Active cutaneous vasodilation in resting humans during mild heat stress

2005 ◽  
Vol 98 (3) ◽  
pp. 829-837 ◽  
Author(s):  
Yoshi-Ichiro Kamijo ◽  
Kichang Lee ◽  
Gary W. Mack

The role of skin temperature in reflex control of the active cutaneous vasodilator system was examined in six subjects during mild graded heat stress imposed by perfusing water at 34, 36, 38, and 40°C through a tube-lined garment. Skin sympathetic nerve activity (SSNA) was recorded from the peroneal nerve with microneurography. While monitoring esophageal, mean skin, and local skin temperatures, we recorded skin blood flow at bretylium-treated and untreated skin sites by using laser-Doppler velocimetry and local sweat rate by using capacitance hygrometry on the dorsal foot. Cutaneous vascular conductance (CVC) was calculated by dividing skin blood flow by mean arterial pressure. Mild heat stress increased mean skin temperature by 0.2 or 0.3°C every stage, but esophageal and local skin temperature did not change during the first three stages. CVC at the bretylium tosylate-treated site (CVCBT) and sweat expulsion number increased at 38 and 40°C compared with 34°C ( P < 0.05); however, CVC at the untreated site did not change. SSNA increased at 40°C ( P < 0.05, different from 34°C). However, SSNA burst amplitude increased ( P < 0.05), whereas SSNA burst duration decreased ( P < 0.05), at the same time as we observed the increase in CVCBT and sweat expulsion number. These data support the hypothesis that the active vasodilator system is activated by changes in mean skin temperature, even at normal core temperature, and illustrate the intricate competition between active vasodilator and the vasoconstrictor system for control of skin blood flow during mild heat stress.

2006 ◽  
Vol 290 (1) ◽  
pp. R172-R179 ◽  
Author(s):  
Glen P. Kenny ◽  
Jane E. Murrin ◽  
W. Shane Journeay ◽  
Francis D. Reardon

The purpose of this study was to evaluate the possible differences in the postexercise cutaneous vasodilatory response between men and women. Fourteen subjects (7 men and 7 women) of similar age, body composition, and fitness status remained seated resting for 15 min or cycled for 15 min at 70% of peak oxygen consumption followed by 15 min of seated recovery. Subjects then donned a liquid-conditioned suit. Mean skin temperature was clamped at ∼34°C for 15 min. Mean skin temperature was then increased at a rate of 4.3 ± 0.8°C/h while local skin temperature was clamped at 34°C. Skin blood flow was measured continuously at two forearm skin sites, one with (UT) and without (BT) (treated with bretylium tosylate) intact α-adrenergic vasoconstrictor activity. The exercise threshold for cutaneous vasodilation in women (37.51 ± 0.08°C and 37.58 ± 0.04°C for UT and BT, respectively) was greater than that measured in men (37.33 ± 0.06°C and 37.35 ± 0.06°C for UT and BT, respectively) ( P < 0.05). Core temperatures were similar to baseline before the start of whole body warming for all conditions. Postexercise heart rate (HR) for the men (77 ± 4 beats/min) and women (87 ± 6 beats/min) were elevated above baseline (61 ± 3 and 68 ± 4 beats/min for men and women, respectively), whereas mean arterial pressure (MAP) for the men (84 ± 3 mmHg) and women (79 ± 3 mmHg) was reduced from baseline (93 ± 3 and 93 ± 4 mmHg for men and women, respectively) ( P < 0.05). A greater increase in HR and a greater decrease in the MAP postexercise were noted in women ( P < 0.05). No differences in core temperature, HR, and MAP were measured in the no-exercise trial. The postexercise threshold for cutaneous vasodilation measured at the UT and BT sites for men (37.15 ± 0.03°C and 37.16 ± 0.04°C, respectively) and women (37.36 ± 0.05°C and 37.42 ± 0.03°C, respectively) were elevated above no exercise (36.94 ± 0.07°C and 36.97 ± 0.05°C for men and 36.99 ± 0.09°C and 37.03 ± 0.11°C for women for the UT and BT sites, respectively) ( P < 0.05). A difference in the magnitude of the thresholds was measured between women and men ( P < 0.05). We conclude that women have a greater postexercise onset threshold for cutaneous vasodilation than do men and that the primary mechanism influencing the difference between men and women in postexercise skin blood flow is likely the result of an altered active vasodilatory response and not an increase in adrenergic vasoconstrictor tone.


2019 ◽  
Vol 84 ◽  
pp. 439-450
Author(s):  
Stephanie Veselá ◽  
Boris R.M. Kingma ◽  
Arjan J.H. Frijns ◽  
Wouter D. van Marken Lichtenbelt

2005 ◽  
Vol 98 (6) ◽  
pp. 2011-2018 ◽  
Author(s):  
Gregg R. McCord ◽  
Christopher T. Minson

The dramatic increase in skin blood flow and sweating observed during heat stress is mediated by poorly understood sympathetic cholinergic mechanisms. One theory suggests that a single sympathetic cholinergic nerve mediates cutaneous active vasodilation (AVD) and sweating via cotransmission of separate neurotransmitters, because AVD and sweating track temporally and directionally when activated during passive whole body heat stress. It has also been suggested that these responses are regulated independently, because cutaneous vascular conductance (CVC) has been shown to decrease, whereas sweat rate increases, during combined hyperthermia and isometric handgrip exercise. We tested the hypothesis that CVC decreases during isometric handgrip exercise if skin blood flow is elevated using local heating to levels similar to that induced by pronounced hyperthermia but that this does not occur at lower levels of skin blood flow. Subjects performed isometric handgrip exercise as CVC was elevated at selected sites to varying levels by local heating (which is independent of AVD) in thermoneutral and hyperthermic conditions. During thermoneutral isometric handgrip exercise, CVC decreased at sites in which blood flow was significantly elevated before exercise (−6.5 ± 1.8% of maximal CVC at 41°C and −10.5 ± 2.0% of maximal CVC at 43°C; P < 0.05 vs. preexercise). During isometric handgrip exercise in the hyperthermic condition, an observed decrease in CVC was associated with the level of CVC before exercise. Taken together, these findings argue against withdrawal of AVD to explain the decrease in CVC observed during isometric handgrip exercise in hyperthermic conditions.


2018 ◽  
Vol 314 (2) ◽  
pp. R171-R180 ◽  
Author(s):  
Zachary J. Schlader ◽  
James R. Sackett ◽  
Suman Sarker ◽  
Blair D. Johnson

The recruitment of thermoeffectors, including thermoregulatory behavior, relative to changes in body temperature has not been quantified in humans. We tested the hypothesis that changes in skin blood flow, behavior, and sweating or metabolic rate are initiated with increasing changes in mean skin temperature (Tskin) in resting humans. While wearing a water-perfused suit, 12 healthy young adults underwent heat (Heat) and cold stress (Cold) that induced gradual changes in Tskin. Subjects controlled the temperature of their dorsal neck to their perceived thermal comfort. Thus neck skin temperature provided an index of thermoregulatory behavior. Neck skin temperature (Tskin), core temperature (Tcore), metabolic rate, sweat rate, and nonglabrous skin blood flow were measured continually. Data were analyzed using segmental regression analysis, providing an index of thermoeffector activation relative to changes in Tskin. In Heat, increases in skin blood flow were observed with the smallest elevations in Tskin ( P < 0.01). Thermal behavior was initiated with an increase in Tskin of 2.4 ± 1.3°C (mean ± SD, P = 0.04), while sweating was observed with further elevations in Tskin (3.4 ± 0.5°C, P = 0.04), which coincided with increases in Tcore ( P = 0.98). In Cold, reductions in skin blood flow occurred with the smallest decrease in Tskin ( P < 0.01). Thermal behavior was initiated with a Tskin decrease of 1.5 ± 1.3°C, while metabolic rate ( P = 0.10) and Tcore ( P = 0.76) did not change throughout. These data indicate that autonomic and behavioral thermoeffectors are recruited in coordination with one another and likely in an orderly manner relative to the comparative physiological cost.


1988 ◽  
Vol 74 (2) ◽  
pp. 201-206 ◽  
Author(s):  
Ahmad A. K. Hassan ◽  
J. E. Tooke

1. The effects of locally induced alterations in skin temperature on the postural changes in skin blood flow of the foot were assessed in 38 healthy subjects in a constant-temperature environment (22 ± 0.5°C, mean ± sd). 2. Moderate local cooling and warming of the foot (26–36°C) was induced by blowing cold or hot air. Higher ranges of temperature (38–44°C) were achieved by a thermostatically controlled disc heater. 3. Skin blood flow was measured before and during each change in local skin temperature using a laser Doppler flowmeter with the foot maintained at heart level, and placed passively 50 cm below the heart. Blood flow was measured in two skin areas: (i) the dorsum of the foot, where arteriovenous anastomoses are absent, and (ii) the pulp of the big toe, where these anastomoses are relatively numerous. 4. It was found that within the physiological temperature range of 26–36°C the normal postural fall in foot skin blood flow was preserved, whereas it was markedly attenuated or totally abolished at higher temperatures (38–44°C). The pattern of response was quite similar in areas having or lacking arteriovenous anastomoses. 5. It is suggested that the failure of postural vasoconstriction observed at the higher skin temperatures might contribute to some of the problems of cardiovascular adaptations seen in a hot environment.


2017 ◽  
Vol 313 (2) ◽  
pp. R140-R148 ◽  
Author(s):  
Nicholas Ravanelli ◽  
Ollie Jay ◽  
Daniel Gagnon

Some studies have observed a functional relationship between sweating and skin blood flow. However, the implications of this relationship during physiologically relevant conditions remain unclear. We manipulated sudomotor activity through changes in sweating efficiency to determine if parallel changes in vasomotor activity are observed. Eight young men completed two trials at 36°C and two trials at 42°C. During these trials, air temperature remained constant while ambient vapor pressure increased from 1.6 to 5.6 kPa over 2 h. Forced airflow across the skin was used to create conditions of high (HiSeff) or low (LoSeff) sweating efficiency. Local sweat rate (LSR), local skin blood flow (SkBF), as well as mean skin and esophageal temperatures were measured continuously. It took longer for LSR to increase during HiSeff at 36°C (HiSeff: 99 ± 11 vs. LoSeff: 77 ± 11 min, P < 0.01) and 42°C (HiSeff: 72 ± 16 vs. LoSeff: 51 ± 15 min, P < 0.01). In general, an increase in LSR preceded the increase in SkBF when expressed as ambient vapor pressure and time for all conditions ( P < 0.05). However, both responses were activated at a similar change in mean body temperature (average across all trials, LSR: 0.26 ± 0.15 vs. SkBF: 0.30 ± 0.18°C, P = 0.26). These results demonstrate that altering the point at which LSR is initiated during heat exposure is paralleled by similar shifts for the increase in SkBF. However, local sweat production occurs before an increase in SkBF, suggesting that SkBF is not necessarily a prerequisite for sweating.


2015 ◽  
Vol 118 (7) ◽  
pp. 898-903 ◽  
Author(s):  
Gary J. Hodges ◽  
Dean L. Kellogg ◽  
John M. Johnson

The vascular response to local skin cooling is dependent in part on a cold-induced translocation of α2C-receptors and an increased α-adrenoreceptor function. To discover whether β-adrenergic function might contribute, we examined whether β-receptor sensitivity to the β-agonist isoproterenol was affected by local skin temperature. In seven healthy volunteers, skin blood flow was measured from the forearm by laser-Doppler flowmetry and blood pressure was measured by finger photoplethysmography. Data were expressed as cutaneous vascular conductance (CVC; laser-Doppler flux/mean arterial blood pressure). Pharmacological agents were administered via intradermal microdialysis. We prepared four skin sites: one site was maintained at a thermoneutral temperature of 34°C (32 ± 10%CVCmax) one site was heated to 39°C (38 ± 11%CVCmax); and two sites were cooled, one to 29°C (22 ± 7%CVCmax) and the other 24°C (16 ± 4%CVCmax). After 20 min at these temperatures to allow stabilization of skin blood flow, isoproterenol was perfused in concentrations of 10, 30, 100, and 300 μM. Each concentration was perfused for 15 min. Relative to the CVC responses to isoproterenol at the thermoneutral skin temperature (34°C) (+21 ± 10%max), low skin temperatures reduced (at 29°C) (+17 ± 6%max) or abolished (at 24°C) (+1 ± 5%max) the vasodilator response, and warm (39°C) skin temperatures enhanced the vasodilator response (+40 ± 9%max) to isoproterenol. These data indicate that β-adrenergic function was influenced by local skin temperature. This finding raises the possibility that a part of the vasoconstrictor response to direct skin cooling could include reduced background β-receptor mediated vasodilation.


2014 ◽  
Vol 116 (8) ◽  
pp. 1088-1095 ◽  
Author(s):  
Nathan B. Morris ◽  
Anthony R. Bain ◽  
Matthew N. Cramer ◽  
Ollie Jay

Two studies were performed to 1) characterize changes in local sweat rate (LSR) following fluid ingestion of different temperatures during exercise, and 2) identify the potential location of thermoreceptors along the gastrointestinal tract that independently modify sudomotor activity. In study 1, 12 men cycled at 50% V̇o2peakfor 75 min while ingesting 3.2 ml/kg of 1.5°C, 37°C, or 50°C fluid 5 min before exercise; and after 15, 30, and 45-min of exercise. In study 2, 8 men cycled at 50% V̇o2peakfor 75 min while 3.2 ml/kg of 1.5°C or 50°C fluid was delivered directly into the stomach via a nasogastric tube (NG trials) or was mouth-swilled only (SW trials) after 15, 30, and 45 min of exercise. Rectal (Tre), aural canal (Tau), and mean skin temperature (Tsk); and LSR on the forehead, upper-back, and forearm were measured. In study 1, Tre, Tau, and Tskwere identical between trials, but after each ingestion, LSR was significantly suppressed at all sites with 1.5°C fluid and was elevated with 50°C fluid compared with 37°C fluid ( P < 0.001). The peak difference in mean LSR between 1.5°C and 50°C fluid after ingestion was 0.29 ± 0.06 mg·min−1·cm−2. In study 2, LSR was similar between 1.5°C and 50°C fluids with SW trials ( P = 0.738), but lower at all sites with 1.5°C fluid in NG trials ( P < 0.001) despite no concurrent differences in Tre, Tau, and Tsk. These data demonstrate that 1) LSR is transiently altered by cold and warm fluid ingestion despite similar core and skin temperatures; and 2) thermoreceptors that independently and acutely modulate sudomotor output during fluid ingestion probably reside within the abdominal area, but not the mouth.


1982 ◽  
Vol 53 (3) ◽  
pp. 744-749 ◽  
Author(s):  
J. M. Johnson ◽  
M. K. Park

To explore further the competition between vasoconstrictor and vasodilator reflexes in the regulation of skin blood flow, responses in forearm blood flow (FBF) to the initiation of supine leg exercise were measured by plethysmography against a background of rising internal temperature. In 17 studies involving six men, skin temperature (Tsk) was controlled with water-perfused suits first at normothermic levels, followed by a 40- to 50-min period during which Tsk was held at 3813;38.5 degrees C. Supine leg exercise at a moderate intensity (100–150 W) was performed for 5–6 min of each 15 min throughout, yielding one period of exercise performed during normothermic conditions and three periods of exercise performed during the period of elevated Tsk. On the average, FBF fell significantly with the beginning of each period of exercise (P less than 0.05). Furthermore, the amount by which FBF fell tended to increase with increasing levels of preexercise FBF. Thus the average fall in FBF associated with the onset of the last period of exercise, 2.45 ml X 100 ml-1 X min-1, significantly exceeded the 1.12 ml X 100 ml-1 X min-1 fall in FBF seen with onset of work in normothermic conditions. These responses were not due to changes in internal temperature as reflected by esophageal temperatures. However, individual studies occasionally revealed a reduction or abolition of the vasoconstrictor response with the last period of exercise. These findings are in agreement with earlier studies showing a cutaneous participation in the vasoconstrictor responses to exercise but also indicate that sufficient hyperthermia can attenuate or even abolish this response.


2010 ◽  
Vol 109 (5) ◽  
pp. 1301-1306 ◽  
Author(s):  
Jonathan E. Wingo ◽  
David A. Low ◽  
David M. Keller ◽  
R. Matthew Brothers ◽  
Manabu Shibasaki ◽  
...  

Sweat rate (SR) is reduced in locally cooled skin, which may result from decreased temperature and/or parallel reductions in skin blood flow. The purpose of this study was to test the hypotheses that decreased skin blood flow and decreased local temperature each independently attenuate sweating. In protocols I and II, eight subjects rested supine while wearing a water-perfused suit for the control of whole body skin and internal temperatures. While 34°C water perfused the suit, four microdialysis membranes were placed in posterior forearm skin not covered by the suit to manipulate skin blood flow using vasoactive agents. Each site was instrumented for control of local temperature and measurement of local SR (capacitance hygrometry) and skin blood flow (laser-Doppler flowmetry). In protocol I, two sites received norepinephrine to reduce skin blood flow, while two sites received Ringer solution (control). All sites were maintained at 34°C. In protocol II, all sites received 28 mM sodium nitroprusside to equalize skin blood flow between sites before local cooling to 20°C (2 sites) or maintenance at 34°C (2 sites). In both protocols, individuals were then passively heated to increase core temperature ∼1°C. Both decreased skin blood flow and decreased local temperature attenuated the slope of the SR to mean body temperature relationship (2.0 ± 1.2 vs. 1.0 ± 0.7 mg·cm−2·min−1·°C−1 for the effect of decreased skin blood flow, P = 0.01; 1.2 ± 0.9 vs. 0.07 ± 0.05 mg·cm−2·min−1·°C−1 for the effect of decreased local temperature, P = 0.02). Furthermore, local cooling delayed the onset of sweating (mean body temperature of 37.5 ± 0.4 vs. 37.6 ± 0.4°C, P = 0.03). These data demonstrate that local cooling attenuates sweating by independent effects of decreased skin blood flow and decreased local skin temperature.


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