Reflex control of skin blood flow by skin temperature: role of core temperature

1979 ◽  
Vol 47 (6) ◽  
pp. 1188-1193 ◽  
Author(s):  
J. M. Johnson ◽  
M. K. Park

Two protocols were used to discover whether the reflex response in skin blood flow (SkBF) to rising skin temperature (Tsk) was dependent on the level of internal temperature. Part I. In five subjects, Tsk (controlled with water-perfused suits) was raised to 37 degrees C prior to, between 2 and 5 min, or between 10 and 17 min of exercise. The associated SkBF elevation per degree rise in Tsk averaged 0.20, 1.28, and 1.75 ml/100 ml . min, respectively. When Tsk was raised during the first 5 min of exercise, esophageal temperature (Tes) rose markedly (0.39 degrees C), but transiently fell if Tsk was raised after 10 min of exercise. Part II. In six subjects, different work loads were used to develop different levels of internal temperature. Tsk was elevated to 37 degrees C after 10--15 min at light (50--75 W) or moderate (100--150 W) work loads. At the heavier work load (and higher Tes), the rise in forearm SkBF per degree rise in Tsk averaged 2.33 +/- 0.38 (SE) times that observed at the light work load. These data strongly suggest that the reflex response of SkBF to rising Tsk is dependent on the level of internal temperature.

1994 ◽  
Vol 266 (5) ◽  
pp. H1979-H1984 ◽  
Author(s):  
P. E. Pergola ◽  
D. L. Kellogg ◽  
J. M. Johnson ◽  
W. A. Kosiba

The purpose of this study was to examine whether reflex effects of changes in whole body skin temperature (Tsk) on cutaneous vasculature are mediated through the vasoconstrictor or the active vasodilator arm of the sympathetic nervous system. In six subjects, reflex responses in forearm skin blood flow (SkBF) to changes in Tsk were monitored by laser-Doppler flowmetry. SkBF was monitored at a control site and at a 0.6-cm2 site where bretylium (BT) had been iontophoretically applied to abolish sympathetic vasoconstrictor control. Reflex control of SkBF at BT-treated sites is solely through active vasodilator activity. An index of cutaneous vascular conductance (CVC) was calculated from the blood flow signal and mean arterial pressure, measured noninvasively. Data are expressed relative to maximum CVC (CVCmax) achieved by local warming of measurement sites to 42 degrees C at the end of each study. Tsk was controlled with a water-perfused suit covering the entire body except for the head and arms. Esophageal temperature (Tes) was measured as an index of internal temperature. In part A (rest), raising Tsk at rest from 31.9 +/- 0.3 to 36.7 +/- 0.2 degrees C increased CVC at control sites from 3 +/- 0.2 to 5 +/- 0.6% of CVCmax. CVC did not change at BT-treated sites, suggesting that at rest, with a normal internal temperature, reflex effects of raising Tsk on SkBF are mediated through vasoconstrictor withdrawal. In part B (exercise), exercise at a low Tsk increased Tes to 37.49 +/- 0.1 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)


1975 ◽  
Vol 38 (5) ◽  
pp. 839-845 ◽  
Author(s):  
C. R. Wyss ◽  
G. L. Brengelmann ◽  
J. M. Johnson ◽  
L. B. Rowell ◽  
D. Silverstein

Five subjects were studied during periods of controlled increases and decreases in skin temperature (Ts) over the Ts range of 34–40 degrees C. One protocol was designed to observe changes in forearm blood flow (FBF) and heart rate (HR) with changes in core temperature (Tc; right atrial blood temperature and esophageal temperature were measured) with Ts held constant at two levels. FBF and HR changed linearly with Tc in the Tc range of 37–38 degrees C with Ts constant at 38 degrees C. A second protocol imposed Ts changes at two levels of Ts and Tc; this protocol also included a prolonged cooling period. The influence of Ts on FBF and HR was reduced when Ts changes occurred at an elevated Ts and Tc, and FBF showed considerable hysteresis during cooling. We conclude that a linear model for the control of FBF or HR is inadequate as a tool for predicting the control of these variables.


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.


1986 ◽  
Vol 61 (5) ◽  
pp. 1613-1622 ◽  
Author(s):  
J. M. Johnson

Although it is well accepted that skin blood flow (SkBF) in humans is controlled by thermoregulatory reflexes, the conclusion that the cutaneous circulation is also controlled by reflexes of nonthermoregulatory origin is not universally held. This review considers the extent to which the cutaneous circulation participates in baroreceptor-mediated reflexes and in the reflexes associated with exercise. Exercise is explored in some detail, because it elicits both thermoregulatory and nonthermoregulatory reflexes. The overall conclusion reached is that thermoregulatory control of SkBF is subject to modification by or competition from several other sources. The fundamental pattern for control of SkBF is described by the threshold and slope of the SkBF-internal temperature relationship. Reflex effects of skin temperature act to shift the threshold of this relationship such that lower levels of skin temperature are associated with higher threshold internal temperatures at which cutaneous vasodilation begins. Similarly, baroreceptor reflexes, reflexes associated with exercise, and effects of some cardiovascular disease also operate against this background. Although modification of the SkBF-internal temperature slope is occasionally seen, the most consistent effect of these nonthermoregulatory factors is to elevate the threshold internal temperature for cutaneous vasodilation. The consequence of this modification of thermoregulatory control of SkBF is that temperature regulation will often suffer when increases in SkBF are delayed or limited. Blood flow to other regions, possibly including active skeletal muscle, may also be compromised when thermoregulatory demands for SkBF are high.


1984 ◽  
Vol 56 (5) ◽  
pp. 1283-1288 ◽  
Author(s):  
J. M. Johnson ◽  
D. S. O'Leary ◽  
W. F. Taylor ◽  
M. K. Park

To find whether sweat rate (SR) and forearm skin blood flow ( SkBF ) were reflexly affected by skin temperature (Tsk) we used water-perfused suits to rapidly elevate Tsk during exercise. With this elevation in Tsk, there was a period of little net change in esophageal temperature (Tes) but marked responses in SR and SkBF . During this period a rise in Tsk of 4.2 +/- 0.3 degrees C was associated with an increase in SR of 0.44 +/- 0.09 mg X cm-2 X min-1 and an increase in SkBF of 3.27 +/- 0.42 ml X 100 ml-1 X min-1. Multiple linear regression analysis as well as comparison with control studies in which Tsk was kept cool also reveal a consistent role for Tsk in the reflex regulation of SR and SkBF . Responses in SR and FBF were much more marked at levels of Tsk below 33 degrees C. Below a Tsk of 33 degrees C, SR rose 0.30 +/- 0.06 mg X cm-2 X min-1 per degrees C rise in Tsk, whereas above 33 degrees SR rose only 0.05 +/- 0.01 mg X cm2 X min per degrees C. FBF rose 2.81 +/- 0.60 and 0.77 +/- 0.18 ml X 100 ml-1 X min-1 per degrees C rise in Tsk at the lower and upper ranges of Tsk, respectively.


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 (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.


2009 ◽  
Vol 11 (1) ◽  
pp. 39-43 ◽  
Author(s):  
Colleen Maloney-Hinds ◽  
Jerrold S. Petrofsky ◽  
Grenith Zimmerman ◽  
David A. Hessinger

2000 ◽  
Vol 278 (2) ◽  
pp. H321-H330 ◽  
Author(s):  
José González-Alonso ◽  
Ricardo Mora-Rodríguez ◽  
Edward F. Coyle

Euhydrated and dehydrated subjects exercised in a hot and a cold environment with our aim to identify factors that relate to reductions in stroke volume (SV). We hypothesized that reductions in SV with heat stress are related to the interaction of several factors rather than the effect of elevated skin blood flow. Eight male endurance-trained cyclists [maximal O2 consumption (V˙o 2 max) 4.5 ± 0.1 l/min; means ± SE] cycled for 30 min (72%V˙o 2 max) in the heat (H; 35°C) or the cold (C; 8°C) when euhydrated or dehydrated by 1.5, 3.0, or 4.2% of their body weight. When euhydrated, SV and esophageal temperature (Tes 38.2–38.3°C) were similar in H and C, whereas skin blood flow was much higher in H vs. C (365 ± 64% higher; P < 0.05). With each 1% body weight loss, SV declined 6.4 ± 1.3 ml (4.8%) in H and 3.4 ± 0.4 ml (2.5%) in C, whereas Tes increased 0.21 ± 0.02 and 0.10 ± 0.02°C in H and C, respectively ( P < 0.05). However, reductions in SV were not associated with increases in skin blood flow. The reduced SV was highly associated with increased heart rate and reduced blood volume in both H ( R = 0.96; P < 0.01) and C ( R = 0.85; P < 0.01). In conclusion, these results suggest that SV is maintained in trained subjects during exercise in euhydrated conditions despite large differences in skin blood flow. Furthermore, the lowering of SV with dehydration appears largely related to increases in heart rate and reductions in blood volume.


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