The Experts below are selected from a list of 147 Experts worldwide ranked by ideXlab platform
Michael J. Buono - One of the best experts on this subject based on the ideXlab platform.
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blocking the beta adrenergic system does not affect Sweat Gland Function during heat acclimation
Autonomic Neuroscience: Basic and Clinical, 2012Co-Authors: Ricardo Perez Martinez, Douglas M Jones, Daniel Hodge, Michael J. BuonoAbstract:The purpose of the current study was to test the hypothesis that the beta-adrenergic innervation of the human eccrine Sweat Gland facilitates greater Sweat production following heat acclimation. Eight healthy subjects (mean ± SD age: 25.1 ± 4.1 years, weight: 79.0 ± 16.1 kg, and VO(2)max: 48.5 ± 8.0 ml/kg/min) underwent active heat acclimation by walking at 40% of their VO(2)max for 8 days (90 min a day) in an environmental chamber (35.3 ± 0.8°C and 40.2 ± 2.1% rH). To test the hypothesis, the adrenergic component of Sweat Gland innervation was inhibited by continuously administering a 0.5% solution of the beta-adrenergic antagonist propranolol via iontophoresis to a 5 cm(2) area of one forearm during each 90-min exercise bout. The opposing control forearm underwent iontophoresis with a saline solution. Following heat acclimation, mean Sweat rate in the inhibited and control forearm was 0.47 ± 0.30 mg/cm(2)/min and 0.44 ± 0.25mg/cm(2)/min, respectively. Findings of the current study fail to support the hypothesis that adrenergic innervation facilitates human eccrine Sweat Gland Function during heat acclimation, as no significant differences in Sweating were observed. In light of the above, the physiological significance of the dual cholinergic and adrenergic innervation of the eccrine Sweat Gland has yet to be determined.
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peripheral Sweat Gland Function but not whole body Sweat rate increases in women following humid heat acclimation
Journal of Thermal Biology, 2010Co-Authors: Michael J. Buono, Sandra Leichliter Martha, Jay H HeaneyAbstract:The purpose of this study was to compare both the whole-body and pharmacological-induced Sweat rates of men and women following humid heat acclimation. Whole-body Sweat rate was significantly (P<0.05) increased 20% in men following heat acclimation; however, it was essentially unchanged in women. The most important new finding was that humid heat acclimation produced a significant (P<0.05) 60–70% increase in pilocarpine-induced Sweat rate in both men and women. These results suggest that humid heat acclimation significantly improves peripheral Sweat Gland Function equally in both men and women. However, during exercise in humid heat, the increased peripheral Sweat capacity in women is suppressed via either pre- or post-Glandular mechanisms, thus limiting wasteful Sweat production.
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is active Sweating during heat acclimation required for improvements in peripheral Sweat Gland Function
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2009Co-Authors: Michael J. Buono, Travis R Numan, Ryan Claros, Stephanie K Brodine, Fred W. KolkhorstAbstract:We investigated whether the eccrine Sweat Glands must actively produce Sweat during heat acclimation if they are to adapt and increase their capacity to Sweat. Eight volunteers received intradermal...
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peripheral Sweat Gland Function is improved with humid heat acclimation
Journal of Thermal Biology, 2009Co-Authors: Michael J. Buono, Sandra Leichliter Martha, Jay H HeaneyAbstract:Article history: 2. Mean rectal temperature and heart rate were significantly (p
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peripheral Sweat Gland Function improves with humid heat acclimation
2009Co-Authors: Michael J. Buono, Sandra Leichliter Martha, Jay H HeaneyAbstract:Abstract : Background: This study was conducted to determine if humid heat acclimation improves thermoregulatory Function at the level of eccrine Sweat Gland. Methods: Thirteen male volunteers participated in this study, which consisted of 2 h of exercise in a thermal environment of 35 degrees C and 75% relative humidity for 8 consecutive days. All trials were randomized and consisted of four 25-min exercise intervals with 5 min of seated rest. The four exercise intervals consisted of two bouts of treadmill walking (3 mph, 3% grade) and two bouts of cycle ergometry (power output of 60 W). Heart rate and core temperature were measured each minute during the trials and whole-body Sweat rate was calculated for the duration of the exposure. On days 1, 4, and 8 peripheral Sweat production was induced via pilocarpine iontophoresis on the flexor surface of both forearms. Results: Mean rectal temperature and heart rate were significantly reduced by 0.5 degrees C and 17 bpm, respectively, and whole body Sweat rate significantly increased by 20% during the 8-day heat acclimation protocol. Humid heat acclimation produced a significant 63% increase in pilocarpine-induced Sweat rate. Conclusion: The results strongly suggest that heat acclimation improves Sweat Gland Function via a peripheral mechanism.
Fred W. Kolkhorst - One of the best experts on this subject based on the ideXlab platform.
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is active Sweating during heat acclimation required for improvements in peripheral Sweat Gland Function
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2009Co-Authors: Michael J. Buono, Travis R Numan, Ryan Claros, Stephanie K Brodine, Fred W. KolkhorstAbstract:We investigated whether the eccrine Sweat Glands must actively produce Sweat during heat acclimation if they are to adapt and increase their capacity to Sweat. Eight volunteers received intradermal...
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Effect of acute normobaric hypoxia on peripheral Sweat rate.
High altitude medicine & biology, 2002Co-Authors: Dana M. Dipasquale, Fred W. Kolkhorst, Jeanne F. Nichols, Michael J. BuonoAbstract:Peripheral Sweat rate was measured to determine if acute normobaric hypoxia exerted a local inhibition on Sweat Gland Function. It was hypothesized that peripheral Sweat rate would be reduced during hypoxia, following cholinergic stimulation. Nineteen subjects (24 ± 3 yr; 177 ± 9 cm; 75.5 ± 20.1 kg), 8 females and 11 males, were tested once during normobaric hypoxia, simulating an altitude of approximately 3050 m (PO2 = 13.9%; PB ~ 730 mmHg), and once at sea level (200 m; PO2 = 20.9%; PB ~ 730 mmHg). While seated at rest, a ~7-cm2 area of the anterior forearm was stimulated using pilocarpine iontophoresis to produce localized Sweating at the site. Following stimulation, Sweat was collected from the area for 15 min using a Macroduct Sweat Collection System. One-way repeated measures ANOVA indicated a significantly lower Sweat rate during normobaric hypoxia (4.6 ± 2.6 g · m-2 · min-1) compared to sea level (5.5 ± 3.0 g · m-2 · min-1; p = 0.006). Because Sweating was initiated directly at the Sweat Gland, th...
Glen P Kenny - One of the best experts on this subject based on the ideXlab platform.
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ageing attenuates muscarinic mediated Sweating differently in men and women with no effect on nicotinic mediated Sweating
Experimental Dermatology, 2019Co-Authors: Takeshi Nishiyasu, Naoto Fujii, Gregory W Mcgarr, Ronald J Sigal, Pierre Boulay, Glen P KennyAbstract:Ageing attenuates muscarinic-mediated Sweating. However, whether ageing also impairs nicotinic-mediated Sweating remains unclear. Further, despite the known sex-related differences in peripheral Sweat Gland Function, it remains unclear whether age-related modifications of muscarinic and nicotinic-mediated Sweating, if any, are similar between men and women. We assessed local Sweating in young and older healthy men and women (n = 11, each group) at two dorsal forearm skin sites receiving either: (a) methacholine (muscarinic receptor agonist, 5 doses: 0.0125, 0.25, 5, 100, 2000 mmol/L) or (b) nicotine (nicotinic receptor agonist, 5 doses: 1.2, 3.6, 11, 33, 100 mmol/L) via intradermal microdialysis. Age-related reductions in methacholine-induced Sweating were observed at low-to-moderate doses (0.0125-5 mmol/L; all P ≤ 0.05) in men, whereas a reduction was only evident at the highest methacholine dose (2000 mmol/L; P ≤ 0.05) in women. No effect of ageing was observed for nicotine-induced Sweating (all P > 0.26 for main effects of age, dose and all interactions). We showed that while healthy ageing attenuates low-to-moderate levels of muscarinic-mediated Sweating in men, reductions are only observed at high levels of muscarinic-mediated Sweating in women. However, healthy ageing does not modulate nicotinic-mediated Sweating in either men or women.
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age related differences in postsynaptic increases in Sweating and skin blood flow postexercise
Physiological Reports, 2014Co-Authors: Jill M Stapleton, Naoto Fujii, Ryan Mcginn, Katherine Mcdonald, Glen P KennyAbstract:The influence of peripheral factors on the control of heat loss responses (i.e., Sweating and skin blood flow) in the postexercise period remains unknown in young and older adults. Therefore, in eight young (22 ± 3 years) and eight older (65 ± 3 years) males, we examined dose-dependent responses to the administration of acetylcholine (ACh) and methacholine (MCh) for Sweating (ventilated capsule), as well as to ACh and sodium nitroprusside (SNP) for cutaneous vascular conductance (CVC, laser-Doppler flowmetry, % of max). In order to assess if peripheral factors are involved in the modulation of thermoeffector activity postexercise, pharmacological agonists were perfused via intradermal microdialysis on two separate days: (1) at rest (DOSE) and (2) following a 30-min bout of exercise (Ex+DOSE). No differences in Sweat rate between the DOSE and Ex+DOSE conditions at either ACh or MCh were observed for the young (ACh: P = 0.992 and MCh: P = 0.710) or older (ACh: P = 0.775 and MCh: P = 0.738) adults. Similarly, CVC was not different between the DOSE and Ex+DOSE conditions for the young (ACh: P = 0.123 and SNP: P = 0.893) or older (ACh: P = 0.113 and SNP: P = 0.068) adults. Older adults had a lower Sweating response for both the DOSE (ACh: P = 0.049 and MCh: P = 0.006) and Ex+DOSE (ACh: P = 0.050 and MCh: P = 0.029) conditions compared to their younger counterparts. These findings suggest that peripheral factors do not modulate postexercise Sweating and skin blood flow in both young and older adults. Additionally, Sweat Gland Function is impaired in older adults, albeit the impairments were not exacerbated during postexercise recovery.
Weidinger Carl - One of the best experts on this subject based on the ideXlab platform.
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Store-operated Ca2+ entry regulates Ca2+-activated chloride channels and eccrine Sweat Gland Function
'American Society for Clinical Investigation', 2016Co-Authors: Concepcion, Axel R, Vaeth Martin, Wagner, Larry E, Eckstein Miriam, Hecht Lee, Yang Jun, Crottes David, Seidl Maximilian, Shin, Hyosup P, Weidinger CarlAbstract:Eccrine Sweat Glands are essential for Sweating and thermoregulation in humans. Loss-of-Function mutations in the Ca2+ release-activated Ca2+ (CRAC) channel genes ORAI1 and STIM1 abolish store-operated Ca2+ entry (SOCE), and patients with these CRAC channel mutations suffer from anhidrosis and hyperthermia at high ambient temperatures. Here we have shown that CRAC channel-deficient patients and mice with ectodermal tissue-specific deletion of Orai1 (Orai1K14Cre) or Stim1 and Stim2 (Stim1/2K14Cre) failed to Sweat despite normal Sweat Gland development. SOCE was absent in agonist-stimulated Sweat Glands from Orai1K14Cre and Stim1/2K14Cre mice and human Sweat Gland cells lacking ORAI1 or STIM1 expression. In Orai1K14Cre mice, abolishment of SOCE was associated with impaired chloride secretion by primary murine Sweat Glands. In human Sweat Gland cells, SOCE mediated by ORAI1 was necessary for agonist-induced chloride secretion and activation of the Ca2+-activated chloride channel (CaCC) anoctamin 1 (ANO1, also known as TMEM16A). By contrast, expression of TMEM16A, the water channel aquaporin 5 (AQP5), and other regulators of Sweat Gland Function was normal in the absence of SOCE. Our findings demonstrate that Ca2+ influx via store-operated CRAC channels is essential for CaCC activation, chloride secretion, and Sweat production in humans and mice.status: publishe
Carl Weidinger - One of the best experts on this subject based on the ideXlab platform.
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store operated ca2 entry regulates ca2 activated chloride channels and eccrine Sweat Gland Function
Journal of Clinical Investigation, 2016Co-Authors: Axel R Concepcion, Martin Vaeth, Miriam Eckstein, Larry E Wagner, Lee Hecht, Jun Yang, David Crottes, Maximilian Seidl, Hyosup P Shin, Carl WeidingerAbstract:Eccrine Sweat Glands are essential for Sweating and thermoregulation in humans. Loss-of-Function mutations in the Ca2+ release-activated Ca2+ (CRAC) channel genes ORAI1 and STIM1 abolish store-operated Ca2+ entry (SOCE), and patients with these CRAC channel mutations suffer from anhidrosis and hyperthermia at high ambient temperatures. Here we have shown that CRAC channel-deficient patients and mice with ectodermal tissue-specific deletion of Orai1 (Orai1K14Cre) or Stim1 and Stim2 (Stim1/2K14Cre) failed to Sweat despite normal Sweat Gland development. SOCE was absent in agonist-stimulated Sweat Glands from Orai1K14Cre and Stim1/2K14Cre mice and human Sweat Gland cells lacking ORAI1 or STIM1 expression. In Orai1K14Cre mice, abolishment of SOCE was associated with impaired chloride secretion by primary murine Sweat Glands. In human Sweat Gland cells, SOCE mediated by ORAI1 was necessary for agonist-induced chloride secretion and activation of the Ca2+-activated chloride channel (CaCC) anoctamin 1 (ANO1, also known as TMEM16A). By contrast, expression of TMEM16A, the water channel aquaporin 5 (AQP5), and other regulators of Sweat Gland Function was normal in the absence of SOCE. Our findings demonstrate that Ca2+ influx via store-operated CRAC channels is essential for CaCC activation, chloride secretion, and Sweat production in humans and mice.
