scholarly journals Cutaneous adrenergic nerve blockade attenuates sweating during incremental exercise in habitually trained men

2018 ◽  
Vol 125 (4) ◽  
pp. 1041-1050 ◽  
Author(s):  
Tatsuro Amano ◽  
Naoto Fujii ◽  
Yoshimitsu Inoue ◽  
Narihiko Kondo

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.

2017 ◽  
Vol 123 (1) ◽  
pp. 182-189 ◽  
Author(s):  
Tatsuro Amano ◽  
Yosuke Shitara ◽  
Naoto Fujii ◽  
Yoshimitsu Inoue ◽  
Narihiko Kondo

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.


2020 ◽  
Vol 319 (5) ◽  
pp. R584-R591
Author(s):  
Tatsuro Amano ◽  
Naoto Fujii ◽  
Glen P. Kenny ◽  
Yumi Okamoto ◽  
Yoshimitsu Inoue ◽  
...  

We evaluated the hypothesis that the activation of L-type voltage-gated Ca2+ channels contributes 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 verapamil-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 was continuously measured throughout both protocols. Pilocarpine-induced sweating in Control was higher in trained than in untrained men for both the concentrations of pilocarpine (both P ≤ 0.001). Pilocarpine-induced sweating at the low-dose site was attenuated at the Verapamil versus the Control site in both the groups (both P ≤ 0.004), albeit the reduction was greater in trained as compared with in untrained men ( P = 0.005). The verapamil-mediated reduction in sweating remained intact at the high-dose pilocarpine site in the untrained men ( 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.


2016 ◽  
Vol 51 (9) ◽  
pp. 696-700 ◽  
Author(s):  
Jorge Aburto-Corona ◽  
Luis Aragón-Vargas

Context: Sunscreen lotions are important to protect the skin during outdoor exercise, but they may interfere with sweating. Objective: To measure the effect of 2 water-resistant sunscreens on local sweat production in men and women exercising in the heat and to compare those effects with the expected inhibition resulting from the use of an antiperspirant. Design: Randomized crossover study. Setting: Exercise in the heat (ambient temperature = 30.2°C ± 0.4°C dry bulb and 58% ± 4.3% relative humidity) in a controlled-environment laboratory. Patients or Other Participants: Twenty physically active, apparently healthy college students, 10 men (age = 22.5 ± 2.8 years, height = 1.771 ± 0.069 m, mass = 70.2 ± 11.0 kg) and 10 women (age = 22.2 ± 3.2 years, height = 1.625 ± 0.075 m, mass = 57.7 ± 7.9 kg). Intervention(s): With sweat-collection patches applied to their right and left scapular regions, the participants performed 2 exercise sessions on consecutive days. We assigned skin treatments (antiperspirant; organic chemical sun filter, sunscreen A; inorganic physical sun block, sunscreen B; no lotion) randomly to side and session. Participants pedaled at 79% ± 1% of maximum heart rate for 20 minutes in the heat. Main Outcome Measure(s): Scapular localized sweat rate. Results: No baseline, environmental, or exercise condition was different among skin treatments. Scapular localized sweat rate was lower for the antiperspirant treatment (88.3 μL/min·dm2; 95% confidence interval [CI] = 82.0, 94.7 μL/min·dm2) and the inorganic physical sun block (sunscreen B) treatment (99.3 μL/min·dm2; 95% CI = 93.1, 105.5 μL/min·dm2) than for the organic chemical sun filter (sunscreen A) treatment (114.8 μL/min·dm2; 95% CI = 108.8, 120.6 μL/min·dm2) or the no-lotion treatment (122.6 μL/min·dm2; 95% CI = 116.2, 129.0 μL/min·dm2; P &lt; .01). Conclusions: The inorganic physical sun block, sunscreen B, hindered effective sweating to the same extent as the antiperspirant, whereas the treatment with the organic chemical sun filter, sunscreen A, was not different from the control treatment. At this stage, it is not possible to identify the specific ingredient responsible for the effect.


1988 ◽  
Vol 254 (5) ◽  
pp. H871-H878 ◽  
Author(s):  
R. A. Cohen ◽  
R. M. Weisbrod

The overflow of endogenous norepinephrine caused by transmural electrical stimulation or depolarization with potassium was smaller in superfused segments of the rabbit carotid artery with intact endothelium than in segments denuded of endothelium. In segments preincubated with [3H]norepinephrine, the lesser overflow was found to be partially due to metabolism by the endothelium of the neurotransmitter. Even after treatment to block the disposition of norepinephrine, the endothelium acted as a partial physical barrier to the overflow of norepinephrine into the lumen of arteries superfused and perfused selectively. However, a lesser overflow of norepinephrine to the adventitia of the artery accounted for the majority of the difference in overflow between segments with and without endothelium. The inhibition by the endothelium of the overflow of norepinephrine from adrenergic nerves was unaffected by blocking prejunctional alpha 2-adrenoceptors, prostaglandin synthesis, free radicals, or guanylate cyclase. Vasodilators released from the endothelium of a donor artery inhibited contractions caused by adrenergic nerve stimulation of a bioassay artery but failed to inhibit norepinephrine release. These observations indicate that the endothelium 1) metabolizes norepinephrine, 2) acts as a physical barrier to its overflow into the blood vessel lumen, and 3) inhibits the release of the adrenergic transmitter from adrenergic nerves.


1988 ◽  
Vol 65 (2) ◽  
pp. 811-814 ◽  
Author(s):  
M. J. Buono ◽  
N. T. Sjoholm

The purpose of this study was to determine the in vivo secretory activity of sweat glands from sedentary and trained subjects. Peripheral sweat production was determined using pilocarpine iontophoresis in 40 volunteers (10 sedentary men, 10 endurance-trained men, 10 sedentary women, 10 endurance-trained women). Peripheral sweat rate was significantly (P less than 0.05) greater in trained men [6.9 +/- 0.6 (SE) g.m2.min-1] and women (6.1 +/- 0.7) compared with sedentary men (3.1 +/- 0.5) and women (2.5 +/- 0.4). Furthermore, peripheral sweat rate was significantly correlated (r = 0.73) with maximal O2 uptake. The above two findings would suggest that physical training improves the secretory activity of the human sweat gland. Such a result supports previous findings that have suggested that the potentiation in sweating seen after training is achieved via a peripheral mechanism. In addition, several gender-related differences were found in the sudorific response of men and women. Specifically, women have a significantly greater sweat gland density, whereas men have a greater sweat production per gland.


2010 ◽  
Vol 22 (1) ◽  
pp. 379
Author(s):  
H. Kohram ◽  
G. Mohammadi ◽  
E. Dirandeh

This study was done to consider relationships of luteal phase variables (prior to AI) with follicular waves. The estrous cycles of 15 buffaloes were synchronized with 2 i.m. injections of prostaglandin F2α given 11 days apart. The buffaloes were randomly assigned to 1 of 3 treatments. Buffaloes in the control treatment received no treatment, whereas G6 buffalos received a GnRH injection between Day 5 and 7 and G16 buffalos received a GnRH injection between Day 15 and 17 of the estrous cycle (estrus = Day 0). Daily, from estrus Day 0 to the next estrus Day 23, buffaloes had their ovaries scanned by ultrasound. Blood samples were collected by tail following each ultrasound examination from estrus until next estrus (estrus = 0). Concentrations of plasma progesterone were determined by radioimmunoassay kit. The limit of detection of the assay was 0.1 45 ng mL-1 and the intra- and interassay coeffients of variation were 7.4% and 9.2%, respectively. Data were analyzed by using PROC GLM of SAS (SAS Institute, Cary, NC, USA). For comparisons between groups, the 2-sample t-test was used for continuous traits, such as size of CL or hormone concentrations. Prospective comparisons of indices of progesterone indicated that the length of luteal lifespan was longer in 3-wave than in 2-wave buffaloes (P < 0.01). Plasma progesterone concentrations were similar at peak and measured as area under the curve on Day 5 through 17 preceding insemination in 2-wave (5.30 ± 0.40 ng mL-1) and 3-wave buffaloes (5.10 ± 0.20 ng mL-1). Length of the luteal phase (defined as from the day of estrus until the last day on which plasma progesterone remained >2 ng mL-1) was <2 days shorter in 2-wave buffaloes than in 3-wave buffaloes (15.20 ± 0.40 v. 17.10 ± 0.50 d; P < 0.05). In addition, the day of peak progesterone occurred earlier in 2-wave buffaloes (13.50 ± 0.30 v. 15.30 ± 0.70 d; P < 0.05).


2005 ◽  
Vol 81 (3) ◽  
pp. 399-402 ◽  
Author(s):  
H. Säkkinen ◽  
J. Tornberg ◽  
P. J. Goddard ◽  
E. Eloranta ◽  
E. Dahl ◽  
...  

AbstractPlasma cortisol concentrations were determined from the blood of eight mature female reindeer (Rangifer tarandus tarandus) after an intravenous injection of either saline (control) or 100, 250 or 500 μg of synthetic ACTH. Blood samples were collected at 0, 2, 4, 6, 8, 10, 15, 20, 25, 30, 45, 60, 75, 90, 120, 150, and 180 min after the injections. The aims were to determine the appropriate dose of ACTH for adrenal stimulation tests, to define the dose level of ACTH which elicited a maximal cortisol response and to describe the range of blood cortisol concentrations for reference when evaluating the stress responses of reindeer.The mean plasma cortisol concentrations (s.e.) at the zero sample times (t0) of the control and the ACTH treatments varied between 93·4 (11·8) and 132·5 (18·1) nmol/l. The total plasma cortisol response (area under curve, AUC, nmol/l × min) increased with increasing dose of ACTH (P < 0·001). The AUC of the control treatment was significantly smaller than of the ACTH treatments (P < 0·001). The highest dose of ACTH (500 μg) gave a significantly bigger AUC than the lowest dose (100 μg) (P = 0·008). The maximal plasma cortisol concentrations (CMAX) were achieved within 60 min of the ACTH injections. The ranges of individual CMAX were 59·0 to 136·8 nmol/l for the control treatment, and 110·0 to 252·0, 152·0 to 247·5 and 135·1 to 257·1 nmol/l for 100, 250 and 500 μg ACTH, respectively. The difference in CMAX was significant between the control treatment and the ACTH treatments (P < 0·001) but not between the different doses of ACTH. The plasma cortisol concentrations at the end of the observation period at t180 were not significantly affected by the ACTH treatment (P > 0·05).In conclusion, the 100-μg dose of ACTH was sufficient to produce a significant cortisol response compared with the control treatment. Increasing the dose did not increase the maximal response, but tended to elongate the response profile. The blood sampling frequency used in the study was found suitable for detection of the cortisol response in reindeer.


2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
D Aronson ◽  
Y Nitzan ◽  
S Petcherski ◽  
E Bravo ◽  
M Habib ◽  
...  

Abstract Background Current treatment of fluid retention in heart failure (HF) relies primarily on diuretics. However, adequate decongestion is not achieved in many patients. Purpose To study the feasibility and short-term performance of a novel approach to remove fluids and sodium directly from the interstitial compartment by enhancing sweat rate. Methods We used a device designed to enhance fluid and salt loss via the eccrine sweat glands. Skin temperature in the lower body was increased to 35–38°, where the slope of the relationship between temperature and sweat production is linear. With this wearable device, the sweat evaporates instantaneously, thus avoiding the awareness of perspiration. The primary efficacy endpoint was the ability to increase skin temperature to the desired range without elevating the core temperature above normal range. A secondary efficacy endpoint was a clinically meaningful hourly sweat output, defined as ≥150 mL/h. The primary safety endpoint was any procedure-related adverse events. Results We studied 6 normal subjects and 10 HF patients with clinical evidence of congestion and median NT-proBNP of 602 pg/mL [interquartile range 427 to 1719 pg/mL]. Participants underwent 3 treatment sessions of up to 4h. Skin temperature increased to a median of 37.5°C (interquartile range 37.1–37.9°C) with the core temperature remaining unchanged. The median total weight loss during treatment was 219±67 g/h (Figure) with a range of 100–338 g/h. In 77% of cases, the average sweat rate was ≥150 mL/h. Systolic (P=0.25) and diastolic (P=0.48) blood pressure and heart rate (P=0.11) remained unchanged during the procedure. There were no significant changes in renal function and no procedure-related adverse events. Conclusion Enhancing sweat rate was safe and resulted in a clinically meaningful fluid removal and weight loss. Further evaluation of this concept is warranted. FUNDunding Acknowledgement Type of funding sources: Private company. Main funding source(s): AquaPass Inc Weight loss due to sweat


2019 ◽  
Vol 109 (5) ◽  
pp. 1335-1343 ◽  
Author(s):  
Christina McVeay ◽  
Penelope C E Fitzgerald ◽  
Sina S Ullrich ◽  
Robert E Steinert ◽  
Michael Horowitz ◽  
...  

ABSTRACT Background The fatty acid, lauric acid (‘C12’), and the amino acid, L-tryptophan (‘Trp’), modulate gastrointestinal functions including gut hormones and pyloric pressures, which are important for the regulation of energy intake, and both potently suppress energy intake. Objective We hypothesized that the intraduodenal administration of C12 and Trp, at loads that do not affect energy intake individually, when combined will reduce energy intake, which is associated with greater modulation of gut hormones and pyloric pressures. Design Sixteen healthy, lean males (age: 24 ± 1.5 y) received 90-min intraduodenal infusions of saline (control), C12 (0.3 kcal/min), Trp (0.1 kcal/min), or C12 + Trp (0.4 kcal/min), in a randomized, double-blind, cross-over study. Antropyloroduodenal pressures were measured continuously, and plasma cholecystokinin (CCK), ghrelin, and glucagon-like peptide-1 (GLP-1) concentrations, appetite perceptions, and gastrointestinal symptoms at 15-min intervals. Immediately after the infusions, energy intake from a standardized buffet meal was quantified. Results C12 + Trp markedly reduced energy intake (kcal; control: 1,232 ± 72, C12: 1,180 ± 82, Trp: 1,269 ± 73, C12 + Trp: 1,056 ± 106), stimulated plasma CCK (AUC(area under the curve)0–90 min, pmol/L*min; control: 21 ± 8; C12: 129 ± 15; Trp: 97 ± 16; C12 + Trp: 229 ± 22) and GLP-1 (AUC0–90 min, pmol/L*min; control: 102 ± 41; C12: 522 ± 102; Trp: 198 ± 63; C12 + Trp: 545 ± 138), and suppressed ghrelin (AUC0–90 min, pg/mL*min; control: −3,433 ± 2,647; C12: −11,825 ± 3,521; Trp: −8,417 ± 3,734; C12 + Trp: −18,188 ± 4,165) concentrations, but did not stimulate tonic, or phasic, pyloric pressures, compared with the control (all P < 0.05), or have adverse effects. C12 and Trp each stimulated CCK (P < 0.05), but to a lesser degree than C12 + Trp, and did not suppress energy intake or ghrelin. C12, but not Trp, stimulated GLP-1 (P < 0.05) and phasic pyloric pressures (P < 0.05), compared with the control. Conclusion The combined intraduodenal administration of C12 and Trp, at loads that individually do not affect energy intake, substantially reduces energy intake, which is associated with a marked stimulation of CCK and suppression of ghrelin. The study was registered as a clinical trial at the Australian and New Zealand Clinical Trial Registry (www.anzctr.org.au,) as 12613000899741.


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