Differences in the postexercise threshold for cutaneous active vasodilation between men and women

2006 ◽  
Vol 290 (1) ◽  
pp. R172-R179 ◽  
Author(s):  
Glen P. Kenny ◽  
Jane E. Murrin ◽  
W. Shane Journeay ◽  
Francis D. Reardon
Keyword(s):  
Blood Flow ◽  
Skin Temperature ◽  
Skin Blood Flow ◽  
Peak Oxygen Consumption ◽  
Whole Body ◽  
Mean Skin Temperature ◽  
Local Skin ◽  
Men And Women ◽  
Cutaneous Vasodilation ◽  
Vasodilatory Response

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.

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
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Skin Temperature ◽  
Skin Blood Flow ◽  
Sweat Rate ◽  
Mean Skin Temperature ◽  
Local Skin ◽  
Mild Heat ◽  
Normal Core ◽  
Local Sweat Rate

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.

scholarly journals Effect of local skin blood flow during light and medium activities on local skin temperature predictions

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

Transient receptor potential vanilloid type 1 channels contribute to reflex cutaneous vasodilation in humans

2012 ◽  
Vol 112 (12) ◽  
pp. 2037-2042 ◽  
Author(s):  
Brett J. Wong ◽  
Sarah M. Fieger
Keyword(s):  
Blood Flow ◽  
Skin Blood Flow ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Whole Body ◽  
Transient Receptor Potential Vanilloid ◽  
Cutaneous Vasodilation ◽  
Transient Receptor ◽  
Reflex Cutaneous Vasodilation

Mechanisms underlying the cutaneous vasodilation in response to an increase in core temperature remain unresolved. The purpose of this study was to determine a potential contribution of transient receptor potential vanilloid type 1 (TRPV-1) channels to reflex cutaneous vasodilation. Twelve subjects were equipped with four microdialysis fibers on the ventral forearm, and each site randomly received 1) 90% propylene glycol + 10% lactated Ringer (vehicle control); 2) 10 mM l-NAME; 3) 20 mM capsazepine to inhibit TRPV-1 channels; 4) combined 10 mM l-NAME + 20 mM capsazepine. Whole body heating was achieved via water-perfused suits sufficient to raise oral temperature at least 0.8°C above baseline. Maximal skin blood flow was achieved by local heating to 43°C and infusion of 28 mM nitroprusside. Systemic arterial pressure (SAP) was measured, and skin blood flow was monitored via laser-Doppler flowmetry (LDF). Cutaneous vascular conductance (CVC) was calculated as LDF/SAP and normalized to maximal vasodilation (%CVCmax). Capsazepine sites were significantly reduced compared with control (50 ± 4%CVCmax vs. 67 ± 5%CVCmax, respectively; P < 0.05). l-NAME (33 ± 3%CVCmax) and l-NAME + capsazepine (30 ± 4%CVCmax) sites were attenuated compared with control ( P < 0.01) and capsazepine ( P < 0.05); however, there was no difference between l-NAME and combined l-NAME + capsazepine. These data suggest TRPV-1 channels participate in reflex cutaneous vasodilation and TRPV-1 channels may account for a portion of the NO component. TRPV-1 channels may have a direct neural contribution or have an indirect effect via increased arterial blood temperature. Whether the TRPV-1 channels directly or indirectly contribute to reflex cutaneous vasodilation remains uncertain.

Control of skin blood flow by whole body and local skin cooling in exercising humans

1996 ◽  
Vol 270 (1) ◽  
pp. H208-H215 ◽  
Author(s):  
P. E. Pergola ◽  
J. M. Johnson ◽  
D. L. Kellogg ◽  
W. A. Kosiba
Keyword(s):  
Blood Flow ◽  
Skin Blood Flow ◽  
Threshold Level ◽  
Tissue Temperature ◽  
Whole Body ◽  
Internal Temperature ◽  
Local Cooling ◽  
Local Skin ◽  
Doppler Flowmetry ◽  
Rate Of Increase

We examined the independent roles of whole body skin temperature (Tsk) and tissue temperature (local temperature, Tloc) in the control of skin blood flow (SBF) during cooling and the roles of the vasoconstrictor (VC) and active vasodilator (AVD) systems in mediating these effects. SBF was monitored by laser-Doppler flowmetry (LDF) at untreated sites and sites with local VC blockade by pretreatment with bretylium (BT). Seven subjects underwent four sessions of moderate bicycle exercise (20-30 min duration) at neutral Tsk and Tloc (34 degrees C), neutral Tsk and cool Tloc (27 degrees C), low Tsk (28 degrees C) and neutral Tloc, and low Tsk and Tloc. Cutaneous vascular conductance (CVC; LDF/mean arterial pressure) was expressed relative to the maximum. Cool Tsk increased the threshold level of internal temperature at which CVC began to rise equally at BT-treated and untreated sites (P < 0.05). The rate of increase in CVC relative to internal temperature was reduced by local cooling. BT pretreatment partially reversed this effect (P < 0.05). Thus a cool environment results in reflex inhibition of the onset of AVD activity by cool Tsk and a reduced rate of increase in CVC due, in part, to norepinephrine release stimulated by cool Tloc.

The sympathetic release test: a test used to assess thermoregulation and autonomic control of blood flow

2014 ◽  
Vol 38 (1) ◽  
pp. 87-92 ◽  
Author(s):  
E. A. Tansey ◽  
S. M. Roe ◽  
C. D. Johnson
Keyword(s):  
Blood Flow ◽  
Skin Temperature ◽  
Skin Blood Flow ◽  
Whole Body ◽  
Temperature Sensitive ◽  
Typical Sample ◽  
Release Test ◽  
Sample Data ◽  
The Subject ◽  
Clinical Conditions

When a subject is heated, the stimulation of temperature-sensitive nerve endings in the skin, and the raising of the central body temperature, results in the reflex release of sympathetic vasoconstrictor tone in the skin of the extremities, causing a measurable temperature increase at the site of release. In the sympathetic release test, the subject is gently heated by placing the feet and calves in a commercially available foot warming pouch or immersing the feet and calves in warm water and wrapping the subject in blankets. Skin blood flow is estimated from measurements of skin temperature in the fingers. Normally skin temperature of the fingers is 65–75°F in cool conditions (environmental temperature: 59–68°F) and rises to 85–95°F during body heating. Deviations in this pattern may mean that there is abnormal sympathetic vasoconstrictor control of skin blood flow. Abnormal skin blood flow can substantially impair an individual's ability to thermoregulate and has important clinical implications. During whole body heating, the skin temperature from three different skin sites is monitored and oral temperature is monitored as an index of core temperature. Students determine the fingertip temperature at which the reflex release of sympathetic activity occurs and its maximal attainment, which reflects the vasodilating capacity of this cutaneous vascular bed. Students should interpret typical sample data for certain clinical conditions (Raynaud's disease, peripheral vascular disease, and postsympathectomy) and explain why there may be altered skin blood flow in these disorders.

scholarly journals Antagonism of soluble guanylyl cyclase attenuates cutaneous vasodilation during whole body heat stress and local warming in humans

2011 ◽  
Vol 110 (5) ◽  
pp. 1406-1413 ◽  
Author(s):  
Dean L. Kellogg ◽  
Joan L. Zhao ◽  
Yubo Wu ◽  
John M. Johnson
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Guanylyl Cyclase ◽  
Soluble Guanylyl Cyclase ◽  
Whole Body ◽  
Local Skin ◽  
Cutaneous Vasodilation ◽  
Local Skin Temperature ◽  
Whole Body Heat Stress ◽  
Body Heat

We hypothesized that nitric oxide activation of soluble guanylyl cyclase (sGC) participates in cutaneous vasodilation during whole body heat stress and local skin warming. We examined the effects of the sGC inhibitor, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), on reflex skin blood flow responses to whole body heat stress and on nonreflex responses to increased local skin temperature. Blood flow was monitored by laser-Doppler flowmetry, and blood pressure by Finapres to calculate cutaneous vascular conductance (CVC). Intradermal microdialysis was used to treat one site with 1 mM ODQ in 2% DMSO and Ringer, a second site with 2% DMSO in Ringer, and a third site received Ringer. In protocol 1, after a period of normothermia, whole body heat stress was induced. In protocol 2, local heating units warmed local skin temperature from 34 to 41°C to cause local vasodilation. In protocol 1, in normothermia, CVC did not differ among sites [ODQ, 15 ± 3% maximum CVC (CVCmax); DMSO, 14 ± 3% CVCmax; Ringer, 17 ± 6% CVCmax; P > 0.05]. During heat stress, ODQ attenuated CVC increases (ODQ, 54 ± 4% CVCmax; DMSO, 64 ± 4% CVCmax; Ringer, 63 ± 4% CVCmax; P < 0.05, ODQ vs. DMSO or Ringer). In protocol 2, at 34°C local temperature, CVC did not differ among sites (ODQ, 17 ± 2% CVCmax; DMSO, 18 ± 4% CVCmax; Ringer, 18 ± 3% CVCmax; P > 0.05). ODQ attenuated CVC increases at 41°C local temperature (ODQ, 54 ± 5% CVCmax; DMSO, 86 ± 4% CVCmax; Ringer, 90 ± 2% CVCmax; P < 0.05 ODQ vs. DMSO or Ringer). sGC participates in neurogenic active vasodilation during heat stress and in the local response to direct skin warming.

Effect of changes in local skin temperature on postural vasoconstriction in man

1988 ◽  
Vol 74 (2) ◽  
pp. 201-206 ◽  
Author(s):  
Ahmad A. K. Hassan ◽  
J. E. Tooke
Keyword(s):  
Blood Flow ◽  
Skin Temperature ◽  
Skin Blood Flow ◽  
Arteriovenous Anastomoses ◽  
Local Cooling ◽  
Local Skin ◽  
Hot Air ◽  
Postural Changes ◽  
Local Skin Temperature ◽  
Heart Blood

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.

scholarly journals A comparison of whole body vibration and moist heat on lower extremity skin temperature and skin blood flow in healthy older individuals

2012 ◽  
Vol 18 (7) ◽  
pp. CR415-CR424 ◽  
Author(s):  
Everett B. Lohman III ◽  
Kanikkai Steni Balan Sackiriyas ◽  
Gurinder S. Bains ◽  
Giovanni Calandra ◽  
Crystal Lobo ◽  
...  
Keyword(s):  
Blood Flow ◽  
Lower Extremity ◽  
Skin Temperature ◽  
Skin Blood Flow ◽  
Whole Body Vibration ◽  
Whole Body ◽  
Older Individuals ◽  
Body Vibration ◽  
Moist Heat

scholarly journals Skin blood flow and nitric oxide during body heating in type 2 diabetes mellitus

2009 ◽  
Vol 106 (2) ◽  
pp. 566-570 ◽  
Author(s):  
Lynn A. Sokolnicki ◽  
Nicholas A. Strom ◽  
Shelly K. Roberts ◽  
Shirley A. Kingsley-Berg ◽  
Ananda Basu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Blood Flow ◽  
Type 2 Diabetes Mellitus ◽  
Skin Blood Flow ◽  
Whole Body ◽  
Control Subjects ◽  
Cutaneous Vasodilation

Individuals with type 2 diabetes mellitus (T2DM) often exhibit microvascular dysfunction that may contribute to impaired thermoregulation, but potential mechanisms remain unclear. Our goals were to quantify skin blood flow responses and nitric oxide-mediated vasodilation during body heating in individuals with T2DM compared with nondiabetic control subjects of similar age. We measured skin blood flow (laser-Doppler flowmetry) in conjunction with intradermal microdialysis of NG-nitro-l-arginine methyl ester (l-NAME; nitric oxide synthase inhibitor) or vehicle during 45–60 min of whole body heating (WBH) in 10 individuals with T2DM and 14 control subjects. In six individuals from each group, we also measured forearm blood flow (FBF) by venous occlusion plethysmography on the contralateral forearm. FBF responses showed diminished absolute cutaneous vasodilation during WBH in the T2DM group ( PANOVA < 0.01; peak FBF in control 13.1 ± 1.7 vs. T2DM 9.0 ± 1.6 ml·100 ml−1·min−1). However, the relative contribution of nitric oxide to the cutaneous vasodilator response (expressed as % of maximal cutaneous vascular conductance) was not different between groups ( P > 0.05). We conclude that cutaneous vasodilator responses to WBH are decreased in individuals with T2DM, but the contribution of nitric oxide to this smaller vasodilation is similar between T2DM and control individuals. This decrease in cutaneous vasodilation is likely an important contributor to impaired thermoregulation in T2DM.

scholarly journals Effect of skin temperature on cutaneous vasodilator response to the β-adrenergic agonist isoproterenol

2015 ◽  
Vol 118 (7) ◽  
pp. 898-903 ◽  
Author(s):  
Gary J. Hodges ◽  
Dean L. Kellogg ◽  
John M. Johnson
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Skin Temperature ◽  
Skin Blood Flow ◽  
Local Skin ◽  
Vasodilator Response ◽  
Skin Cooling ◽  
Local Skin Temperature ◽  
Β Receptor ◽  
Skin Temperatures

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.

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