provide a fundamental framework for understanding the neural circuitry maintaining thermal homeostasis, which is critical to survive severe environmental temperatures.

Photobiomodulation, also referred to as Low-Level Light Therapy (LLLT), has emerged as a promising intervention for pruritus, a prevalent and often distressing symptom. This study investigated the efficacy of low-level light therapy (LLLT) in alleviating pruritus, hyperknesis, and alloknesis induced by histamine and Mucuna pruriens. In a double-blind, randomized, sham-controlled trial with a split-body design, healthy volunteers underwent 6 minutes of LLLT and sham treatments in separate upper back quadrants. The histamine model was applied to the upper quadrants, and Mucuna pruriens to the lower quadrants. Pruritus intensity, alloknesis, hyperknesis, flare area, and skin temperature were measured pre and post treatment. Seventeen individuals (eight females, nine males) participated in the study. In the histamine model, LLLT notably reduced itch intensity (difference = 13.9 (95% CI: 10.5 - 17.4), p = 0.001), alloknesis (difference = 0.80 (95% CI: 0.58-1.02), p = 0.001), and hyperknesis (difference = 0.48 (95% CI: 0.09-0.86), p = 0.01). Skin temperature changes were not significantly different between the two groups (difference = -2.0 (95% CI: -6.7-2.6), p = 0.37). For the Mucuna pruriens model, no significant differences were observed in any measures, including itch intensity (difference = 0.8 (95% CI: -2.3 - 3.8), p = 0.61) hyperknesis (difference = 0.08 (95% CI: -0.06-0.33), p = 0.16) and alloknesis (difference = 0. 0.09 (95% CI: -0.08-0.256), p = 0.27). LLLT effectively reduced histamine-induced pruritus, alloknesis, and hyperknesis; however, LLLT was ineffective against Mucuna pruriens-induced pruritus. Further investigations are required to determine LLLT's effectiveness of LLLT in various pruritus models.

Thermosensory signals may contribute to the sense of body ownership, but their role remains highly debated. We test this assumption within the framework of pathological body ownership, hypothesising that skin temperature and thermoception differ between right-hemisphere stroke patients with and without Disturbed Sensation of Ownership (DSO) for the contralesional plegic upper limb. Patients with DSO exhibit lower basal hand temperatures bilaterally and impaired perception of cold and warm stimuli. Lesion mapping reveals associations in the right Rolandic Operculum and Insula, with these regions linked to lower skin temperature located posterior to those associated with thermoception deficits. Disconnections in bilateral parietal regions are associated with lower hand temperature, while disconnections in a right-lateralized thalamus-parietal hub correlate with thermoception deficits. We discuss the theoretical implications of these findings in the context of the ongoing debate on the role of homeostatic signals in shaping a coherent sense of body ownership. Salvato et al. reveal that thermosensory signals may play a role in bodily self-awareness. Their study on right-brain stroke patients highlights behavioural and neural contribution of temperature and thermoception to disorders of body ownership.

Following the global progressive deployment of 5G networks, considerable attention has focused on assessing their potential impact on human health. This study aims to investigate autonomous nervous system changes by exploring skin temperature and electrodermal activity (EDA) among 44 healthy young individuals of both sexes during and after exposure to 3.5 GHz antenna‐emitted signals, with an electrical field intensity ranging from 1 to 2 V/m. The study employed a randomized, cross‐over design with triple‐blinding, encompassing both ‘real’ and ‘sham’ exposure sessions, separated by a maximum interval of 1 week. Each session comprised baseline, exposure and postexposure phases, resulting in the acquisition of seven runs. Each run initiated with a 150 s segment of EDA recordings stimulated by 10 repeated beeps. Subsequently, the collected data underwent continuous decomposition analysis, generating specific indicators assessed alongside standard metrics such as trough‐to‐peak measurements, global skin conductance and maximum positive peak deflection. Additionally, non‐invasive, real‐time skin temperature measurements were conducted to evaluate specific anatomical points (hand, head and neck). The study suggests that exposure to 3.5 GHz signals may potentially affect head and neck temperature, indicating a slight increase in this parameter. Furthermore, there was a minimal modulation of certain electrodermal metrics after the exposure, suggesting a potentially faster physiological response to auditory stimulation. However, while the results are significant, they remain within the normal physiological range and could be a consequence of an uncontrolled variable. Given the preliminary nature of this pilot study, further research is needed to confirm the effects of 5G exposure. What is the central question of this study? Does autonomous nervous system activity, represented by skin temperature and electrodermal activity, change during and after exposure to 3.5 GHz antenna‐emitted signals typical of 5G mid‐band frequencies? What is the main finding and its importance? Head temperature significantly increased after exposure to 3.5 GHz signals, while neck temperature rose both during and after the exposure. Furthermore, a subtle but significant change in certain electrodermal parameters (CDA. Tonic activity as well as CDA and TTP Lateny) was detected following exposure, suggesting a potentially faster physiological response to auditory stimuli. However, while the findings are noteworthy, they remain within the normal physiological range and could be influenced by an uncontrolled factor.