The role of in vivo β-adrenergic stimulation on sweat production during exercise

Buono, Michael J.; González, Gabriela; Guest, Shaun; Hare, A.; Numan, Travis; Tabor, Brian; White, Ailish C.

doi:10.1016/j.autneu.2009.12.006

Cited by 15 publications

(8 citation statements)

References 18 publications

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“…Human eccrine sweating during heat stress is governed exclusively by the sympathetic cholinergic system (5,19,25). Thus our observations of an involvement of K V channels in cholinergic sweating support a role for K V channels in thermal sweating.…”

Section: Perspectives and Significancesupporting

confidence: 74%

K⁺ channel mechanisms underlying cholinergic cutaneous vasodilation and sweating in young humans: roles of K_Ca, K_ATP, and K_V channels?

Fujii

Louie

McNeely

et al. 2016

American Journal of Physiology-Regulatory, Integrative and Comp

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Acetylcholine released from cholinergic nerves is involved in heat loss responses of cutaneous vasodilation and sweating. K(+) channels are thought to play a role in regulating cholinergic cutaneous vasodilation and sweating, though which K(+) channels are involved in their regulation remains unclear. We evaluated the hypotheses that 1) Ca(2+)-activated K(+) (KCa), ATP-sensitive K(+) (KATP), and voltage-gated K(+) (KV) channels all contribute to cholinergic cutaneous vasodilation; and 2) KV channels, but not KCa and KATP channels, contribute to cholinergic sweating. In 13 young adults (24 ± 5 years), cutaneous vascular conductance (CVC) and sweat rate were evaluated at intradermal microdialysis sites that were continuously perfused with: 1) lactated Ringer (Control), 2) 50 mM tetraethylammonium (KCa channel blocker), 3) 5 mM glybenclamide (KATP channel blocker), and 4) 10 mM 4-aminopyridine (KV channel blocker). At all sites, cholinergic cutaneous vasodilation and sweating were induced by coadministration of methacholine (0.0125, 0.25, 5, 100, and 2,000 mM, each for 25 min). The methacholine-induced increase in CVC was lower with the KCa channel blocker relative to Control at 0.0125 (1 ± 1 vs. 9 ± 6%max) and 5 (2 ± 5 vs. 17 ± 14%max) mM methacholine, whereas it was lower in the presence of KATP (69 ± 7%max) and KV (57 ± 14%max) channel blocker compared with Control (79 ± 6%max) at 100 mM methacholine. Furthermore, methacholine-induced sweating was lower at the KV channel blocker site (0.42 ± 0.17 mg·min(-1)·cm(-2)) compared with Control (0.58 ± 0.15 mg·min(-1)·cm(-2)) at 2,000 mM methacholine. In conclusion, we show that KCa, KATP, and KV channels play a role in cholinergic cutaneous vasodilation, whereas only KV channels contribute to cholinergic sweating in normothermic resting humans.

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Section: Perspectives and Significancesupporting

confidence: 74%

K⁺ channel mechanisms underlying cholinergic cutaneous vasodilation and sweating in young humans: roles of K_Ca, K_ATP, and K_V channels?

Fujii

Louie

McNeely

et al. 2016

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Eccrine sweat glands, which are predominantly responsive to cholinergic stimulation, can also respond to adrenergic stimulation (Sato & Sato, 1981). While numerous studies have reported that adrenergic stimulation of sweat glands within the forearm produces minimal or no changes in local sweating (Morgan et al 2006; Buono et al 2010), the local sweating response to the administration of adrenergic agonists has not been investigated in the forehead. According to this hypothesis, cholinergic stimulation of whole‐body and local forearm (i.e.…”

Section: Discussionmentioning

confidence: 99%

Local sweating on the forehead, but not forearm, is influenced by aerobic fitness independently of heat balance requirements during exercise

Cramer

Bain

Jay

2012

Experimental Physiology

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The present study investigated the influence of maximal oxygen uptake (V O 2 max ) on local steadystate sudomotor responses to exercise, independently of evaporative requirements for heat balance (E req ). Eleven fit (F;V O 2 max 61.9 ± 6.0 ml kg −1 min −1 ) and 10 unfit men (UF;V O 2 max 40.4 ± 3.8 ml kg −1 min −1 ) cycled for 60 min at an air temperature of 24.5 ± 0.8 • C and ambient humidity of 0.9 ± 0.3 kPa at a set metabolic heat production per unit surface area, producing the same E req in all participants (BAL trial) and, in a second trial, at 60% ofV O 2 max . During the BAL trial, absolute power (F 107 ± 2 and UF 102 ± 2 W; P = 0.126), E req (F 175 ± 5 and UF 176 ± 9 W m −2 ; P = 0.855), steady-state whole-body sweat rate (F 0.44 ± 0.02 and UF 0.47 ± 0.02 mg cm −2 min −1 ; P = 0.385) and local sweat rate on the arm (F 0.29 ± 0.03 and UF 0.35 ± 0.03 mg cm −2 min −1 ; P = 0.129) were not different between groups; however, local sweat rate on the forehead in UF (1.67 ± 0.20 mg cm −2 min −1 ) was almost double (P = 0.002) that of F (0.87 ± 0.11 mg cm −2 min −1 ). Heart rate, ratings of perceived exertion and relative exercise intensity were also significantly greater in UF (P < 0.05). There was a trend towards an elevated minute ventilation in UF (P = 0.052), while end-tidal P CO 2 was significantly lower in UF (P = 0.028). At 60%V O 2 max , absolute power (F 174 ± 6 and UF 110 ± 5 W; P < 0.001), E req (F 291 ± 14 and UF 190 ± 17 W m −2 ; P < 0.001), steady-state whole-body sweat rate (F 0.84 ± 0.05 and UF 0.53 ± 0.03 mg cm −2 min −1 ; P < 0.001) and local sweat rate on the arm (F 0.75 ± 0.04 and UF 0.35 ± 0.03 mg cm −2 min −1 ; P < 0.001) and on the forehead (F 2.92 ± 0.42 and UF 1.68 ± 0.23 mg cm −2 min −1 ; P = 0.022) were all significantly greater in F compared with UF. Heart rate and ratings of perceived exertion were similar at all time points (P > 0.05). Significantly greater minute ventilation (P < 0.001) and end-tidal P CO 2 responses (P = 0.017) were found in F. In conclusion, aerobic fitness alters local sweating on the forehead, but not the forearm, independently of evaporative requirements for heat balance, and may be the result of differential control of sweating in these skin areas associated with the relative intensity of exercise.

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“…During in vitro investigation of isolated monkey palmar eccrine sweat glands, Sato and Sato (1981) observed relative effects of 4:2:1 for cholinergic, β-adrenergic, and α-adrenergic stimulation on sweating rate, respectively. In other studies of β-adrenergic blockade on sweating rate, using oral propranolol, also elicited mixed results, with sweating rates increasing (Wilcox et al, 1984;Freund et al, 1987), decreasing (Buono et al, 2010), or showing no change (Pescatello et al, 1990). This is likely due to the systemic effects of propranolol, including decreases in heart rate (Wilcox et al, 1984;Pescatello et al, 1987), blood pressure (Wilcox et al, 1984), cardiac output, both skeletal and SkBF, and reported decreases in Tsk (Freund et al, 1987;Mack et al, 1986) and increased Tcore during exercise (Pescatello et al, 1987;Mack et al, 1986).…”

Section: Non-cholinergic Signaling Mechanisms Of Eccrine Sweatingmentioning

confidence: 99%

Responses to hyperthermia. Optimizing heat dissipation by convection and evaporation: Neural control of skin blood flow and sweating in humans

Smith

Johnson

2016

Autonomic Neuroscience

102

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Under normothermic, resting conditions, humans dissipate heat from the body at a rate approximately equal to heat production. Small discrepancies between heat production and heat elimination would, over time, lead to significant changes in heat storage and body temperature. When heat production or environmental temperature is high the challenge of maintaining heat balance is much greater. This matching of heat elimination with heat production is a function of the skin circulation facilitating heat transport to the body surface and sweating, enabling evaporative heat loss. These processes are manifestations of the autonomic control of cutaneous vasomotor and sudomotor functions and form the basis of this review. We focus on these systems in the responses to hyperthermia. In particular, the cutaneous vascular responses to heat stress and the current understanding of the neurovascular mechanisms involved. The available research regarding cutaneous active vasodilation and vasoconstriction is highlighted, with emphasis on active vasodilation as a major responder to heat stress. Involvement of the vasoconstrictor and active vasodilator controls of the skin circulation in the context of heat stress and nonthermoregulatory reflexes (blood pressure, exercise) are also considered. Autonomic involvement in the cutaneous vascular responses to direct heating and cooling of the skin are also discussed. We examine the autonomic control of sweating, including cholinergic and noncholinergic mechanisms, the local control of sweating, thermoregulatory and nonthermoregulatory reflex control and the possible relationship between sudomotor and cutaneous vasodilator function. Finally, we comment on the clinical relevance of these control schemes in conditions of autonomic dysfunction.

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The role of in vivo β-adrenergic stimulation on sweat production during exercise

Cited by 15 publications

References 18 publications

K⁺ channel mechanisms underlying cholinergic cutaneous vasodilation and sweating in young humans: roles of K_Ca, K_ATP, and K_V channels?

K⁺ channel mechanisms underlying cholinergic cutaneous vasodilation and sweating in young humans: roles of K_Ca, K_ATP, and K_V channels?

Local sweating on the forehead, but not forearm, is influenced by aerobic fitness independently of heat balance requirements during exercise

Responses to hyperthermia. Optimizing heat dissipation by convection and evaporation: Neural control of skin blood flow and sweating in humans

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The role of in vivo β-adrenergic stimulation on sweat production during exercise

Cited by 15 publications

References 18 publications

K+ channel mechanisms underlying cholinergic cutaneous vasodilation and sweating in young humans: roles of KCa, KATP, and KV channels?

K+ channel mechanisms underlying cholinergic cutaneous vasodilation and sweating in young humans: roles of KCa, KATP, and KV channels?

Local sweating on the forehead, but not forearm, is influenced by aerobic fitness independently of heat balance requirements during exercise

Responses to hyperthermia. Optimizing heat dissipation by convection and evaporation: Neural control of skin blood flow and sweating in humans

Contact Info

Product

Resources

About

K⁺ channel mechanisms underlying cholinergic cutaneous vasodilation and sweating in young humans: roles of K_Ca, K_ATP, and K_V channels?

K⁺ channel mechanisms underlying cholinergic cutaneous vasodilation and sweating in young humans: roles of K_Ca, K_ATP, and K_V channels?