scholarly journals Evidence for β-adrenergic modulation of sweating during incremental exercise in habitually trained males

2017 ◽  
Vol 123 (1) ◽  
pp. 182-189 ◽  
Author(s):  
Tatsuro Amano ◽  
Yosuke Shitara ◽  
Naoto Fujii ◽  
Yoshimitsu Inoue ◽  
Narihiko Kondo
Keyword(s):  
Relative Intensity ◽  
Sweat Rate ◽  
Absolute Intensity ◽  
Control Site ◽  
Incremental Exercise ◽  
Saline Control ◽  
Maximum Workload ◽  
Sweat Production ◽  
Adrenergic Mechanism

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.

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
Keyword(s):  
Sweat Rate ◽  
Area Under The Curve ◽  
Incremental Exercise ◽  
Adrenergic Nerves ◽  
Control Treatment ◽  
Adrenergic Nerve ◽  
Saline Control ◽  
Nerve Blockade ◽  
Maximum Workload ◽  
Sweat Production

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.

Effects of L-type voltage-gated Ca2+ channel blockade on cholinergic and thermal sweating in habitually trained and untrained men

2020 ◽  
Vol 319 (5) ◽  
pp. R584-R591
Author(s):  
Tatsuro Amano ◽  
Naoto Fujii ◽  
Glen P. Kenny ◽  
Yumi Okamoto ◽  
Yoshimitsu Inoue ◽  
...  
Keyword(s):  
Rectal Temperature ◽  
Low Dose ◽  
Sweat Rate ◽  
Control Site ◽  
Hot Water ◽  
Saline Control ◽  
High Dose ◽  
Voltage Gated ◽  
Sweat Production ◽  
Forearm Skin

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.

Effect of physical training on peripheral sweat production

1988 ◽  
Vol 65 (2) ◽  
pp. 811-814 ◽  
Author(s):  
M. J. Buono ◽  
N. T. Sjoholm
Keyword(s):  
Physical Training ◽  
Sweat Gland ◽  
Sweat Rate ◽  
Secretory Activity ◽  
Sweat Glands ◽  
Trained Subjects ◽  
Peripheral Mechanism ◽  
Sweat Production ◽  
Sedentary Women

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.

Effect of local acetylcholinesterase inhibition on sweat rate in humans

2001 ◽  
Vol 90 (3) ◽  
pp. 757-762 ◽  
Author(s):  
Manabu Shibasaki ◽  
Craig G. Crandall
Keyword(s):  
Sweat Rate ◽  
Ringer Solution ◽  
Control Site ◽  
Acetylcholinesterase Inhibition ◽  
Whole Body ◽  
Sweat Glands ◽  
Ache Inhibitor ◽  
Temperature Threshold ◽  
Treated Site

ACh is the neurotransmitter responsible for increasing sweat rate (SR) in humans. Because ACh is rapidly hydrolyzed by acetylcholinesterase (AChE), it is possible that AChE contributes to the modulation of SR. Thus the primary purpose of this project was to identify whether AChE around human sweat glands is capable of modulating SR during local application of various concentrations of ACh in vivo, as well as during a heat stress. In seven subjects, two microdialysis probes were placed in the intradermal space of the forearm. One probe was perfused with the AChE inhibitor neostigmine (10 μM); the adjacent membrane was perfused with the vehicle (Ringer solution). SR over both membranes was monitored via capacitance hygrometry during microdialysis administration of various concentrations of ACh (1 × 10−7–2 M) and during whole body heating. SR was significantly greater at the neostigmine-treated site than at the control site during administration of lower concentrations of ACh (1 × 10−7–1 × 10−3 M, P < 0.05), but not during administration of higher concentrations of ACh (1 × 10−2–2 M, P > 0.05). Moreover, the core temperature threshold for the onset of sweating at the neostigmine-treated site was significantly reduced relative to that at the control site. However, no differences in SR were observed between sites after 35 min of whole body heating. These results suggest that AChE is capable of modulating SR when ACh concentrations are low to moderate (i.e., when sudomotor activity is low) but is less effective in governing SR after SR has increased substantially.

THYROID STIMULATORS AND THYROID STIMULATION

1971 ◽  
Vol 66 (3) ◽  
pp. 558-576 ◽  
Author(s):  
Gerald Burke
Keyword(s):  
Regulatory System ◽  
Control Site ◽  
Thyroid Cell ◽  
Primary Control ◽  
Physico Chemical ◽  
Site Of Action ◽  
Long Acting

ABSTRACT A long-acting thyroid stimulator (LATS), distinct from pituitary thyrotrophin (TSH), is found in the serum of some patients with Graves' disease. Despite the marked physico-chemical and immunologic differences between the two stimulators, both in vivo and in vitro studies indicate that LATS and TSH act on the same thyroidal site(s) and that such stimulation does not require penetration of the thyroid cell. Although resorption of colloid and secretion of thyroid hormone are early responses to both TSH and LATS, available evidence reveals no basic metabolic pathway which must be activated by these hormones in order for iodination reactions to occur. Cyclic 3′, 5′-AMP appears to mediate TSH and LATS effects on iodination reactions but the role of this compound in activating thyroidal intermediary metabolism is less clear. Based on the evidence reviewed herein, it is suggested that the primary site of action of thyroid stimulators is at the cell membrane and that beyond the(se) primary control site(s), there exists a multifaceted regulatory system for thyroid hormonogenesis and cell growth.

scholarly journals Role of Bradykinin Type 2 Receptors in Human Sweat Secretion: Translational Evidence Does Not Support a Functional Relationship

2021 ◽  
Vol 34 (3) ◽  
pp. 162-166
Author(s):  
Thad E. Wilson ◽  
Seetharam Narra ◽  
Kristen Metzler-Wilson ◽  
Artur Schneider ◽  
Kelsey A. Bullens ◽  
...  
Keyword(s):  
Healthy Subjects ◽  
Sweat Rate ◽  
Sweat Glands ◽  
Potential Therapeutic Target ◽  
Sweat Secretion ◽  
Hoe 140 ◽  
A Current

Bradykinin increases skin blood flow via a cGMP mechanism but its role in sweating in vivo is unclear. There is a current need to translate cell culture and nonhuman paw pad studies into in vivo human preparations to test for therapeutic viability for disorders affecting sweat glands. Protocol 1: physiological sweating was induced in 10 healthy subjects via perfusing warm (46–48°C) water through a tube-lined suit while bradykinin type 2 receptor (B2R) antagonist (HOE-140; 40 μM) and only the vehicle (lactated Ringer’s) were perfused intradermally via microdialysis. Heat stress increased sweat rate (HOE-140 = +0.79 ± 0.12 and vehicle = +0.64 ± 0.10 mg/cm<sup>2</sup>/min), but no differences were noted with B2R antagonism. Protocol 2: pharmacological sweating was induced in 6 healthy subjects via intradermally perfusing pilocarpine (1.67 mg/mL) followed by the same B2R antagonist approach. Pilocarpine increased sweating (HOE-140 = +0.38 ± 0.16 and vehicle = +0.32 ± 0.12 mg/cm<sup>2</sup>/min); again no differences were observed with B2R antagonism. Last, 5 additional subjects were recruited for various control experiments which identified that a functional dose of HOE-140 was utilized and it was not sudorific during normothermic conditions. These data indicate B2R antagonists do not modulate physiologically or pharmacologically induced eccrine secretion volumes. Thus, B2R agonist/antagonist development as a potential therapeutic target for hypo- and hyperhidrosis appears unwarranted.

Fat and carbohydrate metabolism during exercise in elderly and young subjects

1996 ◽  
Vol 271 (6) ◽  
pp. E983-E989 ◽  
Author(s):  
S. Sial ◽  
A. R. Coggan ◽  
R. Carroll ◽  
J. Goodwin ◽  
S. Klein
Keyword(s):  
Young Adults ◽  
Carbohydrate Metabolism ◽  
Relative Intensity ◽  
The Elderly ◽  
Absolute Intensity ◽  
Substrate Oxidation ◽  
Carbohydrate Oxidation ◽  
Moderate Intensity ◽  
Elderly Subjects ◽  
Moderate Intensity Exercise

We evaluated the effect of aging on fat and carbohydrate metabolism during moderate intensity exercise. Glycerol, free fatty acid (FFA), and glucose rate of appearance (Ra) in plasma and substrate oxidation were determined during 60 min of cycle ergometer exercise in six elderly (73 +/- 2 yr) and six young adults (26 +/- 2 yr) matched by gender and lean body mass. The elderly group was studied during exercise performed at 56 +/- 3% of maximum oxygen uptake, whereas the young adults were studied during exercise performed at the same absolute and at a similar relative intensity as the elderly subjects. Mean fat oxidation during exercise was 25-35% lower in the elderly subjects than in the young adults exercising at either the same absolute or similar relative intensities (P < 0.05). Mean carbohydrate oxidation in the elderly group was 35% higher than the young adults exercising at the same absolute intensity (P < 0.001) but 40% lower than the young adults exercising at the same relative intensity (P < 0.001). Average FFA Ra in the elderly subjects was 85% higher than in the young adults exercising at the same absolute intensity (P < 0.05) but 35% lower than the young adults exercising at a similar relative intensity (P < 0.05). We conclude that fat oxidation is decreased while carbohydrate oxidation is increased during moderate intensity exercise in elderly men and women. The shift in substrate oxidation was caused by age-related changes in skeletal muscle respiratory capacity because lipolytic rates and FFA availability were not rate limiting in the older subjects.

scholarly journals Effects of Formyl Peptide Receptor Agonists Ac9-12 and WKYMV in In Vivo and In Vitro Acute Inflammatory Experimental Models

Cells ◽  
2022 ◽  
Vol 11 (2) ◽  
pp. 228
Author(s):  
Izabella Lice ◽  
José Marcos Sanches ◽  
Rebeca D. Correia-Silva ◽  
Mab P. Corrêa ◽  
Marcelo Y. Icimoto ◽  
...  
Keyword(s):  
Therapeutic Potential ◽  
Biological Effects ◽  
Experimental Models ◽  
Formyl Peptide Receptor ◽  
Saline Control ◽  
Acute Peritonitis ◽  
Formyl Peptide ◽  
Leukocyte Influx

Formyl peptide receptors (Fprs) are a G-protein-coupled receptor family mainly expressed on leukocytes. The activation of Fpr1 and Fpr2 triggers a cascade of signaling events, leading to leukocyte migration, cytokine release, and increased phagocytosis. In this study, we evaluate the effects of the Fpr1 and Fpr2 agonists Ac9-12 and WKYMV, respectively, in carrageenan-induced acute peritonitis and LPS-stimulated macrophages. Peritonitis was induced in male C57BL/6 mice through the intraperitoneal injection of 1 mL of 3% carrageenan solution or saline (control). Pre-treatments with Ac9-12 and WKYMV reduced leukocyte influx to the peritoneal cavity, particularly neutrophils and monocytes, and the release of IL-1β. The addition of the Fpr2 antagonist WRW4 reversed only the anti-inflammatory actions of WKYMV. In vitro, the administration of Boc2 and WRW4 reversed the effects of Ac9-12 and WKYMV, respectively, in the production of IL-6 by LPS-stimulated macrophages. These biological effects of peptides were differently regulated by ERK and p38 signaling pathways. Lipidomic analysis evidenced that Ac9-12 and WKYMV altered the intracellular lipid profile of LPS-stimulated macrophages, revealing an increased concentration of several glycerophospholipids, suggesting regulation of inflammatory pathways triggered by LPS. Overall, our data indicate the therapeutic potential of Ac9-12 and WKYMV via Fpr1 or Fpr2-activation in the inflammatory response and macrophage activation.

Endocrinologic and metabolic effects of interleukin-6 in humans

1995 ◽  
Vol 268 (5) ◽  
pp. E813-E819 ◽  
Author(s):  
J. M. Stouthard ◽  
J. A. Romijn ◽  
T. Van der Poll ◽  
E. Endert ◽  
S. Klein ◽  
...  
Keyword(s):  
Energy Expenditure ◽  
Interleukin 6 ◽  
Cell Cancer ◽  
Metabolic Effects ◽  
Isotope Dilution Method ◽  
Saline Control ◽  
Dilution Method ◽  
Plasma Norepinephrine ◽  
Metabolic Clearance

Interleukin-6 (IL-6) is one of the major circulating cytokines in catabolic states. To investigate its endocrinologic and metabolic actions in vivo, we studied eight patients with metastatic renal cell cancer two times, once during infusion of saline (control) and once during a 4-h infusion of 150 micrograms recombinant human IL-6 (rhIL-6). Rates of appearance (Ra) of glucose and free fatty acids (FFA) in plasma were measured by using the isotope dilution method. Energy expenditure and substrate oxidation were determined by indirect calorimetry. rhIL-6 induced increases in plasma norepinephrine (+261 +/- 97%, P < 0.001), cortisol (+210 +/- 48%, P < 0.001), and glucagon (+70 +/- 18%, P < 0.001), in resting energy expenditure (+25 +/- 2%, P < 0.001 vs. control), and in plasma FFA concentration (+60 +/- 30%, P < 0.001), FFA Ra (+105 +/- 18%, P < 0.001), and fat oxidation (+38 +/- 16%, P < 0.001). Glucose Ra increased by 20 +/- 5% (P < 0.01) during rhIL-6 infusion with a concomitant increase in the metabolic clearance rate of glucose. In conclusion, our data demonstrate that rhIL-6 induces many of the endocrinologic and metabolic changes found in catabolic states and thus may mediate some of the metabolic effects previously ascribed to other cytokines.

scholarly journals Electrophysiological measurement of the number of rhodopsin molecules in single Limulus photoreceptors.

1977 ◽  
Vol 70 (5) ◽  
pp. 621-633 ◽  
Author(s):  
J E Lisman ◽  
H Bering
Keyword(s):  
Relative Intensity ◽  
Surface Density ◽  
Receptor Potential ◽  
Absolute Intensity ◽  
Charge Movement ◽  
Half Time ◽  
Quantal Response ◽  
Early Receptor Potential ◽  
Electrophysiological Measurement ◽  
Electrophysiological Methods

Two partly independent electrophysiological methods are described for measuring the number of rhodopsin molecules (R) in single ventral photoreceptors. Method 1 is based on measurements of the relative intensity required to elicit a quantal response and the relative intensity required to half-saturate the early receptor potential (ERP). Method 2 is based on measurements of the absolute intensity required to elicit a quantal response. Both methods give values of R approximately equal to 10(9). From these and other measurements, estimates are derived for the surface density of rhodopsin (8,000/micrometer2), the charge movement during the ERP per isomerized rhodopsin (20 X 10(-21) C), and the half-time for thermal isomerization of rhodopsin (36yr).

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