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Sweat absorbed by clothing forms a moisture film on fabric surfaces, reducing fabric breathability and disrupting thermoregulation during exercise in a hot environment. We investigated whether T‐shirts made from a newly developed fabric with hydrophobic and water‐repellent fibers near the through holes could prevent sweat film formation, thereby enhancing intraclothing microclimate and thermoregulatory responses. Thirteen male runners completed 30‐min treadmill sessions at moderate and high intensities while wearing either the new fabric T‐shirt (Dry Aeroflow, DAF) or a polyester T‐shirt (CONT) at an ambient temperature of 32°C and a relative humidity of 50% with an air velocity of 0.8 m/s. Compared with CONT, intraclothing humidity was decreased on the chest and back, and chest but not back skin temperature was decreased by 2°C in DAF. However, thermoregulatory key variables such as rectal temperature, mean skin temperature, sweat rates, and heart rate did not differ between the T‐shirts. We concluded that the a T‐shirt with enhanced breathability does not affect overall thermoregulatory response during exercise in the heat despite the partial improvements in intraclothing microclimate and in reducing local skin temperature. [ABSTRACT FROM AUTHOR]

Brown adipose tissue (BAT) plays an important role in energy metabolism because it uses fatty acids for thermogenesis during cold exposure. Preclinical studies found that boysenberry anthocyanins (BoyACs) activate BAT. Therefore, the aim of this preliminary study was to evaluate how BoyAC intake affects BAT in humans. We performed an open-label single-arm nonrandomized study in healthy volunteers. Before and after 4 weeks of daily consumption of 100 ml boysenberry juice (BoyJ) containing 61 mg of BoyACs, participants were assessed at 24 °C and then after 1 h of mild cold exposure (18 °C). An infrared thermography camera was used to measure skin surface temperatures in the supraclavicular BAT region (Tscv) and the non-BAT region of the upper chest (Tch). Energy metabolism was measured by indirect calorimetry. For each endpoint, we calculated Δ as the difference between values before and after cold exposure and compared the values before and after BoyJ intake. 10 volunteers participated (age: 36.1 ± 4.1, body mass index (BMI): 20.9 ± 0.6). After BoyJ intake, ΔTscv-ch was significantly higher (p = 0.029), but Δ energy expenditure, Δ fat oxidation, and Δ carbohydrate oxidation were not significantly different. We found a significant positive correlation between BMI and Δfat oxidation with BoyJ intake. The results indicate that 4 weeks of BoyJ intake activates cold-induced thermogenesis in the scv-BAT but does not have a significant effect on energy metabolism. BoyJ intake may increase fat oxidation during cold exposure in individuals with higher BMI. Trial registry number: UMIN000043476, 05/03/2021. [ABSTRACT FROM AUTHOR]

Changes in hydration status occur throughout the day affecting physiological and behavioural functions. However, little is known about the hydration status of free-living Japanese children and the seasonality of this response. We evaluated hydration status estimated by urine osmolality (Uosm) in 349 children (189 boys and 160 girls, 9.5 ± 2.6 years, range: 6–15 years) upon waking at home and during a single school day in spring (April) and summer (July). Further, we assessed the efficacy of employing self-assessment of urine colour (UC; based on an 8-point scale) by children to monitor their hydration status. Early morning Uosm was greater in the spring (903 ± 220 mOsm L−1; n = 326) as compared to summer (800 ± 244 mOsm L−1; n = 125) (P = 0.003, paired t test, n = 104). No differences, however, were observed in Uosm during the school day (P = 0.417, paired t test, n = 32). While 66% and 50% of children were considered underhydrated (Uosm ≥ 800 mOsm L−1) upon waking in the spring and summer periods, respectively, more children were underhydrated (∼12%) during the school day. Self-reported UC was similar between seasons as assessed in the morning and school day (P ≥ 0.101, paired t test), which differed from the pattern of responses observed with Uosm. We showed that a significant number of Japanese children are likely underhydrated especially in the spring period. Children do not detect seasonal changes in hydration from self-assessed UC, limiting its utility to manage hydration status in children. [ABSTRACT FROM AUTHOR]

To determine whether using nicotine exacerbates exertional heat strain through an increased metabolic heat production (Hprod) or decreased skin blood flow (SkBF), 10 nicotine-naïve trained males [37 ± 12 yr; peak oxygen consumption (V̇ o 2peak): 66 ± 10 mL·min−1·kg−1] completed four trials at 20°C and 30°C following overnight transdermal nicotine (7 mg·24 h−1) and placebo use in a crossover, double-blind design. They cycled for 60 min (55% V̇ o 2peak) followed by a time trial (∼75% V̇ o 2peak) during which measures of gastrointestinal (Tgi) and mean weighted skin ( T ¯ sk) temperatures, SkBF, Hprod, and mean arterial pressure (MAP) were made. The difference in ΔTgi between nicotine and placebo trials was greater during 30°C (0.4 ± 0.5°C) than 20°C (0.1 ± 0.7°C), with T ¯ sk higher during nicotine than placebo trials (0.5 ± 0.5°C, P = 0.02). SkBF became progressively lower during nicotine than placebo trials (P = 0.01) and progressively higher during 30°C than 20°C trials (P < 0.01); MAP increased from baseline (P < 0.01) and remained elevated in all trials. The difference in Hprod between 30°C and 20°C trials was lower during nicotine than placebo (P = 0.01) and became progressively higher during 30°C than 20°C trials with exercise duration (P = 0.03). Mean power output during the time trial was lower during 30°C than 20°C trials (24 ± 25 W, P = 0.02), and although no effect of nicotine was observed (P > 0.59), two participants (20%) were unable to complete their 30°C nicotine trials as one reached the ethical limit for Tgi (40.0°C), whereas the other withdrew due to "nausea and chills" (Tgi = 39.7°C). These results demonstrate that nicotine use increases thermal strain and risk of exertional heat exhaustion by reducing SkBF. NEW & NOTEWORTHY: In naïve participants, acute nicotine use exerts a hyperthermic effect that increases the risk of heat exhaustion during exertional heat strain, which is driven by a blunted skin blood flow response. This has implications for 1) populations that face exertional heat strain and demonstrate high nicotine use (e.g., athletes and military, 25%–50%) and 2) study design whereby screening and exclusion for nicotine use or standardization of prior use (e.g., overnight abstinence) is encouraged. [ABSTRACT FROM AUTHOR]

We evaluated changes in hyperhydration and beverage hydration index (BHI, a composite measure of fluid balance after consuming a test beverage relative to water) during resting, induced by the consumption of beverages containing glycerol and sodium supplemented with fast-absorbing sucrose or slow-absorbing isomaltulose. In a randomized crossover, single-blinded protocol (clinical trials registry: UMIN000042644), 14 young physically active adults (three women) consumed 1 L of beverage containing either 7% glycerol + 0.5% sodium (Gly + Na), Gly + Na plus 7% sucrose (Gly + Na + Suc), Gly + Na plus 7% isomaltulose (Gly + Na + Iso), or water (CON) over a 40 min period. We assessed the change in plasma volume (ΔPV), BHI (calculated from cumulative urine output following consumption of water relative to that of the beverage), and blood glucose and sodium for 180 min after initiating ingestion. Total urine volume was reduced in all beverages containing glycerol and sodium compared to CON (all P ≤ 0.002). The addition of isomaltulose increased BHI by ∼45% (3.43 ± 1.0 vs. 2.50 ± 0.7 for Gly + Na, P = 0.011) whereas sucrose did not (2.6 ± 0.6, P = 0.826). The PV expansion was earliest for Gly + Na (30 min), slower for Gly + Na + Suc (90 min), and slowest for Gly + Na + Iso (120 min) with a concomitant lag in the increase of blood glucose and sodium concentrations. Supplementation of beverages containing glycerol and sodium with isomaltulose but not sucrose enhances BHI from those of glycerol and sodium only under a resting state, likely due to the slow absorption of isomaltulose-derived monosaccharides (i.e., glucose and fructose). [ABSTRACT FROM AUTHOR]

Whether high‐intensity exercise training and detraining combined with skeletal muscle pump (MP) could alter the magnitude of postexercise hypotension has not been investigated. We therefore sought to determine whether the combination of MP (unloaded back‐pedaling) with 4 weeks of high‐intensity exercise training and detraining could alter the magnitude of postexercise hypotension. Fourteen healthy men underwent 4 weeks of high‐intensity exercise training (5 consecutive days per week for 15 min per session at 40% of the difference between the gas exchange threshold and maximal oxygen uptake [i.e., Δ40%]) followed by detraining for 4 weeks. Assessments were conducted at Pre‐training (Pre), Post‐training (Post) and after Detraining with (MP) and without MP (Con). The exercise test in the Pre, Post and the Detraining consisted of 15 min exercise at Δ40% followed by 1 h of recovery. At all time‐points, the postexercise reduction in mean arterial pressure (MAP) was reduced in MP compared to Con (all p < 0.01). Four weeks of high‐intensity exercise training resulted in a reduction in the magnitude of postexercise hypotension (i.e., the change in MAP from baseline was mitigated) across both trials (All p < 0.01) when compared to Pre and Detraining. Following Detraining, the reduction of MAP from baseline was reduced compared to Pre, but was not different from Post. We conclude that high‐intensity exercise training combined with skeletal MP reduces the magnitude of postexercise hypotension, and this effect is partially retained for 4 weeks following the complete cessation of high‐intensity exercise training. [ABSTRACT FROM AUTHOR]

With global warming, workers are increasingly exposed to strenuous occupations in hot environments. Given age- and disease-associated declines in thermoregulatory function, older workers are at an elevated risk of developing heat-related injuries. Brain-derived neurotrophic factor (BDNF) is thought to confer neuroprotection during acute exercise, however, the influence of environmental heat on BDNF responses during prolonged work remains unclear. Therefore, we evaluated serum BDNF concentrations before and after 180 min of moderate-intensity treadmill walking (200 W/m2) and after 60 min of post-exercise recovery in temperate (wet-bulb globe temperature (WBGT) 16°C) and hot (WBGT 32°C) environments in 13 healthy young men (mean [SD; 22 [3] years), 12 healthy older men (59 [4] years), 10 men with hypertension (HTN) (60 [4] years), and 9 men with type 2 diabetes (T2D) (60 [5] years). In the temperate condition, all but one participant (1 HTN) completed the 180 min of exercise. While exercise tolerance in the heat was lower in older men with HTN (117 min [45]) and T2D (123 min [42]) compared to healthy older men (159 min [31]) (both p ≤ 0.049), similar end-exercise rectal temperatures (38.9°C [0.4]) were observed across groups, paralleled by similar elevations in serum BDNF across groups at end-exercise (+1106 pg/mL [203]) and end-recovery (+938 pg/mL [146]; all p ≤ 0.01) in the heat. No changes in serum BDNF were observed in the temperate condition. Our findings indicate similar BDNF responses in individuals with HTN or T2D compared to their healthy counterparts, despite exhibiting reduced tolerance to heat. [ABSTRACT FROM AUTHOR]

Hyperthermia increases intravascular adenosine triphosphate (ATP) and is associated with greater hyperthermia‐induced cutaneous vasodilation. Hyperthermia may also increase skin interstitial fluid ATP thereby activating cutaneous vascular smooth muscle cells and sweat glands. We evaluated the hypothesis that whole‐body heating would increase skin interstitial fluid ATP, and this response would be associated with an increase in cutaneous vasodilation and sweating. Nineteen (8 females) young adults underwent whole‐body heating using a water‐perfusion suit to increase core temperature by ~1°C during which time cutaneous vascular conductance (CVC, ratio of laser‐Doppler blood flow to mean arterial pressure) and sweat rate (ventilated capsule technique) were measured at four forearm skin sites to minimize between‐site variations. Dialysate from the skin sites were collected via intradermal microdialysis. Heating increased serum ATP, CVC, and sweat rate (all p ≤ 0.031). However, heating did not modulate dialysate ATP (median, baseline vs. end‐heating: 2.38 vs. 2.70 nmol/ml) (p = 0.068), though the effect size was moderate (Cohen's d = 0.566). While the heating‐induced increase in CVC was not correlated with changes in serum ATP (r = 0.439, p = 0.060), we observed a negative correlation (rs = −0.555, p = 0.017) between dialysate ATP and CVC. We did not observe a significant correlation between the heating‐induced sweating and serum, dialysate, or sweat ATP (rs = 0.091 to −0.322, all p ≥ 0.222). Altogether, we showed that passive heating increases ATP in blood and possibly skin interstitial fluid, with the latter potentially blunting cutaneous vasodilation. However, ATP does not appear to modulate sweating. [ABSTRACT FROM AUTHOR]

Background: With rising temperature extremes, older workers are becoming increasingly vulnerable to heat‐related injuries because of age‐ and disease‐associated decrements in thermoregulatory function. Endothelial monocyte‐activating polypeptide‐II (EMAP‐II) is a proinflammatory cytokine that has not yet been well‐characterized during heat stress, and which may mediate the inflammatory response to high levels of physiological strain. Methods: We evaluated serum EMAP‐II concentrations before and after 180 min of moderate‐intensity work (200 W/m2) in temperate (wet‐bulb globe temperature [WBGT] 16°C) and hot (WBGT 32°C) environments in heat‐unacclimatized, healthy young (n = 13; mean [SD]; 22 [3] years) and older men (n = 12; 59 [4] years), and unacclimatized older men with hypertension (HTN) (n = 10; 60 [4] years) or type 2 diabetes (T2D) (n = 9; 60 [5] years). Core temperature and heart rate were measured continuously. Results: In the hot environment, work tolerance time was lower in older men with HTN and T2D compared to healthy older men (both p < 0.049). While core temperature and heart rate reserve increased significantly (p < 0.001), they did not differ across groups. End‐exercise serum EMAP‐II concentrations were higher in young men relative to their older counterparts due to higher baseline levels (both p ≤ 0.02). Elevations in serum EMAP‐II concentrations were similar between healthy older men and older men with HTN, while serum EMAP‐II concentrations did not change in older men with T2D following prolonged work in the heat. Conclusion: Serum EMAP‐II concentrations increased following prolonged moderate‐intensity work in the heat and this response is influenced by age and the presence of HTN or T2D. [ABSTRACT FROM AUTHOR]

Nitric oxide synthase (NOS) contributes to the heat loss responses of cutaneous vasodilatation and sweating during exercise. However, the contribution of NOS may be attenuated in individuals with uncomplicated, controlled hypertension due to elevated oxidative stress, which can reduce NO bioavailability. We evaluated the hypothesis that the acute local intradermal administration of the antioxidant ascorbate would enhance cutaneous vasodilatation and sweating via NOS-dependent mechanisms during an exercise-heat stress in adults with hypertension. Habitually active adultswho were normotensive (n = 14, 7 females, 62 ± 4 years) or had uncomplicated, controlled hypertension (n=13, 6 females, 62±5 years) performed 30 min of moderate-intensity (50% of their pre-determined peak oxygen uptake) semi-recumbent cycling in the heat (35°C, 20% relative humidity). Cutaneous vascular conductance (CVC) and sweat rate were assessed at four forearm skin sites continuously perfused with (1) lactated Ringer solution (Control), (2) 10 mM antioxidant ascorbate, (3) 10 mM NG-nitro-Larginine methyl ester (L-NAME), a non-selective NOS inhibitor, or (4) a combination of ascorbate and L-NAME. Relative to Control, no effect of ascorbate was observed on CVC or sweating in either group (P = 0.619). However, L-NAME reduced CVC relative to Control in both groups (P = 0.038). No effect of any treatment on sweating was observed (P = 0.306). Thus, acute local administration of ascorbate to forearm skin does not enhance the activation of heat loss responses of cutaneous vasodilatation and sweating in older adults, and those with hypertension during an exercise-heat stress. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study?Does inhibition of K+ channels modulate the exercise‐training‐induced augmentation in cholinergic and thermal sweating?What is the main finding and its importance?Iontophoretic administration of tetraethylammonium, a K+ channel blocker, blunted sweating induced by a low dose (0.001%) of the cholinergic agent pilocarpine, but not heat‐induced sweating. However, no differences in the cholinergic sweating were observed between young endurance‐trained and untrained men. Thus, while K+ channels play a role in the regulation of eccrine sweating, they do not contribute to the increase in sweating commonly observed in endurance‐trained adults. Our findings provide important new insights into the mechanisms underlying the regulation of sweating by endurance conditioning. We evaluated the hypothesis that the activation of K+ channels mediates the exercise‐training‐induced augmentation of cholinergic and thermal sweating. On separate days, 11 endurance‐trained and 10 untrained men participated in two experimental protocols. Prior to each protocol, we administered 2% tetraethylammonium (TEA, K+ channels blocker) and saline (Control) at forearm skin sites on both arms via transdermal iontophoresis. In protocol 1, low (0.001%) and high (1%) doses of pilocarpine were administered at the TEA‐treated and Control sites over a 60‐min period. In protocol 2, participants were passively heated by immersing their lower limbs in hot water (43°C) until core (rectal) temperature (Tc) increased by 0.8°C above resting levels. Administration of TEA attenuated cholinergic sweating (P = 0.001) during the initial 20 min after the treatment of low dose of pilocarpine only whilst the response was similar between the groups (P = 0.163). Cholinergic and thermal sweating were higher in the trained relative to the untrained men (all P ≤ 0.033). Thermal sweating reached ∼90% of the response at a Tc elevation of 0.8°C during the initial 20 min of passive heating, which corresponds to the period wherein TEA attenuated cholinergic sweating in protocol 1. However, sweating did not differ between the Control and TEA sites in either group (P = 0.704). We showed that activation of K+ channels does not appear to mediate the elevated sweating response induced by a low dose of pilocarpine in trained men. We also demonstrated that K+ channels do not contribute to sweating during heat stress in either group. [ABSTRACT FROM AUTHOR]

Temperature elevation due to global warming increases the risks of dehydration, which can induce heat-related illness. Proper rehydration with appropriate amounts of water and electrolytes is essential to aid body fluid homeostasis. Wearable sweat sensors which can monitor both the sweat rate and sweat electrolyte concentration may be an effective tool for determining appropriate rehydration. Here, we developed a novel potentially wearable sensor that can monitor both the local sweat rate and sweat electrolyte concentration continuously. The new device includes a system with a short microfluidic pathway that guides the sweat appearing on the skin to a small space in the device to form a quantifiable droplet. The sweat rate is assessed from the time for the droplet to appear and droplet volume, while an integrated electric sensor detects the sodium chloride concentration in each sweat droplet. We demonstrated that this new device could record both the flow rates of artificial sweat and its sodium chloride concentration in ranges of human sweating with an accuracy within ±10%. This is equivalent to the accuracy of commercially available sweat rate meters and sweat ion sensors. The present study provides a new perspective for the design of wearable sensors that can continuously monitor sweat rates and sweat electrolyte concentrations for potential application to a healthcare device. [ABSTRACT FROM AUTHOR]

Objective: Reports evaluating age‐related impairments in cutaneous vascular function assessed by either the venoarteriolar reflex (VAR) induced by venous congestion, or post‐occlusive reactive hyperemia (PORH) activated by arterial occlusion, have yielded mixed findings. This may be due to region‐specific variability that occurs when assessing local cutaneous vascular responses. We evaluated the hypothesis that aging attenuates VAR and PORH responses in forearm skin assessed across four adjacent sites, each separated by ~4 cm to account for inter‐site variability. Methods: In twenty young (24 ± 4 years, 10 females) and twenty older (60 ± 7 years, 9 females) adults, VAR and PORH were achieved by a 3‐min venous occlusion and 5‐min arterial occlusion, each induced by inflating a pressure cuff to 45 and 240 mmHg, respectively. Cutaneous blood flow at all skin sites was measured by laser‐Doppler flowmetry with the average response from all sites used for between‐group comparisons. Results: VAR and PORH responses were similar between groups with the exception that the time required to achieve peak PORH was delayed in older adults (mean difference of 5.5 ± 4.4 s, p = 0.003, Cohen's d = 0.812). Conclusions: We showed that aging had a negligible influence on VAR and PORH responses in forearm skin even when controlling for region‐specific variability. [ABSTRACT FROM AUTHOR]

The venoarteriolar reflex (VAR) is a local mechanism by which vasoconstriction is mediated in response to venous congestion. This response may minimize tissue overperfusion, preventing capillary damage and oedema. Post‐occlusive reactive hyperaemia (PORH) is used to assess microvascular function by performing a brief local arterial occlusion resulting in a subsequent rapid transient vasodilation. In the current study, we hypothesized that type 2 diabetes (T2D) attenuates VAR and PORH responses in forearm skin in vivo. In 11 healthy older adults (Control, 58 ± 8 years) and 13 older adults with controlled T2D (62 ± 10 years), cutaneous blood flow measured by laser‐Doppler flowmetry was monitored following a 3‐min venous occlusion of 45 mm Hg that elicited the VAR, followed by a 3‐min recovery period and then a 5‐min arterial occlusion of 240 mm Hg that induced PORH. Finally, sodium nitroprusside, a nitric oxide donor, was administered to induce maximum vasodilation. VAR and PORH variables were similar between groups. By contrast, maximal cutaneous blood flow induced by sodium nitroprusside was lower in the T2D group. Taken together, our observations indicate that T2D impairs vascular smooth muscle responsiveness to nitric oxide, but not VAR and PORH in forearm skin. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study?Do sex and menstrual cycle modulate sweating during isometric handgrip exercise and muscle metaboreceptor stimulation?What is the main finding and its importance?Sex modulates sweating during isometric handgrip exercise, as indicated by the lower sweat output per gland in women than in men, but not during muscle metaboreceptor stimulation. Sweat output per gland during isometric handgrip exercise and muscle metaboreceptor stimulation were lower in the mid‐luteal phase than in the early follicular phase in women. Cholinergic sweat gland sensitivity might explain, in part, the individual variation of the response. Our results provide new insights regarding sex‐ and menstrual cycle‐related modulation of the sweating response. We investigated whether sex and menstrual cycle could modulate sweating during isometric handgrip (IH) exercise and muscle metaboreceptor stimulation. Twelve young, healthy women in the early follicular (EF) and mid‐luteal (ML) phases and 14 men underwent two experimental sessions consisting of a 1.5 min IH exercise at 25 and 50% of maximal voluntary contraction (MVC) in a hot environment (35°C, relative humidity 50%) followed by 2 min forearm occlusion to stimulate muscle metaboreceptors. Sweat rates, the number of activated sweat glands and the sweat output per gland (SGO) on the forearm and chest were assessed. Pilocarpine‐induced sweating was also assessed via transdermal iontophoresis to compare the responses with those of IH exercise and muscle metaboreceptor stimulation, based on correlation analysis. Sweat rates on the forearm and chest during IH exercise and muscle metaboreceptor stimulation did not differ between men and women in either menstrual cycle phase (all P ≥ 0.144). However, women in both phases showed lower SGO on the forearm and/or chest compared with men during IH exercise at 50% of MVC, with no differences in muscle metaboreceptor stimulation. Women in the ML phase had a lower forearm sweat rate during IH exercise at 50% of MVC (P = 0.015) and SGO during exercise and muscle metaboreceptor stimulation (main effect, both P ≤ 0.003) compared with those in the EF phase. Overall, sweat rate and SGO during IH exercise and muscle metaboreceptor stimulation were correlated with pilocarpine‐induced responses (all P ≤ 0.064, r ≥ 0.303). We showed that sex and menstrual cycle modulate sudomotor activity during IH exercise and/or muscle metaboreceptor stimulation. Cholinergic sweat gland sensitivity might explain, in part, the individual variation of the response. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study?Does short‐term heat acclimation enhance whole‐body evaporative heat loss and augment nitric oxide synthase (NOS)‐dependent cutaneous vasodilatation and NOS‐ and cyclooxygenase (COX)‐dependent sweating, in exercising older men?What is the main finding and its importance?Our preliminary data (n = 8) demonstrated that short‐term heat acclimation improved whole‐body evaporative heat loss, but it did not influence the effects of NOS and/or COX inhibition on cutaneous vasodilatation or sweating in older men during an exercise–heat stress. These outcomes might imply that although short‐term heat acclimation enhances heat dissipation in older men, it does not modulate NOS‐ and COX‐dependent control of cutaneous vasodilatation or sweating on the forearm. Ageing is associated with decrements in whole‐body heat loss (evaporative + dry heat exchange), which might stem from alterations in nitric oxide synthase (NOS)‐ and cyclooxygenase (COX)‐dependent cutaneous vasodilatation and sweating. We evaluated whether short‐term heat acclimation would (i) enhance whole‐body heat loss primarily by increasing evaporative heat loss, and (ii) augment NOS‐dependent cutaneous vasodilatation and NOS‐ and COX‐dependent sweating, in exercising older men. Eight older men [mean (SD) age, 59 (8) years] completed a calorimetry and microdialysis trial before and after 7 days of exercise–heat acclimation. For the calorimetry trials, whole‐body evaporative and dry heat exchange were assessed using direct calorimetry during 30 min bouts of cycling at light, moderate and vigorous metabolic heat productions (150, 200 and 250 W/m2, respectively) in dry heat (40°C, 20% relative humidity). For the microdialysis trials, local cutaneous vascular conductance and sweat rate were assessed during 60 min exercise in the heat (35°C, 20% relative humidity) at four dorsal forearm skin sites treated with lactated Ringer solution (control), NOS inhibitor, COX inhibitor or combined NOS and COX inhibitors, via microdialysis. Evaporative heat loss during moderate (P = 0.036) and vigorous (P = 0.021) exercise increased after acclimation. Inhibition of NOS alone reduced cutaneous vascular conductance to a similar extent before and after acclimation (P < 0.040), whereas separate and combined NOS and COX inhibition had no significant effects on sweating relative to the control site (P = 0.745). Our preliminary results might suggest that short‐term heat acclimation improves evaporative heat loss, but does not significantly modulate the contributions of NOS or COX to cutaneous vasodilatation or sweating on the forearm in older men during an exercise–heat stress. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question to this study?Do the sweat glands' maximum ion reabsorption rates increase following heat acclimation in healthy older individuals and is this associated with elevated aldosterone concentrations?What is the main finding and its importance?Sweat gland maximum ion reabsorption rates improved heterogeneously across body sites, which occurred without any changes in aldosterone concentration following a controlled hyperthermic heat acclimation protocol in healthy older individuals. We examined whether the eccrine sweat glands' ion reabsorption rates improved following heat acclimation (HA) in older individuals. Ten healthy older adults (>65 years) completed a controlled hyperthermic (+0.9°C rectal temperature, Tre) HA protocol for nine non‐consecutive days. Participants completed a passive heat stress test (lower leg 42°C water submersion) pre‐HA and post‐HA to assess physiological regulation of sweat gland ion reabsorption at the chest, forearm and thigh. The maximum ion reabsorption rate was defined as the inflection point in the slope of the relation between galvanic skin conductance and sweat rate (SR). We explored the responses again after a 7‐day decay. During passive heating, the Tb thresholds for sweat onset on the chest and forearm were lowered after HA (P < 0.05). However, sweat sensitivity (i.e. the slope), the SR at a given Tre and gross sweat loss did not improve after HA (P > 0.05). Any changes observed were lost during the decay. Pilocarpine‐induced sudomotor responses to iontophoresis did not change after HA (P ≥ 0.801). Maximum ion reabsorption rate was only enhanced at the chest (P = 0.001) despite unaltered aldosterone concentration after HA. The data suggest that this adaptation is lost after 7 days' decay. The HA protocol employed in the present study induced partial adaptive sudomotor responses. Eccrine sweat gland ion reabsorption rates improved heterogeneously across the skin sites. It is likely that aldosterone secretion did not alter the chest sweat ion reabsorption rates observed in the older adults. [ABSTRACT FROM AUTHOR]

While human eccrine sweat glands respond to adrenergic agonists, there remains a paucity of information on the factors modulating this response. Thus, we assessed the relative contribution of α‐ and β‐adrenergic sweating during a heat exposure and as a function of individual factors of sex and training status. α‐ and β‐adrenergic sweating was assessed in forty‐eight healthy young men (n = 35) and women (n = 13) including endurance‐trained (n = 12) and untrained men (n = 12) under non–heat exposure (temperate, 25°C; n = 17) and heat exposure (hot, 35°C; n = 48) conditions using transdermal iontophoresis of phenylephrine (α‐adrenergic agonist) and salbutamol (β‐adrenergic agonist) on the ventral forearm, respectively. Adrenergic sweating was also measured after iontophoretic administration of atropine (muscarinic receptor antagonist) or saline (control) to evaluate how changes in muscarinic receptor activity modulate the adrenergic response to a heat exposure (n = 12). α‐ and β‐adrenergic sweating was augmented in hot compared with temperate conditions (both P ≤.014), albeit the relative increase was greater in β (~5.4‐fold)‐ as compared to α (~1.5‐fold)‐adrenergic‐mediated sweating response. However, both α‐ and β‐adrenergic sweating was abolished by atropinization (P =.001). Endurance‐trained men showed an augmentation in α‐ (P =.043) but not β (P =.960)‐adrenergic sweating as compared to untrained men. Finally, a greater α‐ and β‐adrenergic sweating response (both P ≤.001) was measured in habitually active men than in women. We show that heat exposure augments α‐and β‐adrenergic sweating differently via mechanisms associated with altered muscarinic receptor activity. Sex and training status modulate this response. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study?Does the administration of the adrenergic presynaptic release inhibitor bretylium tosylate modulate sweating during exercise in the heat, and does this response differ between habitually trained and untrained men?What is the main finding and its importance?Iontophoretic administration of bretylium tosylate attenuates sweating during exercise in the heat in habitually trained and untrained men. However, a greater reduction occurred in trained men. The findings demonstrate a role for cutaneous adrenergic nerves in the regulation of eccrine sweating during exercise in the heat and highlight a need to advance our understanding of neural control of human eccrine sweat gland activity. We recently reported an influence of cutaneous adrenergic nerves on eccrine sweat production in habitually trained men performing an incremental exercise bout in non‐heat stress conditions. Based on an assumption that increasing heat stress induces cholinergic modulation of sweating, we evaluated the hypothesis that the contribution of cutaneous adrenergic nerves on sweating would be attenuated during exercise in the heat. Twenty young habitually trained and untrained men (n = 10/group) underwent three successive bouts of 15 min of light‐, moderate‐ and vigorous‐intensity cycling (equivalent to 30, 50, and 70% of peak oxygen uptake (V̇O2peak) respectively), each separated by a 15 min recovery while wearing a perfusion suit perfused with warm water (43°C). Sweat rate (ventilated capsule) was measured continuously at two bilateral forearm skin sites treated with 10 mm bretylium tosylate (an inhibitor of neurotransmitter release from adrenergic nerve terminals) and saline (control) via transdermal iontophoresis. A greater sweat rate was measured during vigorous exercise only in trained as compared to untrained men (P = 0.014). In both groups, sweating was reduced at the bretylium tosylate versus control sites, albeit the magnitude of reduction was greater in the trained men (P ≤ 0.024). These results suggest that cutaneous adrenergic nerves modulate sweating during exercise performed under a whole‐body heat stress, albeit a more robust response occurs in trained men. While it is accepted that a cholinergic mechanism plays a primary role in the regulation of sweating during an exercise‐heat stress, our findings highlight the need for additional studies aimed at understanding the neural control of human eccrine sweating. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study?β‐Adrenergic receptor activation modulates cutaneous vasodilatation and sweating in young adults. In this study, we assessed whether age‐related differences in β‐adrenergic regulation of these responses exist and whether they differ between men and women.What is the main finding and its importance?We showed that ageing augmented β‐adrenergic cutaneous vasodilatation, although the pattern of response differed between men and women. Ageing had no effect on β‐adrenergic sweating in men or women. Our findings advance our understanding of age‐related changes in the regulation of cutaneous vasodilatation and sweating and provide new directions for research on the significance of enhanced β‐adrenergic cutaneous vasodilatation in older adults. β‐Adrenergic receptor agonists, such as isoprenaline, can induce cutaneous vasodilatation and sweating in young adults. Given that cutaneous vasodilatation and sweating responses to whole‐body heating and to pharmacological agonists, such as acetylcholine, ATP and nicotine, can differ in older adults, we assessed whether ageing also modulates β‐adrenergic cutaneous vasodilatation and sweating and whether responses differ between men and women. In the context of the latter, prior reports showed that the effects of ageing on cutaneous vasodilatation (evoked with ATP and nicotine) and sweating (stimulated by acetylcholine) were sex dependent. Thus, in the present study, we assessed the role of β‐adrenergic receptor activation on forearm cutaneous vasodilatation and sweating in 11 young men (24 ± 4 years of age), 11 young women (23 ± 5 years of age), 11 older men (61 ± 8 years of age) and 11 older women (60 ± 8 years of age). Initially, a high dose (100 µm) of isoprenaline was administered via intradermal microdialysis for 5 min to induce maximal β‐adrenergic sweating. Approximately 60 min after the washout period, three incremental doses of isoprenaline were administered (1, 10 and 100 µm, each for 25 min) to assess dose‐dependent cutaneous vasodilatation. Isoprenaline‐mediated cutaneous vasodilatation was greater in both older men and older women relative to their young counterparts. Augmented cutaneous vasodilatory responses were observed at 1 and 10 µm in women and at 100 µm in men. Isoprenaline‐mediated sweating was unaffected by ageing, regardless of sex. We show that ageing augments β‐adrenergic cutaneous vasodilatation differently in men and women, without influencing β‐adrenergic sweating. [ABSTRACT FROM AUTHOR]

Purpose: Human eccrine sweat glands respond to α1-adrenergic receptor agonists. We recently reported that adrenergic mechanisms contribute to sweating in endurance-trained men during an incremental exercise to volitional fatigue. However, it remains unclear if this response is mediated by α1-adrenergic receptor activation.Methods: Twelve endurance-trained men performed an incremental cycling bout until exhaustion while wearing a water-perfused suit to clamp skin temperature at ~ 34 °C. Bilateral forearm sweat rates were measured wherein the distal area was treated with either 1% terazosin (α1-adrenergic receptor antagonist) or saline solution on the opposite limb (Control) via transdermal iontophoresis. We also measured proximal bilateral forearm sweat rate in untreated sites to confirm that no between-limb differences in forearm sweat rate occurred. Once sweat rate returned to pre-exercise resting levels at ~ 20 min postexercise, 0.25% phenylephrine (α1-adrenergic receptor agonist) was iontophoretically administered to skin to verify α1-adrenergic receptor blockade.Results: Sweat rates at the proximal untreated right and left forearm sites were similar during exercise (interaction, P = 0.581). Similarly, no effect of terazosin on sweat rate was measured relative to control site (interaction, P = 0.848). Postexercise administration of phenylephrine increased sweat rate at the control site (0.08 ± 0.09 mg cm-2 min-1), which was suppressed by ~ 90% at the terazosin-treated site (0.01 ± 0.02 mg cm-2 min-1) (P = 0.026), confirming that α1-adrenergic receptor blockade was intact.Conclusion: Our findings demonstrate that α1-adrenergic receptors located at eccrine sweat glands do not contribute to eccrine sweating during incremental exercise in young endurance-trained men. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study?Do regional differences exist in nitric oxide synthase (NOS)‐dependent cutaneous vasodilatation and sweating during exercise‐heat stress in young men.What is the main finding and its importance?Exercise‐induced increases in cutaneous vasodilatation and sweating were greater on the chest and upper back compared to the forearm, although the NOS contribution to cutaneous vasodilatation was similar across all regions. Conversely, there was a greater NOS‐dependent rate of change in sweating on the chest compared to the forearm, with a similar trend on the back. While it is established that nitric oxide synthase (NOS) is an important modulator of forearm cutaneous vasodilatation and sweating during an exercise‐heat stress in young men, it remains unclear if regional differences exist in this response. In 15 habitually active young men (24 ± 4 (SD) years), cutaneous vascular conductance (CVC) and local sweat rate (LSR) were assessed at three body regions. On each of the dorsal forearm, chest and upper‐back (trapezius), sites were continuously perfused with either (1) lactated Ringer solution (control) or (2) 10 Mm Nω‐nitro‐l‐arginine (l‐NNA, NOS inhibitor), via microdialysis. Participants rested in the heat (35°C) for ∼75 min, followed by 60 min of semi‐recumbent cycling performed at a fixed rate of heat production of 200 W m−2 (equivalent to ∼42% V̇O2peak). During exercise, the chest and upper‐back regions showed higher CVC and LSR responses relative to the forearm (all P < 0.05). Within each region, l‐NNA attenuated CVC and LSR relative to control (all P < 0.05). However, the NOS contribution was not different across regions for the rate of change and plateau for CVC or for the LSR plateau (all P > 0.05). Conversely, there was a greater NOS contribution to the rate of change for LSR at the chest relative to the forearm (P < 0.05) with a similar trend for the back. In habitually active young men, NOS‐dependent cutaneous vasodilatation was similar across regions while the NOS contribution to LSR was greater on the chest relative to the forearm. These findings advance our understanding of the mechanisms influencing regional variations in cutaneous vasodilatation and sweating during an exercise‐heat stress. [ABSTRACT FROM AUTHOR]

Local skin heating to 42°C causes cutaneous thermal hyperemia largely via nitric oxide (NO) synthase (NOS)-related mechanisms. We assessed the hypothesis that ATP-sensitive K+ (KATP) channels interact with NOS to mediate cutaneous thermal hyperemia. In 13 young adults (6 women, 7 men), cutaneous vascular conductance (CVC) was measured at four intradermal microdialysis sites that were continuously perfused with 1) lactated Ringer solution (control), 2) 5 mM glibenclamide (KATP channel blocker), 3) 20 mM NG-nitro-l-arginine methyl ester (NOS inhibitor), or 4) a combination of KATP channel blocker and NOS inhibitor. Local skin heating to 42°C was administered at all four treatment sites to elicit cutaneous thermal hyperemia. Thirty minutes after the local heating, 1.25 mM pinacidil (KATP channel opener) and subsequently 25 mM sodium nitroprusside (NO donor) were administered to three of the four sites (each 25–30 min). The local heating-induced prolonged elevation in CVC was attenuated by glibenclamide (19%), but the transient initial peak was not. However, glibenclamide had no effect on the prolonged elevation in CVC in the presence of NOS inhibition. Pinacidil caused an elevation in CVC, but this response was abolished at the glibenclamide-treated skin site, demonstrating its effectiveness as a KATP channel blocker. The pinacidil-induced increase in CVC was unaffected by NOS inhibition, whereas the increase in CVC elicited by sodium nitroprusside was partly (15%) inhibited by glibenclamide. In summary, we showed an interactive effect of KATP channels and NOS for the plateau of cutaneous thermal hyperemia. This interplay may reflect a vascular smooth muscle cell KATP channel activation by NO. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study?We evaluated whether regional variations exist in NO‐dependent cutaneous vasodilatation and sweating during cholinergic stimulation.What is the main finding and its importance?Peak cutaneous vasodilatation and sweating were greater on the torso than the forearm. Furthermore, we found that NO was an important modulator of cholinergic cutaneous vasodilatation, but not sweating, across body regions, with a greater contribution of NO to cutaneous vasodilatation in the limb compared with the torso. These findings advance our understanding of the mechanisms influencing regional variations in cutaneous vasodilator and sweating responses to pharmacological stimulation. Regional variations in cutaneous vasodilatation and sweating exist across the body. Nitric oxide (NO) is an important modulator of these heat loss responses in the forearm. However, whether regional differences in NO‐dependent cutaneous vasodilatation and sweating exist remain uncertain. In 14 habitually active young men (23 ± 4 years of age), cutaneous vascular conductance (CVC%max) and local sweat rates were assessed at six skin sites. On each of the dorsal forearm, chest and upper back (trapezius), sites were continuously perfused with either lactated Ringer solution (control) or 10 mm Nω‐nitro‐l‐arginine (l‐NNA; an NO synthase inhibitor) dissolved in Ringer solution, via microdialysis. At all sites, cutaneous vasodilatation and sweating were induced by co‐administration of the cholinergic agonist methacholine (1, 10, 100, 1000 and 2000 mm; 25 min per dose) followed by 50 mm sodium nitroprusside (20–25 min) to induce maximal vasodilatation. The l‐NNA attenuated CVC%max relative to the control conditions for all regions (all P < 0.05), and NO‐dependent vasodilatation was greater at the forearm compared with the back and chest (both P < 0.05). Furthermore, maximal vasodilatation was higher at the back and chest relative to the forearm (both P < 0.05). Conversely, l‐NNA had negligible effects on sweating across the body (all P > 0.05). Peak local sweat rate was higher at the back relative to the forearm (P < 0.05), with a similar trend observed for the chest. In habitually active young men, NO‐dependent cholinergic cutaneous vasodilatation varied across the body, and the contribution to cholinergic sweating was negligible. These findings advance our understanding of the mechanisms influencing regional variations in cutaneous vasodilatation and sweating during pharmacological stimulation. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study?What is the role of nicotinic receptors in the regulation of normothermic cutaneous blood flow and cutaneous vasodilatation and sweating during whole‐body heating induced following resting in a non‐heat‐stress condition?What is the main finding and its importance?Nicotinic receptors modulated cutaneous vascular tone during rest in a non‐heat‐stress condition and in the early stage of heating, but they had a limited role in mediating cutaneous vasodilatation when core temperature increased >0.4°C. Further, the contribution of nicotinic receptors to sweating was negligible during whole‐body heating. Our findings provide new insights into the role of nicotinic receptors in end‐organ function of skin vasculature and sweat glands in humans. Nicotinic receptors are present in human skin including cutaneous vessels and eccrine sweat glands as well as peripheral nerves. We tested the hypothesis that nicotinic receptors do not contribute to the control of cutaneous vascular tone in the normothermic state, but are involved in mediating cutaneous vasodilatation and sweating during a whole‐body passive heat stress in humans. We first performed a nicotinic receptor blocker verification protocol in six young adults (one female) wherein increases in cutaneous vascular conductance and sweating elicited by 10 mm nicotine were blocked by administration of 500 µm hexamethonium to confirm effective blockade. Thereafter, 12 young males participated in a passive heating protocol. After an instrumentation period in a non‐heat‐stress condition, participants rested for a 10 min baseline period. Thereafter, oesophageal temperature was increased by 1.0°C using water‐perfusion suits. Cutaneous vascular conductance, sweat rate, active sweat gland density and sweat output per individual gland were assessed with and without 500 µm hexamethonium administered via intradermal microdialysis. Hexamethonium reduced cutaneous vascular conductance by 22–34% during normothermia and the early stage of heating. However, this effect was diminished as oesophageal temperature increased >0.4°C. Active sweat gland density was reduced by hexamethonium when oesophageal temperature was elevated by 0.4–0.6°C above baseline resting. However, this was paralleled by a marginal increase in sweat gland output. Consequently, sweat rate remained unchanged. We showed that nicotinic receptors modulate cutaneous perfusion during normothermia and the early stage of heating, but not when core temperature increases >0.4°C. Additionally, they play a limited role in mediating sweating during heating. [ABSTRACT FROM AUTHOR]

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. 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 mmNG‐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. [ABSTRACT FROM AUTHOR]