Authorship：Lead author,　Last author,　Corresponding author   Language：English   Publishing type：Research paper (scientific journal)  

The development of an effective transdermal drug delivery protocol to eccrine sweat glands is important for the advancement of research on the human sweating response. We investigated whether microneedle treatment prior to the application of pilocarpine, a hydrophilic and sudorific agent that does not induce sweating due to a limited percutaneous passive diffusion by skin application alone, augments sweat production. We applied three microneedle arrays to forearm skin sites simultaneously (n = 20). Upon removal of the microneedles, 1 % pilocarpine was applied to each site for 5-, 15-, and 30-min for the assessment of sweat gland function. In parallel, pilocarpine was administered by transdermal iontophoresis (5-min) at a separate site. Sweat rate was assessed continuously via the ventilated capsule technique. Pilocarpine augmented sweat rate at the 15- and 30-min periods as compared to the application at 5-min. The sweating responses induced by the 15- and 30-min application of pilocarpine were equivalent to ∼ 80 % of that measured at the iontophoretically treated sites. Notably, we observed a correlation in sweat rate between these two transdermal drug delivery methods. Altogether, our findings show that pre-treatment of microneedle arrays can enhance transdermal delivery efficiency of pilocarpine to human eccrine sweat glands.

DOI： 10.1016/j.ijpharm.2024.124497

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Authorship：Lead author,　Corresponding author   Language：English   Publishing type：Research paper (scientific journal)  

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.

DOI： 10.1139/apnm-2023-0464

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Authorship：Last author,　Corresponding author   Publishing type：Research paper (scientific journal)   Publisher：Wiley  

Abstract

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.

DOI： 10.1002/hfm.21044

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PURPOSE: Sweat glands and cutaneous vessels possess growth hormone (GH) and insulin-like growth factor 1 (IGF-1) receptors. Here, we assessed if exercise increases GH and IGF-1 in skin interstitial fluid, and whether baseline and exercise-induced increases in GH and IGF-1 concentrations in skin interstitial fluid/blood are associated with heat loss responses of sweating and cutaneous vasodilation. METHODS: Sixteen young adults (7 women) performed a 50-min moderate-intensity exercise bout (50% VO2peak) during which skin dialysate and blood samples were collected. In a sub-study (n = 7, 4 women), we administered varying concentrations of GH (0.025-4000 ng/mL) and IGF-1 (0.000256-100 µg/mL) into skin interstitial fluid via intradermal microdialysis. Sweat rate (ventilated capsule) and cutaneous vascular conductance (CVC) were measured continuously for both studies. RESULTS: Exercise increased sweating and CVC (both P < 0.001), paralleled by increases of serum GH and skin dialysate GH and IGF-1 (all P ≤ 0.041) without changes in serum IGF-1. Sweating was positively correlated with baseline dialysate and serum GH levels, as well as exercise-induced increases in serum GH and IGF-1 (all P ≤ 0.044). Increases in CVC were not correlated with any GH and IGF-1 variables. Exogenous administration of GH and IGF-1 did not modulate resting sweat rate and CVC. CONCLUSION: (1) Exercise increases GH and IGF-1 levels in the skin interstitial fluid, (2) exercise-induced sweating is associated with baseline GH in skin interstitial fluid and blood, as well as exercise-induced increases in blood GH and IGF-1, and (3) cutaneous vasodilation during exercise is not associated with GH and IGF-1 in skin interstitial fluid and blood.

DOI： 10.1007/s00421-024-05448-9

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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), fourteen young physically active adults (3 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).

DOI： 10.1139/apnm-2023-0483

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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.

DOI： 10.14814/phy2.15862

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Publishing type：Research paper (scientific journal)   Publisher：Elsevier BV  

DOI： 10.1016/j.jtherbio.2023.103724

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To date, the thermoregulatory response between continuous and intermittent exercises has been investigated whilst limited studies are available to examine the thermoregulatory responses between different modes of intermittent exercises. We sought to determine the effect of two patterns of short duration intermittent exercises (180:180 (3-min) and 30:30 s (30-s) work: rest) on thermoregulatory responses in a temperate environment (25 °C, 50% RH, vapor pressure: 1.6 kPa) with low airflow (0.2 m/s). Twelve male participants (Age:24.0(5.0) year; VO2max: 53(8) mL.kg-1.min-1; BSA:1.7(0.1) m2) cycled at 50% VO2max for 60 min in 3-min and 30-s intervals to result in the same 30-min net exercise duration. Core and skin temperatures, the percent increase of skin blood flow (forearm and chest) from baseline and local sweat rate (forearm and chest) were not different between 3-min and 30-s (all P > 0.35) from the onset of exercise to the end of the exercise. Similarly, the mean body temperature onsets of skin blood flow (forearm and chest) and local sweat rates (forearm and chest) were not different between different mode of intermittent exercises (all P > 0.1). Furthermore, thermal sensitivities of skin blood flow (forearm and chest) and local sweat rate (forearm and chest) with increasing mean body temperature were not different between different mode of intermittent exercises (all P > 0.1). We conclude that intermittent exercises with different work periods at moderate exercise intensity did not alter core temperature and thermoeffector responses in a temperate environment. (241/250).

DOI： 10.1016/j.jtherbio.2023.103750

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Galanin receptor subtypes GAL1, GAL2, and GAL3 are involved in several biological functions. We hypothesized that 1) GAL3 receptor activation contributes to sweating but limits cutaneous vasodilation induced by whole-body and local heating without a contribution of GAL2; and 2) GAL1 receptor activation attenuates both sweating and cutaneous vasodilation during whole-body heating. Young adults underwent whole-body (n = 12, 6 females) and local (n = 10, 4 females) heating. Forearm sweat rate (ventilated capsule) and cutaneous vascular conductance (CVC; ratio of laser-Doppler blood flow to mean arterial pressure) were assessed during whole-body heating (water-perfusion suit circulated with warm (35 °C) water), while CVC was also assessed by local forearm heating (from 33 °C to 39 °C and elevated to 42 °C thereafter; each level of heating maintained for ∼30 min). Sweat rate and CVC were evaluated at four intradermal microdialysis forearm sites treated with either 1) 5% dimethyl sulfoxide (control), 2) M40, a non-selective GAL1 and GAL2 receptor antagonist, 3) M871 to selectively antagonize GAL2 receptor, or 4) SNAP398299 to selectively antagonize GAL3 receptor. Sweating was not modulated by any GAL receptor antagonist (P > 0.169), whereas only M40 reduced CVC (P ≤ 0.003) relative to control during whole-body heating. Relative to control, SNAP398299 augmented the initial and sustained increase in CVC during local heating to 39 °C, and the transient increase at 42 °C (P ≤ 0.028). We confirmed that while none of the galanin receptors modulate sweating during whole-body heating, GAL1 receptors mediate cutaneous vasodilation. Further, GAL3 receptors blunt cutaneous vasodilation during local heating.

DOI： 10.1016/j.ejphar.2023.175904

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Iontophoretic transdermal administration of NG-nitro-l-arginine methyl ester hydrochloride [l-NAME, a nitric oxide synthase (NOS) inhibitor] has been used as a non-invasive evaluation of NOS-dependent mechanisms in human skin. However, the availability has yet to be investigated in sweating research. Prior observations using invasive techniques (e.g., intradermal microdialysis technique) to administer l-NAME have implicated that NOS reduces sweating induced by heat stress but rarely influences the response induced by the administration of cholinergic muscarinic receptor agonists. Therefore, we investigated whether the transdermal iontophoretic administration of l-NAME modulates sweating similar to those prior observations. Twenty young healthy adults (10 males, 10 females) participated in two experimental protocols on separate days. Before each protocol, saline (control) and 1% l-NAME were bilaterally administered to the forearm skin via transdermal iontophoresis. In protocol 1, 0.001% and 1% pilocarpine were iontophoretically administered at l-NAME-treated and untreated sites. In protocol 2, passive heating was applied by immersing the lower limbs in hot water (43 °C) until the rectal temperature increased by 0.8 °C above baseline. The sweat rate was continuously measured throughout both protocols. Pilocarpine-induced sweat rate was not significantly different between the control and l-NAME-treated sites in both pilocarpine concentrations (P ≥ 0.316 for the treatment effect and interaction of treatment and pilocarpine concentration). The sweat rate during passive heating was attenuated at the l-NAME-treated site relative to the control (treatment effect, P = 0.020). Notably, these observations are consistent with prior sweating studies administrating l-NAME into human skin using intradermal microdialysis techniques. Based on the similarity of our results with already known observations, we conclude that transdermal iontophoresis of l-NAME is a valid non-invasive technique for the investigation of the mechanisms of sweating related to NOS during heat stress.

DOI： 10.1016/j.niox.2023.08.001

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Authorship：Lead author,　Corresponding author   Language：English   Publishing type：Research paper (scientific journal)  

Emotional stress-induced sweating in glabrous skin of the palm and sole, which can be excessive in some individuals (hyperhidrosis), can negatively impact quality of life. Understanding the mechanisms underlying this response can lead to potential treatments. Transdermal iontophoresis is a method to administer ionized sudorific agents to sweat glands within the dermis. However, due to the reduced permeability of pharmacological agents in thicker skin such as the palms, this technique has been shown to be less effective when applied in thicker skin. Thus, we assessed the effectiveness of pre-treating palmar skin with microneedles to create micropores on the stratum corneum of the palm to enhance the iontophoretic delivery of pilocarpine to modulate sweat production. On three separate sessions, we applied microneedles (0.78 cm2, 190 needles with a length of 875 μm) to palm and forearm skin sites. Upon removal of the microneedles, we assessed the number of perforations colored by gentian violet in the forearm only (Protocol 1, n = 20), skin barrier function indexed by transepidermal water loss (TEWL) (Protocol 2, n = 21), and sweating induced by the iontophoretic application of 1% pilocarpine (Protocol 3, n = 43). Briefly, we measured 1) ∼172 dyed spots on forearm skin, 2) an increase of ∼300% and ∼ 900% in TEWL on palm and forearm skin, respectively; and 3) a 2-fold increase in sweating on the palm only following the application of the microneedles. Notably, the microneedle array failed to enhance pilocarpine delivery at either the palm or forearm skin sites. We showed the application of a microneedle array enhanced skin permeability and sweat production on the palm without a concomitant increase in pilocarpine delivery. Therefore, this methodology could be employed to advance our understanding of the causes and treatments of medical conditions such as hyperhidrosis.

DOI： 10.1016/j.jconrel.2023.04.044

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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.

DOI： 10.1111/cpf.12825

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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.

DOI： 10.1002/ajim.23477

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Acute dietary nitrate (NO3-) supplementation can increase [NO3-], but not nitrite ([NO2-]), in human skeletal muscle, though its effect on [NO3-] and [NO2-] in skin remains unknown. In an independent group design, 11 young adults ingested 140 mL of NO3--rich beetroot juice (BR; 9.6 mmol NO3-), and 6 young adults ingested 140 mL of a NO3--depleted placebo (PL). Skin dialysate, acquired through intradermal microdialysis, and venous blood samples were collected at baseline and every hour post-ingestion up to 4 h to assess dialysate and plasma [NO3-] and [NO2-]. The relative recovery rate of NO3- and NO2- through the microdialysis probe (73.1% and 62.8%), determined in a separate experiment, was used to estimate skin interstitial [NO3-] and [NO2-]. Baseline [NO3-] was lower, whereas baseline [NO2-] was higher in the skin interstitial fluid relative to plasma (both P < 0.001). Acute BR ingestion increased [NO3-] and [NO2-] in the skin interstitial fluid and plasma (all P < 0.001), with the magnitude being smaller in the skin interstitial fluid (e.g., 183 ± 54 vs. 491 ± 62 μM for Δ[NO3-] from baseline and 155 ± 190 vs. 217 ± 204 nM for Δ[NO2-] from baseline at 3 h post BR ingestion, both P ≤ 0.037). However, due to the aforementioned baseline differences, skin interstitial fluid [NO2-] post BR ingestion was higher, whereas [NO3-] was lower relative to plasma (all P < 0.001). These findings extend our understanding of NO3- and NO2- distribution at rest and indicate that acute BR supplementation increases [NO3-] and [NO2-] in human skin interstitial fluid.

DOI： 10.1016/j.niox.2023.02.003

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Whether whole body heat loss and thermoregulatory function (local sweat rate and skin blood flow) are different between summer and autumn and between autumn and winter seasons during exercise with different air flow in humid heat remain unknown. We therefore tested the hypotheses that whole body sweat rate (WBSR), evaporated sweat rate, and thermoregulatory function during cycling exercise in autumn would be higher than in winter but would be lower than in summer under hot-humid environment (32 C, 75% RH). We also tested the hypothesis that the increase of air velocity would enhance evaporated sweat rate and sweating efficiency across winter, summer, and autumn seasons. Eight males cycled for 1 h at 40% V̇o2max in winter, summer, and autumn seasons. Using an electric fan, air velocity increased from 0.2 m/s to 1.1 m/s during the final 20 min of cycling. The autumn season resulted in a lower WBSR, unevaporated sweat rate, and a higher sweating efficiency compared with summer (all P ≤ 0.05) but WBSR and unevaporated sweat rate in autumn were higher than in winter and thus sweating efficiency was lower when compared with winter only at the air velocity of 0.2 m/s (All P ≤ 0.05). Furthermore, evaporated sweat rate and core temperature (Tcore) were not different among winter, summer, and autumn seasons (All P > 0.19). In conclusion, changes in WBSR across different seasons do not alter Tcore during exercise in a hot humid environment. Furthermore, increasing air velocity enhances evaporated sweat rate and sweating efficiency across all seasons.

DOI： 10.1152/ajpregu.00115.2022

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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.

DOI： 10.1080/23328940.2023.2176107

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PURPOSE: Isomaltulose is a low glycemic and insulinaemic carbohydrate increasingly used as an alternative sweetener in commercial beverages. While isomaltulose beverages can improve hydration status compared to sucrose-based beverages, it remains unclear if ingestion of an isomaltulose beverage prior to exercise in the heat may improve plasma volume (PV) and thermoregulatory responses. METHODS: Twelve endurance-trained men consumed a 1L carbohydrate beverage containing either 6.5%-sucrose (SUC) or 6.5%-isomaltulose (ISO) 60 min prior to 5 successive, 15-min bouts of moderate-intensity (60% of their pre-determined maximum oxygen uptake) in the heat (32 °C, 50% relative humidity), each separated by a 5 min rest. A 6th bout was performed, wherein the participant adjusted running speed to maximize distance covered within the 15-min period. The change (Δ) in PV, heart rate (HR), body core (rectal and gastrointestinal) and skin temperatures, and whole-body sweat loss were assessed during each exercise bout. RESULTS: Ingestion of ISO induced a higher ΔPV at 4th bout only (P < 0.001) and lower HR (P = 0.032, main effect of beverage) during exercise compared to those of SUC. Body core and skin temperatures and whole-body sweat loss did not differ between conditions (all P ≥ 0.192, interaction effect). Running distance covered in final exercise bout tended to increase (~ 5%) in ISO versus SUC (P = 0.057, d = 0.64). CONCLUSIONS: Relative to a sucrose-based beverage, ISO ingestion prior to exercise in the heat reduced cardiovascular strain by preserving PV and attenuating HR, albeit with no corresponding benefit on thermoregulatory function. The former response may facilitate improvements in exercise performance.

DOI： 10.1007/s00421-022-05044-9

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Current labor demographics are changing, with the number of older adults increasingly engaged in physically demanding occupations expected to continually rise, which are often performed in the heat. Given an age-related decline in whole-body heat loss, older adults are at an elevated risk of developing heat injuries that may be exacerbated by hypertension (HTN) and type 2 diabetes (T2D). Elevated irisin production may play a role in mitigating the excess oxidative stress and acute inflammation associated with physically demanding work in the heat. However, the effects of HTN and T2D on this response remain unclear. Therefore, we evaluated serum irisin before and after 3-h of moderate intensity exercise (metabolic rate: 200 W/m2) and at the end of 60-min of post-exercise recovery in a temperate (wet-bulb globe temperature (WBGT) 16 °C) and high-heat stress (WBGT 32 °C) environment in 12 healthy older men (mean ± SD; 59 ± 4 years), 10 men with HTN (60 ± 4 years), and 9 men with T2D (60 ± 5 years). Core temperature (Tco) was measured continuously. In the heat, total exercise duration was significantly lower in older men with HTN and T2D (both, p ≤ 0.049). Despite Tco not being different between groups, Tco was higher in the hot compared to the temperate condition for all groups (p < 0.001). Similarly, serum irisin concentrations did not differ between groups under either condition but were elevated relative to the temperate condition during post-exercise and end-recovery in the heat (+93.9 pg/mL SEM 26 and + 70.5 pg/mL SEM 38 respectively; both p ≤ 0.014). Thus, our findings indicate similar irisin responses in HTN and T2D compared to healthy, age-matched controls, despite reduced exercise tolerance during prolonged exercise in the heat. Therefore, older workers with HTN and T2D may exhibit greater cellular stress during prolonged exercise in the heat, underlying greater vulnerability to heat-induced cellular injury.

DOI： 10.1016/j.jtherbio.2022.103344

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This study aimed to determine whether heat exposure attenuates motor control performance and learning, and blunts cardiovascular and thermoregulatory responses to visuomotor accuracy tracking (VAT) tasks. Twenty-nine healthy young adults (22 males) were divided into two groups performing VAT tasks (5 trials × 10 blocks) in thermoneutral (NEUT: 25 °C, 45% RH, n = 14) and hot (HOT: 35 °C, 45% RH, n = 15) environments (acquisition phase). One block of the VAT task was repeated at 1, 2, and 4 h after the acquisition phase (retention phase). Heat exposure elevated skin temperature to ~3 °C with a marginally increased core body temperature. VAT performance (error distance of curve tracking) was more attenuated overall in HOT than in NEUT in the acquisition phase without improvement in magnitude alteration. Heat exposure did not affect VAT performance in the retention phase. The mean arterial blood pressure and heart rate, but not for sweating and cutaneous vascular responses to VAT acquisition trials, were more attenuated in HOT than in NEUT without any retention phase alternations. We conclude that skin temperature elevation exacerbates motor control performance and blunts cardiovascular response during the motor skill acquisition period. However, these alternations are not sustainable thereafter.

DOI： 10.3390/ijerph191912328

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NEW FINDINGS: What is the central question of this study? Do transmembrane member 16A (TMEM16A) blockers modulate the activation of heat loss responses of sweating and cutaneous vasodilatation? What are the main finding and its importance? Relative to the vehicle control site, TMEM16A blockers T16Ainh-A01 and benzbromarone had no effect on sweat rate or cutaneous vascular conductance during whole-body heating inducing a 1.1 ± 0.1°C increase in core temperature above baseline resting levels. These results suggest that TMEM16A blockers T16Ainh-A01 and benzbromarone do not modulate the regulation of sweating and cutaneous vasodilatation during whole-body heat stress. ABSTRACT: Animal and in vitro studies suggest that transmembrane member 16A (TMEM16A), a Ca2+ -activated Cl- channel, contributes to regulating eccrine sweating. However, direct evidence supporting this possibility in humans is lacking. We assessed the hypothesis that TMEM16A blockers attenuate sweating during whole-body heating in humans. Additionally, we assessed the associated changes in the heat loss response of cutaneous vasodilatation to determine if a functional role of TMEM16A may exist. Twelve young (24 ± 2 years) adults (six females) underwent whole-body heating using a water-perfused suit to raise core temperature 1.1 ± 0.1°C above baseline. Sweat rate and cutaneous vascular conductance (normalized to maximal conductance via administration of sodium nitroprusside) were evaluated continuously at four forearm skin sites treated continuously by intradermal microdialysis with (1) lactated Ringer's solution (control), (2) 5% dimethyl sulfoxide (DMSO) serving as a vehicle control, or (3) TMEM16A blockers 1 mM T16Ainh-A01 or 2 mM benzbromarone dissolved in 5% DMSO solution. All drugs were administered continuously via intradermal microdialysis. Whole-body heating increased core temperature progressively and this was paralleled by an increase in sweat rate and cutaneous vascular conductance at all skin sites. However, sweat rate (all P > 0.318) and cutaneous vascular conductance (all P ≥ 0.073) did not differ between the vehicle control site relative to the TMEM16A blocker-treated sites. Collectively, our findings indicate that TMEM16A blockers T16Ainh-A01 and benzbromarone do not modulate the regulation of sweating and cutaneous vasodilatation during whole-body heating in young adults in vivo.

DOI： 10.1113/EP090521

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NEW FINDINGS: What is the central question of this study? Does acute intradermal administration of the antioxidant ascorbate augment local forearm cutaneous vasodilatation and sweating via nitric oxide synthase (NOS)-dependent mechanisms during exercise-heat stress in older adults with uncomplicated controlled hypertension? What is the main finding and its importance? Relative to control site, ascorbate had no effect on forearm cutaneous vascular conductance (CVC) and sweat rate, although CVC was reduced with NOS-inhibition in older adults with hypertension. We showed that acute local administration of ascorbate to forearm skin does not modulate heat loss responses during exercise-heat stress in older adults with hypertension. ABSTRACT: 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 adults who 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-determine peak oxygen uptake) semi-recumbent cycling in the heat (35°C, 20% relative humidity). Cutaneous vascular conductance and sweat rate were assessed at four forearm skin sites continuously perfused with either: 1) lactated Ringer (Control), 2) 10 mM antioxidant ascorbate, 3) 10 mM 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 cutaneous vascular conductance or sweating in either group (P = 0.619). However, L-NAME reduced cutaneous vascular conductance 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 (236/250 words) This article is protected by copyright. All rights reserved.

DOI： 10.1113/EP090422

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Isomaltulose is a low glycemic and insulinaemic carbohydrate now used as an alternative sweetener in beverages. However, it remains unclear if hydration status may be impacted differently with the consumption of beverages containing isomaltulose as compared to sucrose, a common beverage sweetener. Thirteen young adults (7 women) consumed 1 L of a carbohydrate beverage (with low electrolyte content) containing either 6.5%-sucrose, 6.5%-isomaltulose, or water within a 15 min period. For each beverage, beverage hydration index (BHI, a composite measure of fluid balance after consuming a test beverage relative to water) was calculated from urine volume produced over a 3 h period following ingestion of the carbohydrate beverages relative to water. The change in plasma volume (ΔPV), blood glucose, and lactate concentrations were assessed every 30 min post-beverage consumption. Isomaltulose ingestion attenuated urine production as compared to water and sucrose (P ≤ 0.005) over the 3 h post-ingestion period. However, no differences were observed between sucrose and water (P = 0.055). BHI was 1.53 ± 0.44 for isomaltulose (P ≤ 0.022 vs. sucrose and water) and 1.20±0.29 for sucrose (P = 0.210 vs. water). A transient reduction in ΔPV was observed following the ingestion of the isomaltulose beverage (at 30 min, P = 0.007 vs. sucrose). Thereafter, no differences in ΔPV between beverages were measured. Increases in blood glucose and lactate, indices of absorption and utility of glucose, were delayed in the isomaltulose as compared to sucrose beverage. In summary, we demonstrated a greater BHI with a carbohydrate-electrolyte beverage containing isomaltulose as compared to sucrose. This may in part be attributed to a delayed absorption of isomaltulose reducing diuresis.

DOI： 10.1016/j.physbeh.2022.113770

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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.

DOI： 10.3390/mi13040575

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NEW & NOTEWORTHY: 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 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. ABSTRACT: We evaluated the hypothesis that the activation of K+ channels mediate the exercise-training-induced augmentation in 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, a low (0.001%) and high (1%) doses of pilocarpine was 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 (Tco ) 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 trained relative to the untrained men (all P≤0.033). Thermal sweating reached ∼90% of the response at a Tco elevation of 0.8°C during 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. This article is protected by copyright. All rights reserved.

DOI： 10.1113/EP090251

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ABSTRACT: Transient receptor potential ankyrin 1 (TRPA1) channel activation induces cutaneous vasodilation in humans in vivo. However, the mechanisms underlying this response remains equivocal. We hypothesized that nitric oxide synthase (NOS) and Ca2+ activated K+ (KCa) channels contribute to the TRPA1 channel-induced cutaneous vasodilation with no involvement of cyclooxygenase (COX). Cutaneous vascular conductance (CVC) in 9 healthy young adults was assessed at 4 dorsal forearm skin sites treated by intradermal microdialysis with (1) 1.985% dimethyl sulfoxide + 0.015% lactated Ringer solution with propylene glycol (vehicle control), (2) 10 mM l-NAME, a nonselective NOS inhibitor, (3) 10 mM ketorolac, a nonselective COX inhibitor, or (4) 50 mM tetraethylammonium, a nonselective KCa channel blocker. Cinnamaldehyde, a TRPA1 channel activator, was administered to each skin site in a dose-dependent manner (2.9%, 8.8%, 26%, and 80%, each lasting ≥30 minutes). Administration of ≥8.8% cinnamaldehyde increased CVC from baseline at the vehicle control site by as much as 27.4% (95% confidence interval of 5.3; P < 0.001). NOS inhibitor attenuated the cinnamaldehyde-induced increases in CVC at the 8.8%, 26%, and 80% concentrations relative to the vehicle control site (all P ≤ 0.05). In contrast, both the COX inhibitor and KCa channel blockers did not attenuate the cinnamaldehyde induced-increases in CVC relative to the vehicle control site for all concentrations (all P ≥ 0.130). We conclude that in human skin in vivo, NOS plays a role in modulating the regulation of cutaneous vasodilation in response to TRPA1 channel activation with no detectable contributions of COX and KCa channels.

DOI： 10.1097/FJC.0000000000001188

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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.

DOI： 10.1111/micc.12743

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We investigated the influence of exercise intensities and regional differences in the sudomotor recruitment pattern in boys. Six prepubertal boys (age 11 ± 1 yr) cycled at light, moderate, and high exercise intensity (35%, 50%, and 65% VO2max) for 30 min in a temperate condition (28 °C, 40% relative humidity). Local sweat rate (ventilated capsule) and number of activated sweat glands (starch-iodine technique) at five body sites were assessed and sweat gland output was calculated. Responses in boys were compared with those in nine young men (23 ± 1 yr) tested under identical conditions. The forehead, chest, back, and forearm, but not thigh, sweat rate increased from light to moderate and at high intensities in boys (all p ≤ 0.005) but not from moderate to high (all p ≥ 0.071). The sweat rate on the forehead was relatively higher (p ≤ 0.045) and thigh was lower (p ≤ 0.050) than other sites in boys at moderate and high intensities. Exercise intensity-dependent sweating was associated with activating more sweat glands but not increasing glandular output in boys. The sweat rate in boys was attenuated versus men heterogeneously across body sites concurrent to low glandular outputs (all p ≤ 0.027). We conclude that exercise intensity modulates the sweat rate in boys by changing the number of activated sweat glands heterogeneously among skin sites. Age-related differences in the sudomotor pattern are evident at higher exercise intensities. Development of glandular output per gland occurring from boys to young men may play a key role in modulating sweat rate with respect to exercise intensity and regional differences.

DOI： 10.1016/j.physbeh.2021.113642

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Na+-K+-ATPase is integrally involved in mediating cutaneous vasodilation during an exercise-heat stress, which includes an interactive role with nitric oxide synthase (NOS). Here, we assessed if Na+-K+-ATPase also contributes to cutaneous thermal hyperemia induced by local skin heating, which is commonly used to assess cutaneous endothelium-dependent vasodilation. Furthermore, we assessed the extent to which NOS contributes to this response. Cutaneous vascular conductance (CVC) was measured continuously at four forearm skin sites in 11 young adults (4 women). After baseline measurement, local skin temperature was increased from 33°C to 39°C to induce cutaneous thermal hyperemia. Once a plateau in CVC was achieved, each skin site was continuously perfused via intradermal microdialysis with either: 1) lactated Ringer solution (control), 2) 6 mM ouabain, a Na+-K+-ATPase inhibitor, 3) 20 mM l-NAME, a NOS inhibitor, or 4) a combination of both. Relative to the control site, CVC during the plateau phase of cutaneous thermal hyperemia (∼50% max) was reduced by the lone inhibition of Na+-K+-ATPase (-19 ± 8% max, P = 0.038) and NOS (-32 ± 4% max, P < 0.001), as well as the combined inhibition of both (-37 ± 9% max, P < 0.001). The magnitude of reduction was similar between NOS inhibition alone and combined inhibition (P = 1.000). The administration of both Na+-K+-ATPase and NOS inhibitors fully abolished the plateau of CVC with values returning to preheating baseline values (P = 0.439). We show that Na+-K+-ATPase contributes to cutaneous thermal hyperemia during local skin heating to 39°C, and this response is partially mediated by NOS.NEW & NOTEWORTHY Cutaneous thermal hyperemia during local skin heating to 39°C, which is highly dependent on nitric oxide synthase (NOS), is frequently used to assess endothelium-dependent cutaneous vasodilation. We showed that Na+-K+-ATPase mediates the regulation of cutaneous thermal hyperemia partly via NOS-dependent mechanisms although a component of the Na+-K+-ATPase modulation of cutaneous thermal hyperemia is NOS independent. Thus, as with NOS, Na+-K+-ATPase may be important in the regulation of cutaneous endothelial vascular function.

DOI： 10.1152/japplphysiol.00073.2021

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PURPOSE: We examined whether eccrine sweat glands ion reabsorption rate declined with age in 35 adults aged 50-84 years. Aerobic fitness (VO2max) and salivary aldosterone were measured to see if they modulated ion reabsorption rates. METHODS: During a passive heating protocol (lower leg 42 °C water submersion) the maximum ion reabsorption rates from the chest, forearm and thigh were measured, alongside other thermophysiological responses. The maximum ion reabsorption rate was defined as the inflection point in the slope of the relation between galvanic skin conductance and sweat rate. RESULTS: The maximum ion reabsorption rate at the forearm, chest and thigh (0.29 ± 0.16, 0.33 ± 0.15, 0.18 ± 0.16 mg/cm2/min, respectively) were weakly correlated with age (r ≤  - 0.232, P ≥ 0.05) and salivary aldosterone concentrations (r ≤  - 0.180, P ≥ 0.179). A moderate positive correlation was observed between maximum ion reabsorption rate at the thigh and VO2max (r = 0.384, P = 0.015). Salivary aldosterone concentration moderately declined with age (r =  - 0.342, P = 0.021). Whole body sweat rate and pilocarpine-induced sudomotor responses to iontophoresis increased with VO2max (r ≥ 0.323, P ≤ 0.027) but only moderate (r =  - 0.326, P = 0.032) or no relations (r ≤  - 0.113, P ≥ 0.256) were observed with age. CONCLUSION: The eccrine sweat glands' maximum ion reabsorption rate is not affected by age, spanning 50-84 years. Aldosterone concentration in an aged cohort does not appear to modulate the ion reabsorption rate. We provide further support for maintaining cardiorespiratory fitness to attenuate any decline in sudomotor function.

DOI： 10.1007/s00421-021-04766-6

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Measurement error(s) of exercise tests for women are severely lacking in the literature. The purpose of this investigation was to 1) determine whether ovulatory status or ambient environment were moderating variables when completing a 30-min self-paced work trial, and 2) provide test-retest norms specific to athletic women. A retrospective analysis of three heat stress studies was completed using 33 female participants (31±9 y, 54±10 mL min-1 kg-1) that yielded 130 separate trials. Participants were classified as ovulatory (n=19), anovulatory and/or luteal phase-deficient (n=4) and oral contraceptive pill users (n=10). Participants completed trials ~2 weeks apart in their (quasi-) early follicular and mid-luteal phases in two of moderate (1.3±0.1 kPa, 20.5±0.5 °C, 18 trials), warm-dry (2.2±0.2 kPa, 34.1±0.2 °C, 46 trials) or warm-humid (3.4±0.1 kPa, 30.2±1.1 °C, 66 trials) environments. We quantified reliability using limits of agreement, intraclass correlation coefficient (ICC), Pearson's correlation coefficient (r), standard error of measurement (SEM) and coefficient of variation (CV). Test-retest reliability was high, clinically-valid (ICC=0.90, r=0.83, both p<0.01) and acceptable with a mean CV of 4.7%, SEM of 3.8 kJ (2.1 W) and reliable bias of -2.1 kJ (-1.2 W). The various ovulatory status and contrasting ambient conditions had no appreciable effect on reliability. These results indicate that athletic women can perform 30-min self-paced work trials ~2 weeks apart with an acceptable and low variability irrespective of their hormonal status or heat-stressful environments.

DOI： 10.1152/japplphysiol.00342.2021

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Seasonal acclimatization from winter to summer is known to enhance thermoeffector responses in hot-dry environments during exercise whilst its impact on sweat evaporation and core temperature (Tcore) responses in hot-humid environments remains unknown. We therefore sought to determine whether seasonal acclimatization is able to modulate whole-body sweat rate (WBSR), evaporated sweat rate, sweating efficiency and thermoregulatory function during cycling exercise in a hot-humid environment (32∘C, 75% RH). We also determined whether the increase in air-velocity, could enhance evaporated sweat rate and sweating efficiency before and after seasonal acclimatization. Twelve males cycled for 1-hour at 40% VO2max in winter (pre-acclimatization) and repeated the trial again in summer (after-acclimatization). For the last 20-min of cycling at a steady-state of Tcore, air-velocity increased from 0.2 (0.04) m/s to 1.1 (0.02) m/s by using an electric fan located in front of the participant. Seasonal acclimatization enhanced WBSR, unevaporated sweat rate, local sweat rate and mean skin temperature compared to pre-acclimatization state (all P<0.05) whilst sweating efficiency was lower (P<0.01) until the 55-min of exercise. Tcore and evaporated sweat rate were unaltered by acclimatization status (all P>0.70). In conclusion, seasonal acclimatization enhances thermoeffector responses but does not attenuate Tcore during exercise in a hot-humid environment. Furthermore, increasing air-velocity enhances evaporated sweat rate and sweating efficiency irrespective of acclimated state.

DOI： 10.1152/japplphysiol.00837.2020

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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. ABSTRACT: 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.

DOI： 10.1113/EP089464

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PURPOSE: Isomaltulose is a low glycemic and insulinaemic carbohydrate available as a constituent in sports drink. However, it remains unclear whether postexercise rehydration achieved by isomaltulose drink ingestion alone differs as compared to other carbohydrates. METHODS: Thirteen young men performed intermittent exercise in the heat (35 °C and relative humidity 40%) to induce a state of hypohydration as defined by a 2% loss in body mass. Thereafter, participants were rehydrated by ingesting drinks equal to the volume of body mass loss with either a mixture of 3.25% glucose and 3.25% fructose, 6.5% sucrose (SUC), or 6.5% isomaltulose (ISO) within the first 30 min of a 3-h recovery. The change in plasma volume (ΔPV) from pre-exercise baseline, blood glucose, and plasma insulin concentration were assessed every 30-min. RESULTS: ΔPV was lower in ISO as compared to SUC until 90 min of the recovery (all P ≤ 0.038) with no difference thereafter (all P ≥ 0.391). The ΔPV were paralleled by concomitant changes in blood glucose levels that were greater in ISO as compared to other drinks after 90 min of the recovery (all P ≤ 0.035). Plasma insulin secretion, which potentially enhances renal sodium reabsorption and fluid retention, did not differ between the trials (interaction, P = 0.653). ISO induced a greater net fluid volume retention as compared to SUC (P = 0.010). CONCLUSION: We showed that rehydration with an isomaltulose drink following exercise-heat stress induces comparable recovery of PV and a greater net fluid retention as compared to other drinks, albeit this response is delayed. The delayed water transport along with glucose absorption may modulate this response. This trial was registered in 25th Sep 2019 at https://www.umin.ac.jp/ as UMIN000038099. (249/250).

DOI： 10.1007/s00394-021-02614-z

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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.

DOI： 10.1111/exd.14408

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Isomaltulose is a low glycemic and insulinemic carbohydrate available as a constituent of sports drinks. However, it remains unclear whether thermoregulatory responses (sweating and cutaneous vasodilation) after isomaltulose drink ingestion differ from those of sucrose and water during exercise in a hot environment. Ten young healthy males consumed 10% sucrose, 10% isomaltulose, or water drinks. Thirty-five minutes after ingestion, they cycled for fifteen minutes at 75% peak oxygen uptake in a hot environment (30 °C, 40% relative humidity). Sucrose ingestion induced greater blood glucose concentration and insulin secretion at the pre-exercise state, compared with isomaltulose and/or water trials, with no differences during exercise in blood glucose. Change in plasma volume did not differ between the three trials throughout the experiment, but both sucrose and isomaltulose ingestions similarly increased plasma osmolality, as compared with water (main beverage effect, p = 0.040)-a key response that potentially delays the onset of heat loss responses. However, core temperature thresholds and slopes for heat loss responses were not different between the trials during exercise. These results suggest that ingestion of isomaltulose beverages induces low glycemic and insulinemic states before exercise but does not alter thermoregulatory responses during exercise in a hot environment, compared with sucrose or water.

DOI： 10.3390/ijerph18115760

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Transient receptor potential vanilloid 4 (TRPV4) channels exist on vascular endothelial cells and eccrine sweat gland secretory cells in human skin. Here, we assessed whether TRPV4 channels contribute to cutaneous vasodilation and sweating during whole body passive heat stress (protocol 1) and to cutaneous vasodilation during postocclusive reactive hyperemia and local thermal hyperemia (protocol 2). Intradermal microdialysis was employed to locally deliver pharmacological agents to forearm skin sites, where cutaneous vascular conductance (CVC) and sweat rate were assessed. In protocol 1 (12 young adults), CVC and sweat rate were increased by passive whole body heating, resulting in a body core temperature elevation of 1.2 ± 0.1°C. The elevated CVC and sweat rate assessed at sites treated with TRPV4 channel antagonist (either 200 µM HC-067047 or 125 µM GSK2193874) were not different from the vehicle control site (5% dimethyl sulfoxide). After whole body heating, the TRPV4 channel agonist (100 µM GSK1016790A) was administered to each skin site, eliciting elevations in CVC. Relative to control, this response was partly attenuated by both TRPV4 channel antagonists, confirming drug efficacy. In protocol 2 (10 young adults), CVC was increased following a 5-min arterial occlusion and during local heating from 33 to 42°C. These responses did not differ between the control and the TRPV4 channel antagonist sites (200 µM HC-067047). We show that TRPV4 channels are not required for regulating cutaneous vasodilation or sweating during a whole body passive heat stress. Furthermore, they are not required for regulating cutaneous vasodilation during postocclusive reactive hyperemia and local thermal hyperemia.

DOI： 10.1152/ajpregu.00123.2020

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INTRODUCTION: Caffeine is an exercise performance enhancer widely used by individuals engaged in training or competition under heat-stressed conditions. Caffeine ingestion during exercise in the heat is believed to be safe because it does not greatly affect body temperature responses, heart rate, or body fluid status. However, it remains unknown whether caffeine affects hyperthermia-induced hyperventilation or reductions in the cerebral blood flow index. We tested the hypothesis that under conditions inducing severe hyperthermia, caffeine exacerbates hyperthermia-induced hyperventilation and reduces the cerebral blood flow index during exercise. METHODS: Using a randomized, single-blind, crossover design, 12 physically active healthy young men (23 ± 2 yr) consumed a moderate dose of caffeine (5 mg·kg-1) or placebo in the heat (37°C). Approximately 60 min after the ingestion, they cycled for ~45 min at a workload equal to ~55% of their predetermined peak oxygen uptake (moderate intensity) until their core temperature increased to 2.0°C above its preexercise baseline level. RESULTS: In both trials, ventilation increased and the cerebral blood flow index assessed by middle cerebral artery mean blood velocity decreased as core temperature rose during exercise (P < 0.05), indicating that hyperthermia-induced hyperventilation and lowering of the cerebral blood flow occurred. When core temperature was elevated by 1.5°C or more (P < 0.05), ventilation was higher and the cerebral blood flow was lower throughout the caffeine trial than the placebo trial (P < 0.05). CONCLUSIONS: A moderate dose of caffeine exacerbates hyperthermia-induced hyperventilation and reductions in the cerebral blood flow index during exercise in the heat with severe hyperthermia.

DOI： 10.1249/MSS.0000000000002537

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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. ABSTRACT: 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.

DOI： 10.1113/EP089025

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Authorship：Lead author,　Corresponding author   Language：English   Publishing type：Research paper (scientific journal)  

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.

DOI： 10.1111/exd.14208

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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 glands 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. ABSTRACT: We examined whether the eccrine sweat glands ion reabsorption rates improved following heat acclimation (HA) in older individuals. Ten healthy older adults (>65 yrs) completed a controlled hyperthermic (+0.9˚C rectal temperature, Tre ) HA protocol for 9 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 glands ions 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, neither sweat sensitivity (i.e. the slope), the SR at a given Tre , nor gross sweat loss improved 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 suggests that this adaptation is lost after 7-days decay. The HA protocol employed in the present study induced partial adaptive sudomotor responses. Eccrine sweat glands 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. This article is protected by copyright. All rights reserved.

DOI： 10.1113/EP088486

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Authorship：Lead author,　Corresponding author   Language：English   Publishing type：Research paper (scientific journal)  

We evaluated the hypothesis that the activation of L-type voltage-gated Ca2+ channels contribute to exercise training-induced augmentation in cholinergic sweating. On separate days, 10 habitually trained and 10 untrained men participated in two experimental protocols. Prior to each protocol, we administered 1% verapamil (Verapamil, L-type voltage-gated Ca2+ channel blocker) and saline (Control) at forearm skin sites on both arms via transdermal iontophoresis. In Protocol 1, we administered low (0.001%) and high (1%) doses of pilocarpine at both the verapamil-treated and untreated forearm sites. In protocol 2, participants were passively heated by immersing their limbs in hot water (43°C) until rectal temperature increased by 1.0°C above baseline resting levels. Sweat rate at all forearm sites were continuously measured throughout both protocols. Pilocarpine-induced sweating in Control was higher in trained than in untrained men for both concentrations of pilocarpine (both P≤0.001). Pilocarpine-induced sweating at the low dose site was attenuated at the Verapamil versus Control site in both groups (both P≤0.004), albeit the reduction was greater in trained as compared to untrained men (P=0.005). The verapamil-mediated reduction in sweating remained intact at the high dose pilocarpine site in the untrained (P=0.004) but not the trained men (P=0.180). Sweating did not differ between Control and Verapamil sites with increases in rectal temperature in both groups (interaction, P=0.571). We show that activation of L-type voltage-gated Ca2+ channels modulates sweat production in habitually trained men induced by a low dose of pilocarpine. However, no effect on sweating was observed during passive heating in either group.

DOI： 10.1152/ajpregu.00167.2020

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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. ABSTRACT: 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.

DOI： 10.1113/EP088583

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Authorship：Lead author,　Corresponding author   Language：English   Publishing type：Research paper (scientific journal)  

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. ABSTRACT: 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 (


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) 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.

DOI： 10.1113/EP088797

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Authorship：Lead author,　Corresponding author   Language：English   Publishing type：Research paper (scientific journal)  

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.

DOI： 10.1007/s00421-020-04351-3

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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. ABSTRACT: 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%


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). 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.

DOI： 10.1113/EP088388

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Authorship：Last author,　Corresponding author   Language：English   Publishing type：Research paper (scientific journal)  

Food ingestion has been shown to affect thermoregulation during exercise, while the impact of protein degradant consumption remains unclear. We investigated the effects of casein hydrolysate ingestion on thermoregulatory responses during exercise in the heat. In a randomized, placebo-controlled, double-blind, crossover trial, five men and five women consumed either 5 g of casein hydrolysate or placebo. Thirty minutes after ingestion, participants cycled at 60% VO2max until voluntary exhaustion wearing a hot-water (43 °C) circulation suit. Exercise time to exhaustion, body core temperature, forearm sweat rate, and forearm cutaneous vascular conductance did not differ different between the conditions. However, chest sweat rate and mean skin temperature increased upon casein hydrolysate ingestion compared with placebo during exercise. Increased chest sweat rate upon casein hydrolysate ingestion was associated with elevated sudomotor sensitivity to increasing body core temperature, but not the temperature threshold for initiating sweating. A positive correlation was found between chest sweat rate and plasma total amino acid concentration during exercise. These results suggest that casein hydrolysate ingestion enhances sweating heterogeneously by increasing peripheral sensitivity of the chest's sweating mechanism and elevating skin temperature during exercise in the heat. However, the physiological link between plasma amino acid concentration and sweat rate remains unclear.

DOI： 10.3390/nu12030867

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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.

DOI： 10.1152/ajpregu.00176.2019

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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. ABSTRACT: 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.

DOI： 10.1113/EP088295

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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. ABSTRACT: 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.

DOI： 10.1113/EP088072

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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.

DOI： 10.1113/EP088115

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Language：Japanese   Publisher：日本生理人類学会  

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Language：Japanese   Publisher：日本生理人類学会  

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Authorship：Lead author,　Corresponding author   Language：English   Publishing type：Research paper (scientific journal)  

NEW FINDINGS: What is the central question of this study? What are the effects of isomaltulose, an ingredient in carbohydrate-electrolyte beverages to maintain glycaemia and attenuate the risk of dehydration during exercise heat stress, on postexercise rehydration and physiological heat loss responses? What is the main finding and its importance? Consumption of a 6.5% isomaltulose-electrolyte beverage following exercise heat stress restored hydration following a 2 h recovery as compared to a 2% solution or water only. While the 6.5% isomaltulose-electrolytes increased plasma volume and plasma osmolality, which are known to modulate postexercise heat loss, sweating and cutaneous vascular responses did not differ between conditions. Consequently, ingestion beverages containing 6.5% isomaltulose-electrolytes enhanced postexercise rehydration without affecting heat loss responses. ABSTRACT: Isomaltulose is a disaccharide carbohydrate widely used during exercise to maintain glycaemia and hydration. We investigated the effects of ingesting a beverage containing isomaltulose and electrolytes on postexercise hydration state and physiological heat loss responses. In a randomized, single-blind cross-over design, 10 young healthy men were hypohydrated by performing up to three 30 min successive moderate-intensity (50% heart rate reserve) bouts of cycling, each separated by 10 min, while wearing a water-perfusion suit heated to 45°C. The protocol continued until a 2% reduction in body mass was achieved. Thereafter, participants performed a final 15 min moderate-intensity exercise bout followed by a 2 h recovery. Following cessation of exercise, participants ingested a beverage consisting of (i) water only (Water), (ii) 2% isomaltulose (CHO-2%), or (iii) 6.5% isomaltulose (CHO-6.5%) equal to the volume of 2% body mass loss within the first 30 min of the recovery. Changes in plasma volume (ΔPV) after fluid ingestion were greater for CHO-6.5% compared with CHO-2% (120 min postexercise) and Water (90 and 120 min) (all P ≤ 0.040). Plasma osmolality remained elevated with CHO-6.5% compared with consumption of the other beverages at 30 and 90 min postexercise (all P ≤ 0.050). Urine output tended to be reduced with CHO-6.5% compared to other fluid conditions (main effect, P = 0.069). Rectal and mean skin temperatures, chest sweat rate and cutaneous perfusion did not differ between conditions (all P > 0.05). In conclusion, compared with CHO-2% and Water, consuming a beverage consisting of CHO-6.5% and electrolytes during recovery under heat stress enhances PV recovery without modulating physiological heat loss responses.

DOI： 10.1113/EP087843

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Transient receptor potential vanilloid 4 (TRPV4) channels exist in the endothelial cells of cutaneous blood vessels and the secretory cells of eccrine sweat glands. We assessed if exogenous TRPV4 channel activation elicits cutaneous vasodilatation and sweating in humans in vivo, and if so, whether this response is mediated by nitric oxide synthase (NOS)- cyclooxygenase (COX)- and/or Ca2+-sensitive K+ (KCa) channel-related mechanisms. In ten healthy young adults (24±2 years, 5 women), cutaneous vascular conductance and sweat rate were assessed at four dorsal forearm skin sites continuously treated with either: 1) lactated Ringer's solution (Control), 2) 20 mM L-NAME, a non-selective NOS inhibitor, 3) 10 mM ketorolac, a non-selective COX inhibitor, or 4) 50 mM TEA, a non-selective KCa channel blocker. A potent and selective TRPV4 channel agonist, GSK1016790 A (GSK101), was administered to each skin site in a dose-dependent manner (1, 10, 100, 1000 μM each for ≥30min) via intradermal microdialysis. Administration of 100 and 1000 μM GSK101 increased cutaneous vascular conductance from pre-infusion level at the Control site (48±12 and 57±9%max, respectively, P≤0.004). This response was markedly (53-83%) attenuated by NOS inhibition, COX inhibition, or KCa channel blockade (all P≤0.037), except KCa channel blockade had no effect during 1000 μM GSK101 administration. GSK101 did not influence sweat rate regardless of skin site. We showed that in human skin in vivo, exogenous activation of TRPV4 channels mediates cutaneous vasodilatation, but not sweating through NOS, COX, and KCa channel mechanisms.

DOI： 10.1016/j.ejphar.2019.172462

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：SPRINGER  

PurposeChanges in mean skin temperature (T-sk) have been shown to modify the maximum rate of sweat ion reabsorption. This study aims to extend this knowledge by investigating if modifications could also be caused by local T-sk.MethodsThe influence of local T-sk on the sweat gland maximum ion reabsorption rates was investigated in ten healthy volunteers (three female and seven male; 20.81.2years, 60.47.7kg, 169.4 +/- 10.4cm) during passive heating (water-perfused suit and lower leg water immersion). In two separate trials, in a randomized order, one forearm was always manipulated to 33 degrees C (Neutral), whilst the other was manipulated to either 30 degrees C (Cool) or 36 degrees C (Warm) using water-perfused patches. Oesophageal temperature (T-es), forearm T-sk, sweat rate (SR), galvanic skin conductance (GSC) and salivary aldosterone concentrations were measured. The sweat gland maximum ion reabsorption rates were identified using the SR threshold for an increasing GSC.ResultsThermal [T-es and body temperature (T-b)] and non-thermal responses (aldosterone) were similar across all conditions (p>0.05). A temperature-dependent response for the sweat gland maximum ion reabsorption rates was evident between 30 degrees C (0.18 +/- 0.10mg/cm(2)/min) and 36 degrees C (0.28 +/- 0.14mg/cm(2)/min, d=0.88, p<0.05), but not for 33 degrees C (0.22 +/- 0.12mg/cm(2)/min), d=0.44 and d=0.36, p>0.05.Conclusion The data indicate that small variations in local T-sk may not affect the sweat gland maximum ion reabsorption rates but when the local T-sk increases by >6 degrees C, ion reabsorption rates also increase.

DOI： 10.1007/s00421-018-04059-5

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Two studies were conducted to examine the effects of ice slushy ingestion (ICE) and cold water immersion (CWI) on thermoregulatory and sweat responses during constant (study 1) and self-paced (study 2) exercise. In study 1, 11 men cycled at 40-50% of peak aerobic power for 60 min (33.2 ± 0.3°C, 45.9 ± 0.5% relative humidity, RH). In study 2, 11 men cycled for 60 min at perceived exertion (RPE) equivalent to 15 (33.9 ± 0.2°C and 42.5 ± 3.9%RH). In both studies, each trial was preceded by 30 min of CWI (~22°C), ICE or no cooling (CON). Rectal temperature (Tre), skin temperature (Tsk), thermal sensation, and sweat responses were measured. In study 1, ICE decreased Tre-Tsk gradient versus CON (p = 0.005) during first 5 min of exercise, while CWI increased Tre-Tsk gradient versus CON and ICE for up to 20 min during the exercise (p<0.05). In study 2, thermal sensation was lower in CWI versus CON and ICE for up to 35-40 min during the exercise (p<0.05). ICE reduced thermal sensation versus CON during the first 20 min of exercise (p<0.05). In study 2, CWI improved mean power output (MPO) by ~8 W, compared with CON only (p = 0.024). In both studies, CWI (p<0.001) and ICE (p = 0.019) delayed sweating by 1-5 min but did not change the body temperature sweating threshold, compared with CON (both p>0.05). Increased Tre-Tsk gradient by CWI improved MPO while ICE reduced Tre but did not confer any ergogenic effect. Both precooling treatments attenuated the thermal efferent signals until a specific body temperature threshold was reached.

DOI： 10.1371/journal.pone.0212966

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PURPOSE: This study investigated the influence of β-adrenergic receptor blockade on sweating during bilateral static knee extension (KE) and lateral isometric handgrip (IH) exercises followed by post-exercise muscle ischemia (PEMI) in habitually trained individuals. METHOD: Ten habitually trained men (maximum oxygen uptake, 57.1 ± 3.4 ml kg-1 min-1) were mildly heated by increasing their skin temperature, and bilateral KE or lateral IH exercises at an intensity of 60% maximum voluntary contraction were subsequently performed for 1 min, followed by PEMI to stimulate muscle metaboreceptors for 2 min. Sweat rates were measured on the bilateral forearms (KE) or thighs (IH) transdermally administered with 1% propranolol (propranolol, a non-selective β-adrenergic receptor inhibitor) or saline (control) via iontophoresis. RESULTS: Relative to the pre-exercise baseline values, IH exercise (P = 0.038) followed by PEMI (P = 0.041) similarly increased sweat rates on the thighs at both control and propranolol sites (baseline, 0.05 ± 0.04 vs. 0.05 ± 0.04; IH, 0.14 ± 0.12 vs. 0.15 ± 0.14; PEMI, 0.14 ± 0.16 vs. 0.14 ± 0.16 mg cm-2 min-1). KE increased sweat rates on the forearms (P = 0.001) at both control and propranolol sites similarly (baseline, 0.02 ± 0.03 vs. 0.02 ± 0.03; KE, 0.21 ± 0.19 vs. 0.20 ± 0.18), whereas PEMI did not significantly induce sweating at these sites (P = 0.260) (0.09 ± 0.12 and 0.10 ± 0.12 mg cm-2 min-1, respectively). CONCLUSION: These results suggest that non-thermal drives induced by static exercise and PEMI do not elicit β-adrenergic sweating in habitually trained individuals even when the non-thermal drives are originated from leg(s) under the conditions in the present study.

DOI： 10.1007/s00421-018-3993-x

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It remains unknown whether cutaneous adrenergic nerves functionally contribute to sweat production during exercise. This study examined whether cutaneous adrenergic nerve blockade attenuates sweating during incremental exercise, specifically in habitually trained individuals. Accordingly, 10 habitually trained and 10 untrained males (V̇o2max: 56.7 ± 5.4 and 38.9 ± 6.7 ml·kg-1·min-1, respectively; P < 0.001) performed incremental semirecumbent cycling (20 W/min) until exhaustion. Sweat rates (ventilated capsule) were measured at two bilateral forearm skin sites on which either 10 mM bretylium tosylate (BT) (an inhibitor of neurotransmitter release from sympathetic adrenergic nerve terminals) or saline (Control) was transdermally administered via iontophoresis. BT treatment delayed sweating onset in both groups (∼0.66 min; P = 0.001) and suppressed the sweat rate relative to the Control treatment at ≥70% relative total exercise time in trained individuals (each 10% increment; all P ≤ 0.009) but not in untrained counterparts ( P = 0.122, interaction between relative time × treatment). Changes in total sweat production at the BT site relative to the Control site were greater in trained individuals than in untrained counterparts (area under the curve, -0.86 ± 0.67 and -0.22 ± 0.39 mg/cm2, respectively; P = 0.023). In conclusion, we demonstrated that cutaneous adrenergic nerves do modulate sweating during incremental exercise, which appeared to be more apparent in habitually trained men (e.g., ≥70% maximum workload). Although our results indicated that habitual exercise training may augment neural adrenergic sweat production during incremental exercise, additional studies are required to confirm this possibility. NEW & NOTEWORTHY We demonstrated for the first time that cutaneous adrenergic nerves do modulate sweating during high-intensity exercise in humans (≥70% maximum workload). In addition, neural adrenergic sweating appeared to be greater in habitually trained individuals than in untrained counterparts, although further studies are necessary to confirm such a possibility. Nonetheless, the observations presented herein advance our understanding on human thermoregulation while providing new evidence for the neutral mediation of adrenergic sweating during exercise.

DOI： 10.1152/japplphysiol.00370.2018

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PURPOSE: We investigated the influence of inorganic nitrate ([Formula: see text]) supplementation on local sweating and cutaneous vascular responses during exercise in hot conditions. METHOD: Eight healthy, young subjects were assigned in a randomized, double-blind, crossover design to receive [Formula: see text]-rich beetroot (BR) juice (140 mL/day, containing ~ 8 mmol of [Formula: see text]) and [Formula: see text]-depleted placebo (PL) juice (140 mL/day, containing ~ 0.003 mmol of [Formula: see text]) for 3 days. On day 3 of supplementation, subjects cycled at an intensity corresponding to 55% of [Formula: see text]O2max for 30 min in hot conditions (30 °C, 50% relative humidity). Chest and forearm sweat rate (SR) and skin blood flow (SkBF), were measured continuously. Cutaneous vascular conductance (CVC) was calculated by SkBF/mean arterial pressure (MAP). RESULTS: Prior to exercise, plasma [Formula: see text] (21 ± 6 and 581 ± 161 µM) and nitrite ([Formula: see text], 87 ± 28 and 336 ± 156 nM) concentrations were higher after BR compared to PL supplementation (P ≤ 0.011, n = 6). Oesophageal, mean skin, and mean body temperatures during exercise were not different between conditions. In addition, BR supplementation did not affect SR, SkBF, and CVC during exercise. A lower MAP was found after 30 min of exercise following BR supplementation (112 ± 6 and 103 ± 6 mmHg for PL and BR, respectively, P = 0.021). CONCLUSION: These results suggest that inorganic [Formula: see text] supplementation, which increases the potential for O2-independent NO production, does not affect local sweating and cutaneous vascular responses, but attenuates blood pressure in young healthy subjects exercising in a hot environment.

DOI： 10.1007/s00421-018-3889-9

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The sweat glands maximum ion reabsorption rates were investigated (n = 12, 21.7 ± 3.0 years, 59.4 ± 9.8 kg, 166.9 ± 10.4 cm and 47.1 ± 7.5 mL/kg/min) during two separate endogenous protocols; cycling at 30% (LEX) and 60% VO2max (MEX) and one exogenous trial; passive heating (PH) (43°C water lower leg immersion) in 27°C, 50%RH. Oesophageal temperature (Tes ), skin temperature (Tsk ), and forearm, chest and lower back sweat rate (SR) and galvanic skin conductance (GSC) were measured. Salivary aldosterone was measured pre-and postheating (n = 3). Using the ∆SR threshold for an increasing ∆GSC to identify maximum sweat ion reabsorption rate revealed higher reabsorption rates during MEX compared to PH (mean of all regions: 0.63 ± 0.28 vs. 0.44 ± 0.3 mg/cm2 /min, P < 0.05). It was not possible to identify the ion reabsorption rate during LEX for some participants. Tes and mean Tsk were different between conditions but mean body temperature (Tb ) and local Tsk (forearm, chest and back) were similar (P > 0.05). Aldosterone increased more during MEX (72.8 ± 36.6 pg/mL) compared to PH (39.2 ± 17.5 pg/mL) and LEX (1.8 ± 9.7 pg/mL). The back had a higher threshold than the forearm (P < 0.05) but it was similar to the chest (P > 0.05) (mean of all conditions; 0.64 ± 0.33, 0.42 ± 0.25, 0.54 ± 0.3 mg/cm2 /min, respectively). Although the differences between conditions may be influenced by thermal or nonthermal mechanism, our results indicate a possibility that the sweat glands maximum ion reabsorption rates may be different between exercise and passive heating without mediating skin regional differences.

DOI： 10.14814/phy2.13619

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The aim of our study was to determine if habitual endurance training can influence the relative contribution of nitric oxide synthase (NOS) and cyclooxygenase (COX) in the regulation of sweating during a passive heat stress in young adults. Ten trained athletes and nine untrained counterparts were passively heated until oral temperature (as estimated by sublingual temperature, Tor) increased by 1.5°C above baseline resting. Forearm sweat rate (ventilated capsule) was measured at three skin sites continuously perfused with either lactated Ringer's solution (Control), 10 mmol/L N
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-nitro-L-arginine methyl ester (L-NAME, non-selective NOS inhibitor), or 10 mmol/L ketorolac (Ketorolac, non-selective COX inhibitor) via intradermal microdialysis. Sweat rate was averaged for each 0.3°C increase in Tor Sweat rate at the L-NAME site was lower than Control following a 0.9 and 1.2°C increase in Tor in both groups (all P ≤ 0.05). Relative to the Control site, NOS-inhibition reduced sweating similarly between the groups (P = 0.51). Sweat rate at the Ketorolac site was not different from the Control at any levels of Tor in both groups (P > 0.05). Nevertheless, a greater sweat rate was measured at the end of heating in the trained as compared to the untrained individuals (P ≤ 0.05). We show that NOS contributes similarly to sweating in both trained and untrained individuals during a passive heat stress. Further, no effect of COX on sweating was measured for either group. The greater sweat production observed in endurance-trained athletes is likely mediated by factors other than NOS- and COX-dependent mechanisms.

DOI： 10.14814/phy2.13403

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The aim of the present study was to determine the β-adrenergic contribution to sweating during incremental exercise in habitually trained males. Nine habitually trained and 11 untrained males performed incremental cycling until exhaustion (20 W/min). Bilateral forearm sweat rates (ventilated capsule) were measured at two skin sites that were transdermally administered via iontophoresis with either 1% propranolol (Propranolol, a nonselective β-adrenergic receptor antagonist) or saline (Control). The sweat rate was evaluated as a function of both relative (percentage of maximum workload) and absolute exercise intensities. The sweat rate at the Propranolol site was lower than the control during exercise at 80 (0.57 ± 0.21 and 0.45 ± 0.19 mg·cm-2·min-1 for Control and Propranolol, respectively) and 90% (0.74 ± 0.22 and 0.65 ± 0.17 mg·cm-2·min-1, respectively) of maximum workload in trained males (all P < 0.05). By contrast, no between-site differences in sweat rates were observed in untrained counterparts (all P > 0.05). At the same absolute intensity, higher sweat rates on the control site were observed in trained males relative to the untrained during exercise at 160 (0.23 ± 0.20 and 0.04 ± 0.05 mg·cm-2·min-1 for trained and untrained, respectively) and 180 W (0.40 ± 0.20 and 0.13 ± 0.13 mg·cm-2·min-1, respectively) (all P < 0.05), whereas this between-group difference was not observed at the Propranolol site (all P > 0.05). We show that the β-adrenergic mechanism does modulate sweating during exercise at a submaximal high relative intensity in habitually trained males. The β-adrenergic mechanism may in part contribute to the greater sweat production in habitually trained males than in untrained counterparts during exercise.NEW & NOTEWORTHY We demonstrated for the first time that the β-adrenergic mechanism does modulate sweating (i.e., β-adrenergic sweating) during exercise using a localized β-adrenoceptor blockade in humans in vivo. β-Adrenergic sweating was evident in habitually trained individuals during exercise at a submaximal high relative intensity (80-90% maximal work). This observation advances our understanding of human thermoregulation during exercise and of the mechanism that underlies sweat gland adaptation to habitual exercise training.

DOI： 10.1152/japplphysiol.00220.2017

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PURPOSE: It is recently reported that determining sweat rate (SR) threshold for increasing galvanic skin conductance (GSC) would represent a maximum rate of sweat ion reabsorption in sweat glands. We evaluate the maximum rate of sweat ion reabsorption over skin regions, sex, and long-term exercise training by using the threshold analysis in the present study. METHODS: Ten males (2 untrained, 4 sprinters, and 4 distance runners) and 12 females (5 untrained, 4 sprinters, and 3 distance runners) conducted graded cycling exercise for 45 min at low, middle, and high exercise intensities (heart rate 100-110, 120-130, and 140-150 beats/min, respectively) for 10, 15, and 20 min, respectively, at 30 °C and 50% relative humidity. Comparisons were made between males and females and among untrained individuals, distance runners, and sprinters on the back and forearm. RESULTS: SR threshold for increasing GSC on back was significantly higher than that of forearm (P < 0.05) without any sex differences (back 0.70 ± 0.08 and 0.61 ± 0.04, forearm 0.40 ± 0.05 and 0.45 ± 0.06 mg/cm2/min for males and females, respectively). Distance runners and sprinters showed higher SR threshold for increasing GSC than that of untrained subjects on back (P < 0.05) but not on forearm (back 0.45 ± 0.06, 0.83 ± 0.06, and 0.70 ± 0.04, forearm 0.33 ± 0.04, 0.49 ± 0.02, and 0.39 ± 0.07 mg/cm2/min for untrained subjects, distance runners, and sprinters, respectively). CONCLUSION: These results suggest that the maximum sweat ion reabsorption rate on the back is higher than that of forearm without sex differences. Furthermore, exercise training in distance runners and sprinters improves the maximum sweat ion reabsorption rate on the back.

DOI： 10.1007/s00421-017-3619-8

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This study investigated the influence of dietary inorganic nitrate supplementation on pulmonary and muscle deoxyhemoglobin/myoglobin (i.e. deoxy [Hb+Mb]) kinetics during submaximal cycling exercise. In a randomized, placebo-controlled, cross-over study, eight healthy and physically active male subjects completed two step cycle tests at a work rate equivalent to 50% of the difference between the gas exchange threshold and peak over separate 4-day supplementation periods with NO(BR; providing 8.4mmol NO and NO depleted (placebo; PLA) beetroot juice. Pulmonary was measured breath-by-breath and time-resolved near-infrared spectroscopy was utilized to quantify absolute deoxy [Hb+Mb] and total [Hb+Mb] within the rectus femoris, vastus lateralis, and vastus medialis. There were no significant differences (P>0.05) in the primary deoxy [Hb+Mb] mean response time or amplitude between the PLA and BR trials at each muscle site. BR significantly increased the mean (three-site) end-exercise deoxy [Hb+Mb] witha tendency to increase the mean (three-site) area under the curve for total [Hb + Mb] responses . The mml:mover accent="true"VO2 slow component reduction after BR supplementation (PLA: 0.27 +/- 0.07 vs. BR: 0.23 +/- 0.08Lmin(-1), P=0.07) correlated inversely with the mean increases in deoxy [Hb+Mb] and total [Hb+Mb] across the three muscle regions (r(2)=0.62 and 0.66, P<0.05). Dietary supplementation increased O-2 diffusive conductance across locomotor muscles in association with improved mml:mover accent="true VO2 dynamics during heavy-intensity cycling transitions.

DOI： 10.14814/phy2.13340

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We evaluated the influence of K+ channels (i.e., Ca2+-activated K+ (KCa), ATP-sensitive K+ (KATP), and voltage-gated K+ (KV) channels) and key enzymes (nitric oxide synthase (NOS) and cyclooxygenase (COX)) on nicotine-induced cutaneous vasodilation and sweating. Using intradermal microdialysis, we evaluated forearm cutaneous vascular conductance (CVC) and sweat rate in 2 separate protocols. In protocol 1 (n = 10), 4 separate sites were infused with (i) lactated Ringer (Control), (ii) 50 mmol·L-1 tetraethylammonium (KCa channel blocker), (iii) 5 mmol·L-1 glybenclamide (KATP channel blocker), and (iv) 10 mmol·L-1 4-aminopyridine (KV channel blocker). In protocol 2 (n = 10), 4 sites were infused with (i) lactated Ringer (Control), (ii) 10 mmol·L-1 Nω-nitro-l-arginine (NOS inhibitor), (iii) 10 mmol·L-1 ketorolac (COX inhibitor), or (iv) a combination of NOS+COX inhibitors. At all sites, nicotine was infused in a dose-dependent manner (1.2, 3.6, 11, 33, and 100 mmol·L-1; each for 25 min). Nicotine-induced increase in CVC was attenuated by the KCa, KATP, and KV channel blockers, whereas nicotine-induced increase in sweat rate was reduced by the KCa and KV channel blockers (P ≤ 0.05). COX inhibitor augmented nicotine-induced increase in CVC (P ≤ 0.05), which was absent when NOS inhibitor was co-administered (P > 0.05). In addition, our secondrary experiment (n = 7) demonstrated that muscarinic receptor blockade with 58 μmol·L-1 atropine sulfate salt monohydrate abolished nicotine-induced increases in CVC (1.2-11 mmol·L-1) and sweating (all doses). We show that under a normothermic resting state: (i) KCa, KATP, and KV channels contribute to nicotinic cutaneous vasodilation, (ii) inhibition of COX augments nicotinic cutaneous vasodilation likely through NOS-dependent mechanism(s), and (iii) KCa and KV channels contribute to nicotinic sweating.

DOI： 10.1139/apnm-2016-0615

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We evaluated the association between aerobic power (defined by peak oxygen consumption; VO2peak) and the contribution of nitric oxide synthase (NOS) to the sweating response in young and older individuals during exercise in the heat. Data from 44 young (24 ± 1 years) and 48 older (61 ± 2 years) males with mean VO2peak of 47.8 ± 2.4 (range, 28.0-62.3) and 39.1 ± 2.3 (range, 26.4-55.7) mLO2 kg-1 min-1, respectively, were compiled from our prior studies. Participants performed two 15- to 30-min bouts of exercise at a fixed rate of metabolic heat production of 400 or 500 W, each separated by 15-20 min recovery in the heat (35°C, relative humidity of 20%). Forearm sweat rate (ventilated capsule technique) was measured at two skin sites that were continuously and simultaneously administered with lactated Ringers solution (Control) or 10 mmol/L N
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-nitro-L-arginine methyl ester (L-NAME, nonselective NOS inhibitor) via intradermal microdialysis. Sweat rate during the final 5 min of each exercise bout was lower with L-NAME compared to the Control in both groups (all P < 0.05). The magnitude of the attenuation in sweat rate induced by L-NAME compared to the Control was not correlated with VO2peak (all P ≥ 0.46) while this attenuation was negatively correlated with the sweat rate at the Control in both groups and in both exercise bouts (all P < 0.01, R ≤ -0.43). These results suggest that NOS-dependent sweating is not associated with aerobic power per se, while it becomes evident in individuals who produce larger sweat rates during exercise irrespective of age.

DOI： 10.14814/phy2.13208

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The purpose of the present study was to investigate sweating responses to isometric hand-grip (IH) exercise andmuscle metaboreflex in prepubertal children and the elderly. In hot conditions (ambient temperature, 35 degrees C; relative humidity, 45%), 13 healthy young adults, 10 prepubertal children and 10 elderly subjects (aged 20.4 +/- 1.2, 11.4 +/- 0.5 and 63.5 +/- 3.1 years, respectively) repeated a three hand-grip exercise protocol that consisted of 1 min IH exercise at 15, 30 or 45% of maximal voluntary contraction (MVC) followed by 2 min postexercise forearm occlusion. Local sweat rates (SRs) on the forehead, chest, forearm, thigh and palm were continuously measured (ventilated capsule method). The forehead SR in prepubertal children during IH exercise at 45% MVC was significantly lower than that of young adults (0.26 +/- 0.22 and 0.08 +/- 0.15 mg cm(-2) min(-1) for young adults and children, respectively; P < 0.05) but not of the elderly at any exercise intensities. The SR on the chest (0.22 +/- 0.22 and -0.01 +/- 0.05 mg cm(-2) min(-1) for young adults and children, respectively), forearm (0.14 +/- 0.12 and 0.03 +/- 0.04 mg cm(-2) min(-1)) and thigh (0.13 +/- 0.10 and 0.02 +/- 0.03 mg cm(-2) min(-1)) during postexercise occlusion at 45% MVC was significantly lower in children than in young adults (P < 0.05). Elderly subjects showed a significantly lower SR on the forearm (0.04 +/- 0.04 and 0.01 +/- 0.02 mg cm(-2) min(-1) for young adults and elderly, respectively) and thigh (0.07 +/- 0.07 and 0.01 +/- 0.03 mg cm(-2) min(-1)) at 15% MVC and on the thigh at 45% MVC (0.13 +/- 0.10 and 0.04 +/- 0.04 mg cm-2 min-1) during postexercise occlusion compared with young adults (P< 0.05). These results suggest that sweating responses to IH exercise and muscle metaboreflex were underdeveloped in prepubertal children and that ageing attenuates the response to the muscle metaboreflex in a way that is not consistent across the body.

DOI： 10.1113/EP085908

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We recently showed that intradermal administration of endothelin-1 diminished endothelium-dependent and -independent cutaneous vasodilation. We evaluated the hypothesis that Rho kinase may be a mediator of this response. We also sought to evaluate if endothelin-1 increases sweating. In 12 adults (25 +/- 6 yr), we measured cutaneous vascular conductance (CVC) and sweating during 1) endothelium-dependent vasodilation induced via administration of incremental doses of methacholine (0.25, 5, 100, and 2,000 mM each for 25 min) and 2) endothelium-independent vasodilation induced via administration of 50 mM sodium nitroprusside (20-25 min). Responses were evaluated at four skin sites treated with either 1) lactated Ringer solution (Control), 2) 400 nM endothelin-1, 3) 3 mM HA-1077 (Rho kinase inhibitor), or 4) endothelin-1 + HA-1077. Pharmacological agents were intradermally administered via micro-dialysis. Relative to the Control site, endothelin-1 attenuated endothelium-dependent vasodilation (CVC at 2,000 mM methacholine, 80 +/- 10 vs. 56 +/- 15% max, P < 0.01); however, this response was not detected when the Rho kinase inhibitor was simultaneously administered (CVC at 2,000 mM methacholine for Rho kinase inhibitor vs. endothelin-1 + Rho kinase inhibitor sites: 73 +/- 9 vs. 72 +/- 11% max, P > 0.05). Endothelium-independent vasodilation was attenuated by endothelin-1 compared with the Control site (CVC, 92 +/- 13 vs. 70 +/- 14% max, P < 0.01). However, in the presence of Rho kinase inhibition, endothelin-1 did not affect endotheliumin-dependent vasodilation (CVC at Rho kinase inhibitor vs. endothelin-1 + Rho kinase inhibitor sites: 81 +/- 9 vs. 86 +/- 10% max, P > 0.05). There was no between-site difference in sweating throughout (P > 0.05). We show that in young adults, Rho kinase is an important mediator of the endothelin-1-mediated attenuation of endothelium-dependent and -independent cutaneous vasodilation, and that endothelin-1 does not increase sweating.

DOI： 10.1152/ajpregu.00368.2016

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It is axiomatic that greater aerobic fitness ((V)over dotO(2peak)) derives from enhanced perfusive and diffusive O-2 conductances across active muscles. However, it remains unknown how these conductances might be reflected by regional differences in fractional O-2 extraction (i.e., deoxy [Hb+Mb] and tissue O-2 saturation [StO2]) and diffusive O-2 potential (i.e., total[Hb+Mb]) among muscles spatially heterogeneous in blood flow, fiber type, and recruitment (vastus lateralis, VL; rectus femoris, RF). Using quantitative time-resolved near-infrared spectroscopy during ramp cycling in 24 young participants ((V)over dotO(2peak) range: similar to 37.4-66.4 mL kg(-1) min(-1)), we tested the hypotheses that (1) deoxy [Hb+Mb] and total[Hb+Mb] at (V)over dotO(2peak) would be positively correlated with (V)over dotO(2peak) in both VL and RF muscles; (2) the pattern of deoxygenation (the deoxy[Hb+Mb] slopes) during submaximal exercise would not differ among subjects differing in (V)over dotO(2peak). Peak deoxy [Hb+Mb] and StO2 correlated with (V)over dotO(2peak) for both VL (r = 0.44 and -0.51) and RF (r = 0.49 and -0.49), whereas for total[Hb+Mb] this was true only for RF (r = 0.45). Baseline deoxy[Hb+Mb] and StO2 correlated with (V)over dotO(2peak) only for RF (r = -0.50 and 0.54). In addition, the deoxy[Hb+Mb] slopes were not affected by aerobic fitness. In conclusion, while the pattern of deoxygenation (the deoxy[Hb+Mb] slopes) did not differ between fitness groups the capacity to deoxygenate [Hb+Mb] (index of maximal fractional O-2 extraction) correlated significantly with (V)over dotO(2peak) in both RF and VL muscles. However, only in the RF did total [Hb+Mb] (index of diffusive O-2 potential) relate to fitness.

DOI： 10.14814/phy2.13065

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：PERGAMON-ELSEVIER SCIENCE LTD  

Cutaneous thermal sensitivity to a warm and cold stimulus was compared amongst 12 older (OF, 65.2 +/- 1.0 year) and 29 younger (YF, 21.6 +/- 0.2 years) female participants, and 17 older (OM, 66.2 +/- 1.5 years) and 13 younger (YM, 21.2 +/- 0.4 years) male participants to examine the effects of ageing and sex. In a neutral condition (27.5 degrees C, 50% RH) during rest, warm and cold thermal sensitivity was measured on eight body regions (forehead, chest, back, forearm, hand, thigh, calf, and foot). Using the method of limits, a thermal stimulator was applied to the skin at an adapting temperature and either increased or decreased at a constant rate (0.3 degrees C/s) until the participants detected the temperature with a push button. Thermal sensitivity declined with ageing to both a cold (older: 1468.6 +/- 744.7 W/m(2), younger: 869.8 +/- 654.7 W/m(2), p < 0.001) and warm (older: 2127.0 +/- 12083 W/m(2), younger: 1301.7 +/- 1055.2 W/m(2), p < 0.001) innocuous stimulus. YF and OF were more sensitive than YM and OM to both a warm and cold stimulus (p < 0.05). There was no interaction between age and sex suggesting that whilst thermal sensitivity decreases with age the decrease is similar between the sexes (p > 0.05). There was an interaction between temperatures, age and location and it seemed that cold thermal sensitivity was more homogenous for young and older participants however warm thermal sensitivity was more heterogeneous especially in the younger participants (p < 0.05). Although the pattern was not similar between ages or sexes it was evident that the forehead was the most sensitive region to a warm and cold stimulus. Interestingly the decline in sensitivity observed with ageing occurred for all locations but was attenuated at the forehead in both males and females (p > 0.05). (C) 2016 Elsevier Inc All rights reserved.

DOI： 10.1016/j.physbeh.2016.05.045

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：PERGAMON-ELSEVIER SCIENCE LTD  

Changing stride frequency may influence oxygen uptake and heart rate during running as a function of running economy and central command. This study investigated the influence of stride frequency manipulation on thermoregulatory responses during endurance running. Seven healthy endurance runners ran on a treadmill at a velocity of 15 km/h for 60 min in a controlled environmental chamber (ambient temperature 27 degrees C and relative humidity 50%), and stride frequency was manipulated. Stride frequency was intermittently manipulated by increasing and decreasing frequency by 10% from the pre-determined preferred frequency. These periods of increase or decrease were separated by free frequency running in the order of free stride frequency, stride frequency manipulation (increase or decrease), free stride frequency, and stride frequency manipulation (increase or decrease) for 15 min each. The increased and decreased stride frequencies were 110% and 91% of the free running frequency, respectively (196 +/- 6, 162 +/- 5, and 178 +/- 5 steps/min, respectively, P < 0.01). Compared to the control, stride frequency manipulation did not affect rectal temperature, heart rate, or the rate of perceived exhaustion during running. Whole-body sweat loss increased significantly when stride frequency was manipulated (1.48 +/- 0.11 and 1.57 +/- 0.11 kg for control and manipulated stride frequencies, respectively, P < 0.05), but stride frequency had a small effect on sweat loss overall (Cohen's d=0.31). A higher mean skin temperature was also observed under mixed frequency conditions compared to that in the control (P < 0.05). While the precise mechanisms underlying these changes remain unknown (e.g. running economy or central command), our results suggest that manipulation of stride frequency does not have a large effect on sweat loss or other physiological variables, but does increase mean skin temperature during endurance running. (C) 2016 Published by Elsevier Ltd.

DOI： 10.1016/j.jtherbio.2016.08.005

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：AMER PHYSIOLOGICAL SOC  

We examined whether the sustained activation of metaboreceptor in forearm during cycling exercise can modulate sweating and cutaneous vasodilation. On separate days, 12 young participants performed a 1.5-min isometric handgrip exercise at 40% maximal voluntary contraction followed by 1) 9-min forearm ischemia (Occlusion, to activate metaboreceptor) or 2) no ischemia (Control) in thermoneutral conditions (27(circle)C, 50%) with mean skin temperature clamped at 34(circle)C. Thirty seconds after the handgrip exercise, participants cycled for 13.5 min at 40% VO2 max. For Occlusion, forearm ischemia was maintained for 9 min followed by no ischemia thereafter. Local sweat rate (SR, ventilated capsule) and cutaneous vascular conductance (CVC, laser-Doppler perfusion units/ mean arterial pressure) on the contralateral nonischemic arm as well as esophageal and skin temperatures were measured continuously. The period of ischemia in the early stages of exercise increased SR (+ 0.03 mg(.)cm (-2) (.) min (-1), P < 0.05) but not CVC (P > 0.05) above Control levels. No differences were measured in the esophageal temperature at which onset of sweating (Control 37.19 +/- 0.09 vs. Occlusion 37.07 +/- 0.09(circle)C) or CVC (Control 37.21 +/- 0.08 vs. Occlusion 37.08 +/- 0.10(circle)C) as well as slopes for these responses (all P > 0.05). However, a greater elevation in SR occurred thereafter such that SR was significantly elevated at the end of the ischemic period relative to Control (0.37 +/- 0.05 vs. 0.23 +/- 0.05 mg(.)cm (-2.)min (- 1), respectively, P < 0.05) despite no differences in esophageal temperature. We conclude that the activation of forearm muscle metaboreceptor can modulate sweating, but not CVC, during cycling exercise without affecting the core temperature-SR relationship.

DOI： 10.1152/ajpregu.00545.2015

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：SPRINGER  

Purpose The purpose of the present study was to develop and describe a simple method to evaluate the rate of ion reabsorption of eccrine sweat glands in human using the measurement of galvanic skin conductance (GSC) and local sweating rate (SR). This purpose was investigated by comparing the SR threshold for increasing GSC with following two criteria of sweat ion reabsorption in earlier studies such as (1) the SR threshold for increasing sweat ion was at approximately 0.2-0.5 mg/cm(2)/min and (2) exercise heat acclimation improved the sweat ion reabsorption ability and would increase the criteria 1.Methods Seven healthy non-heat-acclimated male subjects received passive heat treatment both before and after 7 days of cycling in hot conditions (50 % maximum oxygen uptake, 60 min/day, ambient temperature 32 degrees C, and 50 % relative humidity).Results Subjects became partially heat-acclimated, as evidenced by the decreased end-exercise heart rate (p < 0.01), rate of perceived exhaustion (p < 0.01), and oesophageal temperature (p = 0.07), without alterations in whole-body sweat loss, from the first to the last day of training. As hypothesized, we confirmed that the SR threshold for increasing GSC was near the predicted SR during passive heating before exercise heat acclimation, and increased significantly after training (0.19 +/- 0.09-0.32 +/- 0.10 mg/cm(2)/min, p < 0.05).Conclusions The reproducibility of sweat ion reabsorption by the eccrine glands in the present study suggests that the relationship between GSC and SR can serve as a new index for assessing the maximum rate of sweat ion reabsorption of eccrine sweat glands in humans.

DOI： 10.1007/s00421-015-3275-9

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：SPRINGER  

Time-resolved near-infrared spectroscopy (TRS-NIRS) allows absolute quantitation of deoxygenated haemoglobin and myoglobin concentration ([HHb]) in skeletal muscle. We recently showed that the spatial distribution of peak [HHb] within the quadriceps during moderate-intensity cycling is reduced with progressive hypoxia and this is associated with impaired aerobic energy provision. We therefore aimed to determine whether reduced spatial distribution of skeletal muscle [HHb] was associated with impaired aerobic energy transfer during exhaustive ramp-incremental exercise in hypoxia. Seven healthy men performed ramp-incremental cycle exercise (20 W/min) to exhaustion at 3 fractional inspired O-2 concentrations (FIO2): 0.21, 0.16, 0.12. Pulmonary O-2 uptake ((V) over dot O-2) was measured using a flow meter and gas analyser system. Lactate threshold (LT) was estimated non-invasively. Absolute muscle deoxygenation was quantified by multichannel TRS-NIRS from the rectus femoris and vastus lateralis (proximal and distal regions). (V) over dotO(2peak) and LT were progressively reduced (p< 0.05) with hypoxia. There was a significant effect (p< 0.05) of FIO2 on [HHb] at baseline, LT, and peak. However the spatial variance of [HHb] was not different between FIO2 conditions. Peak total Hb ([Hb(tot)]) was significantly reduced between FIO2 conditions (p< 0.001). There was no association between reductions in the spatial distribution of skeletal muscle [HHb] and indices of aerobic energy transfer during ramp-incremental exercise in hypoxia. While regional [HHb] quantified by TRS-NIRS at exhaustion was greater in hypoxia, the spatial distribution of [HHb] was unaffected. Interestingly, peak [Hb(tot)] was reduced at the tolerable limit in hypoxia implying a vasodilatory reserve may exist in conditions with reduced FIO2.

DOI： 10.1007/978-1-4939-3023-4_2

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：WILEY-BLACKWELL  

We investigated the effect of thigh compression, which accelerates activation of central command and muscle metabo- and mechanoreceptors, on the adaptation of sweating and cutaneous vascular responses during exercise heat acclimation. Nine non-heat-acclimated male subjects were acclimated to heat (32 degrees C and 50% RH) while cycling [50% of maximum oxygen uptake ( , acetylcholine-induced forearm sweating rate (iontophoresis), and mean sweating and cutaneous vascular responses on the forehead, chest, and forearm (SRmean and CVCmean) during passive heating were evaluated before and after training. Training significantly increased while did not affect acetylcholine-induced sweating rates in either group. Training significantly decreased T-b thresholds for SRmean and CVCmean during passive heating without the alternations of sensitivities in both groups. Although SRmean during passive heating at a given T-b was not improved in either group, CVCmean was significantly (P<0.05) attenuated after exercise training only in experimental group. Our results indicate that thigh cuff compression during exercise heat acclimation does not influence adaptation of the sweating response but attenuate cutaneous vasodilation.

DOI： 10.1111/sms.12365

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：AMER PHYSIOLOGICAL SOC  

The present study investigated the role of muscle metaboreceptor activation on human thermoregulation by measuring core temperature thresholds and slopes for sweating and cutaneous vascular responses during passive heating associated with central and peripheral mechanisms. Six male and eight female subjects inserted their lower legs into hot water (43 degrees C) while wearing a water perfusion suit on the upper body (34 degrees C). One minute after immersion, an isometric handgrip exercise-40% of maximum voluntary contraction-was conducted for 1.5 min in both control and experimental conditions, while postexercise occlusion was performed in the experimental condition only for 9 min. The postexercise forearm occlusion during passive heating consistently stimulated muscle metaboreceptors, as implicated by significantly elevated mean arterial blood pressure throughout the experimental period (P < 0.05). Stimulation of the forearm muscle metaboreceptors increased sweating and cutaneous vascular responses during passive heating, and was associated with significant reductions in esophageal temperature threshold of sweating and cutaneous vasodilation (Delta threshold, sweating: 0.33 +/- 0.05 and 0.16 +/- 0.04 degrees C, cutaneous vascular conductance: 0.38 +/- 0.08 and 0.16 +/- 0.05 degrees C for control and experimental groups, respectively, P < 0.05). The slopes of these responses were not different between the conditions. These results suggest that muscle metaboreceptor activation in the forearm accelerates sweating and cutaneous vasodilation during passive heating associated with a reduction in core temperature thresholds and may be related to central mechanisms controlling heat loss responses.

DOI： 10.1152/ajpregu.00005.2015

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：AMER PHYSIOLOGICAL SOC  

Skeletal muscle deoxygenated hemoglobin and myoglobin concentration ([HHb]), assessed by near-infrared spectroscopy (NIRS), is commonly used as a surrogate of regional O-2 extraction (reflecting the O-2 delivery-to-consumption ratio, (Q) over dot/(V) over dot O-2). However, [HHb] change (Delta[HHb]) is also influenced by capillary-venous heme concentration, and/or small blood vessel volume (reflected in total heme; [THb]). We tested the hypotheses that Delta[HHb] is associated with O-2 extraction, and insensitive to [THb], over a wide range of (Q) over dot/(V) over dot O-2 elicited by passive head-up tilt (HUT; 10-min, 15 degrees increments, between -10 degrees and 75 degrees). Steady-state common femoral artery blood flow (FBF) was measured by echo-Doppler, and time-resolved NIRS measured [HHb] and [THb] of vastus lateralis (VL) and gastrocnemius (GS) in 13 men. EMG confirmed muscles were inactive. During HUT in VL [HHb] increased linearly (57 +/- 10 to 101 +/- 16 mu M; P < 0.05 above 15 degrees) and was associated (r(2) similar to 0.80) with the reduction in FBF (618 +/- 75 ml/min at 0 degrees to 268 +/- 52 ml/min at 75 degrees; P < 0.05 above 30 degrees) and the increase in [THb] (228 +/- 30 vs. 252 +/- 32 mu M; P < 0.05 above 15 degrees). GS response was qualitatively similar to VL. However, there was wide variation within and among individuals, such that the overall limits of agreement between Delta[HHb] and Delta FBF ranged from -35 to + 19% across both muscles. Neither knowledge of tissue O-2 saturation nor vascular compliance could appropriately account for the Delta[HHb]- FBF dissociation. Thus, under passive tilt, [HHb] is influenced by (Q) over dot/(V) over dot O-2, as well as microvascular hematocrit and/or tissue blood vessel volume, complicating its use as a noninvasive surrogate for muscle microvascular O-2 extraction.

DOI： 10.1152/japplphysiol.00918.2014

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：AMER PHYSIOLOGICAL SOC  

The present study compared peak muscle deoxygenation ([HHb](peak)) responses at three quadriceps sites during occlusion (OCC), ramp incremental (RI), severe-(SVR) and moderate-intensity (MOD) exercise. Seven healthy men (25 +/- 4 yr) each completed a stationary cycling RI (20 W/min) test to determine [HHb](peak) [at distal and proximal vastus lateralis (VLD and VLP) and rectus femoris (RF)], peak (V) over dotO(2) ((V) over dotO(2peak)), gas exchange threshold (GET), and peak work rate (WRpeak). Subjects also completed MOD (WR = 80% GET) and SVR exercise (WR corresponding to 120% (V) over dotO(2peak)) with absolute [HHb] (quantified by multichannel, time-resolved near-infrared spectroscopy) and pulmonary VO2 ((V) over dotO(2p)) monitored continuously. Additionally, [HHb] and total hemoglobin ([Hb](tot)) were monitored at rest and during subsequent OCC (250 mmHg). Site-specific adipose tissue thickness was assessed (B-mode ultrasound), and its relationship with resting [Hb](tot) was used to correct absolute [HHb]. For VLD and RF, [HHb](peak) was higher (P < 0.05) during OCC (VLD = 111 +/- 38, RF = 114 +/- 26 mu M) than RI (VLD 64 +/- 14, RF = 85 +/- 20) and SVR (VLD = 63 +/- 13, RF = 81 +/- 18). [HHb](peak) was similar (P > 0.05) across these conditions at the VLP (OCC = 67 +/- 17, RI = 69 +/- 17, SVR = 63 +/- 17 mu M). [HHb] peaked and then decreased prior to exercise cessation during SVR at all three muscle sites. [HHb](peak) during MOD was consistently lower than other conditions at all sites. A "[HHb] reserve" exists during intense cycling at the VLD and RF, likely implying either sufficient blood flow to meet oxidative demands or insufficient diffusion time for complete equilibration. In VLP this [HHb] reserve was absent, suggesting that a critical PO2 may be challenged during intense cycling.

DOI： 10.1152/japplphysiol.00060.2014

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：AMER PHYSIOLOGICAL SOC  

Activation of muscle metaboreceptors and mechanoreceptors has been shown to independently influence the sweating response, while their integrative control effects remain unclear. We examined the sweating response when the two muscle receptors are concurrently activated in different limbs, as well as the blood pressure response. In total, 27 young males performed passive calf muscle stretches (muscle mechanoreceptor activation) for 30 s in a semisupine position with and without postisometric handgrip exercise muscle ischemia (PEMI, muscle metaboreceptor activation) at exercise intensities of 35 and 50% of maximum voluntary contraction (MVC) under hot conditions (ambient temperature, 35 degrees C, relative humidity, 50%). Passive calf muscle stretching alone increased the mean sweating rate significantly on the forehead, chest, and thigh (SRmean) and mean arterial blood pressure (MAP), but not the heart rate (HR), from prestretching levels by 0.04 +/- 0.01 mg center dot cm(2)center dot min(-1), 4.0 +/- 1.3 mmHg (P < 0.05), and -1.0 +/- 0.5 beats/min (P > 0.05), respectively. The SRmean and MAP during PEMI were significantly higher than those at rest. The passive calf muscle stretch during PEMI increased MAP significantly by 3.4 +/- 1.0 and 2.0 +/- 0.7 mmHg for 35 and 50% of MVC, respectively (P < 0.05), but not that of SRmean or HR at either exercise intensity. These results suggest that sweating and blood pressure responses to concurrent activation of the two muscle receptors in different limbs differ and that the influence of calf muscle mechanoreceptor activation alone on the sweating response disappears during forearm muscle metaboreceptor activation.

DOI： 10.1152/ajpregu.00515.2013

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：WILEY  

It remains unclear whether an overshoot in skeletal muscle deoxygenation (HHb; reflecting a microvascular kinetic mismatch of O-2 delivery to consumption) contributes to the slowed adjustment of oxidative energy provision at the onset of exercise. We progressively reduced the fractional inspired O-2 concentration (F-I,(O2)) to investigate the relationship between slowed pulmonary O-2 uptake ((V) over dot(O2)) kinetics and the dynamics and spatial distribution of absolute [HHb]. Seven healthy men performed 8 min cycling transitions during normoxia (F-I,(O2) = 0.21), moderate hypoxia (F-I,(O2) = 0.16) and severe hypoxia (F-I,(O2) = 0.12). (V) over dot(O2) uptake was measured using a flowmeter and gas analyser system. Absolute [HHb] was quantified by multichannel, time-resolved near-infrared spectroscopy from the rectus femoris and vastus lateralis (proximal and distal regions), and corrected for adipose tissue thickness. The phase II. (V) over dot(O2) time constant was slowed (P < 0.05) as F-I,(O2) decreased (normoxia, 17 +/- 3 s; moderate hypoxia, 22 +/- 4 s; and severe hypoxia, 29 +/- 9 s). The [HHb] overshoot was unaffected by hypoxia, but the transient peak [HHb] increased with the reduction in F-I,(O2) (P < 0.05). Slowed. (V) over dot(O2) kinetics in hypoxia were positively correlated with increased peak [HHb] in the transient (r(2) = 0.45; P < 0.05), but poorly related to the [HHb] overshoot. A reduction of spatial heterogeneity in peak [HHb] was inversely correlated with slowed. (V) over dot(O2) kinetics (r(2) = 0.49; P < 0.05). These data suggest that aerobic energy provision at the onset of exercise may be limited by the following factors: (i) the absolute ratio (i. e. peak [HHb]) rather than the kinetic ratio (i. e. [HHb] overshoot) of microvascular O-2 delivery to consumption; and (ii) a reduced spatial distribution in the ratio of microvascular O-2 delivery to consumption across the muscle.

DOI： 10.1113/expphysiol.2013.073270

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：SPRINGER  

The purpose of this study was to compare sweating function in sprinters who have trained for several years with untrained subjects and trained endurance runners. Two separate experiments were conducted. Nine sprinters, eight untrained men, and nine distance runners ( 50.9 +/- A 1.4, 38.2 +/- A 1.8, and 59.1 +/- A 1.2 mL/kg/min, respectively; P < 0.05) were passively heated for 50 min (Experiment 1), and ten sprinters, 11 untrained men and nine distance runners (similar levels compared with Experiment 1 in each group) had their sweat gland capacity assessed based on acetylcholine-induced sweating rate (SR) (Experiment 2). The slope of the mean non-glabrous SR plotted against change in mean body temperature during passive heating did not differ significantly between sprinters and untrained men (1.21 +/- A 0.10 and 0.97 +/- A 0.12 mg cm(-2)/min/A degrees C, respectively); in contrast, compared with untrained men, distance runners exhibited a significantly greater slope (1.42 +/- A 0.11 mg cm(-2)/min/A degrees C, P < 0.05). The mean body temperature threshold for SR was not significantly different among the groups. Acetylcholine-induced SR did not differ significantly between sprinters and untrained men, whereas distance runners showed a significantly higher induced SR compared with untrained men. The sweating function was not improved in sprinters who have trained 2-3 h/day, 5 days/week, for at least 3 years compared with untrained men, although the was markedly greater in sprinters. Thus, there is a case that daily training was not sufficient to improve sweating function in sprinters relative to those in distance runners.

DOI： 10.1007/s00421-013-2641-8

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：AMER PHYSIOLOGICAL SOC  

Chin LM, Kowalchuk JM, Barstow TJ, Kondo N, Amano T, Shiojiri T, Koga S. The relationship between muscle deoxygenation and activation in different muscles of the quadriceps during cycle ramp exercise. J Appl Physiol 111: 1259-1265, 2011. First published July 28, 2011; doi:10.1152/japplphysiol.01216.2010.-The relationship between muscle deoxygenation and activation was examined in three different muscles of the quadriceps during cycling ramp exercise. Seven young male adults (24 +/- 3 yr; mean +/- SD) pedaled at 60 rpm to exhaustion, with a work rate (WR) increase of 20 W/min. Pulmonary oxygen uptake was measured breath-by-breath, while muscle deoxygenation (HHb) and activity were measured by time-resolved near-infrared spectroscopy (NIRS) and surface electromyography (EMG), respectively, at the vastus lateralis (VL), rectus femoris (RF), and vastus medialis (VM). Muscle deoxygenation was corrected for adipose tissue thickness and normalized to the amplitude of the HHb response, while EMG signals were integrated (iEMG) and normalized to the maximum iEMG determined from maximal voluntary contractions. Muscle deoxygenation and activation were then plotted as a percentage of maximal work rate (%WR(max)). The HHb response for all three muscle groups was fitted by a sigmoid function, which was determined as the best fitting model. The c/d parameter for the sigmoid fit (representing the %WR(max) at 50% of the total amplitude of the HHb response) was similar between VL (47 +/- 12% WR(max)) and VM (43 +/- 11% WR(max)), yet greater (P < 0.05) for RF (65 +/- 13% WR(max)), demonstrating a "right shift" of the HHb response compared with VL and VM. The iEMG also showed that muscle activation of the RF muscle was lower (P < 0.05) compared with VL and VM throughout the majority of the ramp exercise, which may explain the different HHb response in RF. Therefore, these data suggest that the sigmoid function can be used to model the HHb response in different muscles of the quadriceps; however, simultaneous measures of muscle activation are also needed for the HHb response to be properly interpreted during cycle ramp exercise.

DOI： 10.1152/japplphysiol.01216.2010

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Language：English   Publishing type：Research paper (scientific journal)  

AIM: The goals of this study were to investigate changes in the sweating and cutaneous vascular responses on the palm and the volar aspect of the index finger during sustained static exercise of increasing intensity and to determine whether the former can be attributed to altered sweat gland activity. METHODS: Five male and five female subjects performed maximal voluntary handgrip contractions (MVC: right hand) for 60 s at 20, 35 and 50% MVC (ambient temperature 25 °C, relative humidity 50%). RESULTS: The sweat rate and the number of activated sweat glands on the non-exercised hand showed intensity-dependent increases (P < 0.05). At 35 and 50% MVC, finger sweat secretion was significantly higher than on the palm, which was primarily associated with the number of activated sweat glands (P < 0.05). In addition, there was a marked simultaneous decrease in the cutaneous vascular conductance for the finger at 35 and 50% MVC (P < 0.05), but not for the palm. CONCLUSION: Our results suggest that a difference exists between intensity-dependent increases of sudomotor responses within more than one glabrous skin site. Specifically, markedly greater sweating occurs on the volar finger than on the palmar surface during sustained static exercise. These differences in sweat rate mainly resulted from changes in the number of activated sweat glands. In addition, intra-segment variations in cutaneous blood flow on the glabrous hand are shown.

DOI： 10.1111/j.1748-1716.2011.02299.x

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：AMER PHYSIOLOGICAL SOC  

Amano T, Ichinose M, Koga S, Inoue Y, Nishiyasu T, Kondo N. Sweating responses and the muscle metaboreflex under mildly hyperthermic conditions in sprinters and distance runners. J Appl Physiol 111: 524-529, 2011. First published June 9, 2011; doi:10.1152/japplphysiol.00212.2011.-To investigate the effects of different training methods on nonthermal sweating during activation of the muscle metaboreflex, we compared sweating responses during postexercise muscle occlusion in endurance runners, sprinters, and untrained men under mild hyperthermia (ambient temperature, 35 C; relative humidity, 50%). Ten endurance runners, nine sprinters, and ten untrained men (maximal oxygen uptakes: 57.5 +/- 1.5, 49.3 +/- 1.5, and 36.6 +/- 1.6 ml.kg(-1).min(-1), respectively; P < 0.05) performed an isometric handgrip exercise at 40% maximal voluntary contraction for 2 min, and then a pressure of 280 mmHg was applied to the forearm to occlude blood circulation for 2 min. The Delta change in mean arterial blood pressure between the resting level and the occlusion was significantly higher in sprinters than in untrained men (32.2 +/- 4.4 vs. 17.3 +/- 2.6 mmHg, respectively; P < 0.05); however, no difference was observed between distance runners and untrained men. The Delta mean sweating rate (averaged value of the forehead, chest, forearm, and thigh) during the occlusion was significantly higher in distance runners than in sprinters and untrained men (0.38 +/- 0.07, 0.19 +/- 0.03, and 0.11 +/- 0.04 mg.cm(-2).min(-1), respectively; P < 0.05) and did not differ between sprinters and untrained men. Our results suggest that the specificity of training modalities influences the sweating response during activation of the muscle metaboreflex. In addition, these results imply that a greater activation of the muscle metaboreflex does not cause a greater sweating response in sprinters.

DOI： 10.1152/japplphysiol.00212.2011

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Language：English   Publishing type：Research paper, summary (international conference)   Publisher：LIPPINCOTT WILLIAMS & WILKINS  

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Language：Japanese   Publisher：日本発汗学会  

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Language：Japanese   Publisher：(公財)石本記念デサントスポーツ科学振興財団  

高強度のウォームアップ(W-up)運動を用いると,W-up運動後の主運動における活動筋の酸素消費量(VO2)の増加が速くなり,酸素不足が減少する.本研究では,表層筋に加えて深層筋も含めた活動筋の酸素動態を計測し,高強度のW-up運動が活動筋の酸素動態に及ぼす影響を明らかにした.時間分解・近赤外分光装置を用いて,活動筋における脱酸素化ヘモグロビン+ミオグロビン(HHb)を計測した.大腿直筋深層部のHHbは第1運動と第2運動の開始後の約5分目において定常状態を示し,VO2とQの増加速度のマッチングが生じたことが示唆された.さらに,第1運動と第2運動において大腿直筋深層部におけるHHbの時定数と平均応答時間は表層部に比べて有意に遅かった.HHbはVO2/Qを反映するので,表層筋に比べて遅筋線維が多く含まれ,運動中の筋温がより高い深層筋では,酸素供給が十分になって活動筋全体のVO2とQのバランスが改善され,酸素不足が減少したと推測される.(著者抄録)

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Language：English   Publishing type：Research paper, summary (international conference)   Publisher：LIPPINCOTT WILLIAMS & WILKINS  

DOI： 10.1249/01.mss.0000485048.60409.08

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Language：Japanese   Publisher：(株)文光堂  

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J-GLOBAL

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J-GLOBAL

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J-GLOBAL

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Language：Japanese   Publisher：(株)杏林書院  

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