Spectral characteristics of skin sympathetic nerve activity in heat-stressed humans

Cui, Jian; Sathishkumar, Mithra; Wilson, Thad E.; Shibasaki, Manabu; Davis, Scott L.; Crandall, Craig G.

doi:10.1152/ajpheart.00025.2005

Cited by 49 publications

(62 citation statements)

References 27 publications

(46 reference statements)

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“…These responses are accomplished through a combination of local and neurally mediated cutaneous vasodilation, coupled with elevated cardiac output and redistribution of blood flow and volume away from central vascular beds, such as the splanchnic and renal circulations, to the cutaneous circulation (4, 9, 21, 29 -31). In addition, skin and muscle sympathetic nerve activities (SNA) increase during heat stress (3,5,6,17,23,34), with increases in skin SNA being responsible for sweating and cutaneous vasodilation, while increases in muscle SNA have a less clear end result.Earlier studies provided evidence that, during both local and indirect whole body heating, increases in forearm blood flow were exclusive to the skin; that is, muscle blood flow did not change to these perturbations (7,8,15,26). In part due to these and related studies, it was reported that the skin has a capacity to increase blood flow upwards to 7-8 l/min during a profound heat stress (7, 27).…”

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Local heating, but not indirect whole body heating, increases human skeletal muscle blood flow

Heinonen

Kemppainen

Knuuti

et al. 2011

Journal of Applied Physiology

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141

139

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Heinonen I, Brothers RM, Kemppainen J, Knuuti J, Kalliokoski KK, Crandall CG. Local heating, but not indirect whole body heating, increases human skeletal muscle blood flow. J Appl Physiol 111: 818-824, 2011. First published June 16, 2011 doi:10.1152 doi:10. /japplphysiol.00269.2011cades it was believed that direct and indirect heating (the latter of which elevates blood and core temperatures without directly heating the area being evaluated) increases skin but not skeletal muscle blood flow. Recent results, however, suggest that passive heating of the leg may increase muscle blood flow. Using the technique of positronemission tomography, the present study tested the hypothesis that both direct and indirect heating increases muscle blood flow. Calf muscle and skin blood flows were evaluated from eight subjects during normothermic baseline, during local heating of the right calf [only the right calf was exposed to the heating source (water-perfused suit)], and during indirect whole body heat stress in which the left calf was not exposed to the heating source. Local heating increased intramuscular temperature of the right calf from 33.4 Ϯ 1.0°C to 37.4 Ϯ 0.8°C, without changing intestinal temperature. This stimulus increased muscle blood flow from 1.4 Ϯ 0.5 to 2.3 Ϯ 1.2 ml·100 g Ϫ1 ·min Ϫ1 (P Ͻ 0.05), whereas skin blood flow under the heating source increased from 0.7 Ϯ 0.3 to 5.5 Ϯ 1.5 ml·100 g Ϫ1 ·min Ϫ1 (P Ͻ 0.01). While whole body heat stress increased intestinal temperature by ϳ1°C, muscle blood flow in the calf that was not directly exposed to the water-perfused suit (i.e., indirect heating) did not increase during the whole body heat stress (normothermia: 1.6 Ϯ 0.5 ml·100 g Ϫ1 ·min Ϫ1 ; heat stress: 1.7 Ϯ 0.3 ml·100 g Ϫ1 ·min Ϫ1 ; P ϭ 0.87). Whole body heating, however, reflexively increased calf skin blood flow (to 4.0 Ϯ 1.5 ml·100 g Ϫ1 ·min Ϫ1 ) in the area not exposed to the water-perfused suit. These data show that local, but not indirect, heating increases calf skeletal muscle blood flow in humans. These results have important implications toward the reconsideration of previously accepted blood flow distribution during whole body heat stress. positron-emission tomography; skin blood flow; bone blood flow; heat stress WHEN HUMANS ARE EXPOSED to acute heat stress several cardiovascular adjustments occur primarily directed toward increasing skin blood flow, which are necessary to adequately dissipate an internal heat load. These responses are accomplished through a combination of local and neurally mediated cutaneous vasodilation, coupled with elevated cardiac output and redistribution of blood flow and volume away from central vascular beds, such as the splanchnic and renal circulations, to the cutaneous circulation (4, 9, 21, 29 -31). In addition, skin and muscle sympathetic nerve activities (SNA) increase during heat stress (3,5,6,17,23,34), with increases in skin SNA being responsible for sweating and cutaneous vasodilation, while increases in muscle SNA have a less clear end result.Earlier studies p...

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confidence: 99%

mentioning

confidence: 99%

Local heating, but not indirect whole body heating, increases human skeletal muscle blood flow

Heinonen

Kemppainen

Knuuti

et al. 2011

Journal of Applied Physiology

Self Cite

141

139

View full text Add to dashboard Cite

show abstract

“…At the completion of whole body heating, 24°C water was perfused to cool the participant. Whole body heating increases SSNA, cutaneous vascular conductance (CVC), and sweat rate (Cui et al 2006;Normell and Wallin 1974;Wilson et al 2001) and appears to follow a pattern of initial suppression of SSNA and then dramatically increased internal temperature (Iwase et al 2002).…”

Section: Measurementsmentioning

confidence: 99%

“…Physical, mental, and thermal stress increase skin sympathetic outflow (Cui et al 2006;Muller et al 2013;Vissing and Hjortso 1996;Wilson et al 2006), which can be quantified directly via postganglionic skin sympathetic nerve activity (SSNA) and indirectly via sympathetic end-organ responses (skin blood flow and sweat gland secretions). It is currently unknown whether rosacea patients have altered skin sympathetic outflow during triggering stresses.…”

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Augmented supraorbital skin sympathetic nerve activity responses to symptom trigger events in rosacea patients

Metzler-Wilson

Toma

Sammons

et al. 2015

Journal of Neurophysiology

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Facial flushing in rosacea is often induced by trigger events. However, trigger causation mechanisms are currently unclear. This study tested the central hypothesis that rosacea causes sympathetic and axon reflex-mediated alterations resulting in trigger-induced symptomatology. Twenty rosacea patients and age/sex-matched controls participated in one or a combination of symptom triggering stressors. In protocol 1, forehead skin sympathetic nerve activity (SSNA; supraorbital microneurography) was measured during sympathoexcitatory mental (2-min serial subtraction of novel numbers) and physical (2-min isometric handgrip) stress. In protocol 2, forehead skin blood flow (laser-Doppler flowmetry) and transepithelial water loss/sweat rate (capacitance hygrometry) were measured during sympathoexcitatory heat stress (whole body heating by perfusing 50°C water through a tube-lined suit). In protocol 3, cheek, forehead, forearm, and palm skin blood flow were measured during nonpainful local heating to induce axon reflex vasodilation. Heart rate (HR) and mean arterial pressure (MAP) were recorded via finger photoplethysmography to calculate cutaneous vascular conductance (CVC; flux·100/MAP). Higher patient transepithelial water loss was observed (rosacea 0.20 ± 0.02 vs. control 0.10 ± 0.01 mg·cm(-2)·min(-1), P < 0.05). HR and MAP changes were not different between groups during sympathoexcitatory stressors or local heating. SSNA during early mental (32 ± 9 and 9 ± 4% increase) and physical (25 ± 4 and 5 ± 1% increase, rosacea and controls, respectively) stress was augmented in rosacea (both P < 0.05). Heat stress induced more rapid sweating and cutaneous vasodilation onset in rosacea compared with controls. No axon reflex vasodilation differences were observed between groups. These data indicate that rosacea affects SSNA and that hyperresponsiveness to trigger events appears to have a sympathetic component.

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“…During whole body cooling, decreases in mean skin temperature to 30.5°C resulted in a robust increase in efferent skin sympathetic nerve activity (SSNA) in young adults (28,58,59,124) (Fig. 3).…”

Section: Potential Loci For Deficient Skin Vasoconstriction In Agingmentioning

confidence: 99%

Sympathetic control of reflex cutaneous vasoconstriction in human aging

Greaney

Alexander

Kenney

2015

Journal of Applied Physiology

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This Synthesis highlights a series of recent studies that has systematically interrogated age-related deficits in cold-induced skin vasoconstriction. In response to cold stress, a reflex increase in sympathetic nervous system activity mediates reductions in skin blood flow. Reflex vasoconstriction during cold exposure is markedly impaired in aged skin, contributing to the relative inability of healthy older adults to maintain core temperature during mild cold stress in the absence of appropriate behavioral thermoregulation. This compromised reflex cutaneous vasoconstriction in healthy aging can occur as a result of functional deficits at multiple points along the efferent sympathetic reflex axis, including blunted sympathetic outflow directed to the skin vasculature, reduced presynaptic neurotransmitter synthesis and/or release, and altered end-organ responsiveness at several loci, in addition to potential alterations in afferent thermoreceptor function. Arguments have been made that the relative inability of aged skin to appropriately constrict is due to the aging cutaneous arterioles themselves, whereas other data point to the neural circuitry controlling those vessels. The argument presented herein provides strong evidence for impaired efferent sympathetic control of the peripheral cutaneous vasculature during whole body cold exposure as the primary mechanism responsible for attenuated vasoconstriction.

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Spectral characteristics of skin sympathetic nerve activity in heat-stressed humans

Cited by 49 publications

References 27 publications

Local heating, but not indirect whole body heating, increases human skeletal muscle blood flow

Local heating, but not indirect whole body heating, increases human skeletal muscle blood flow

Augmented supraorbital skin sympathetic nerve activity responses to symptom trigger events in rosacea patients

Sympathetic control of reflex cutaneous vasoconstriction in human aging

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