scholarly journals Ten days of repeated local forearm heating does not affect cutaneous vascular function

2017 ◽  
Vol 123 (2) ◽  
pp. 310-316 ◽  
Author(s):  
Michael A. Francisco ◽  
Vienna E. Brunt ◽  
Krista Nicole Jensen ◽  
Santiago Lorenzo ◽  
Christopher T. Minson

The aim of the present study was to determine whether 10 days of repeated local heating could induce peripheral adaptations in the cutaneous vasculature and to investigate potential mechanisms of adaptation. We also assessed maximal forearm blood flow to determine whether repeated local heating affects maximal dilator capacity. Before and after 10 days of heat training consisting of 1-h exposures of the forearm to 42°C water or 32°C water (control) in the contralateral arm (randomized and counterbalanced), we assessed hyperemia to rapid local heating of the skin ( n = 14 recreationally active young subjects). In addition, sequential doses of acetylcholine (ACh, 1 and 10 mM) were infused in a subset of subjects ( n = 7) via microdialysis to study potential nonthermal microvascular adaptations following 10 days of repeated forearm heat training. Skin blood flow was assessed using laser-Doppler flowmetry, and cutaneous vascular conductance (CVC) was calculated as laser-Doppler red blood cell flux divided by mean arterial pressure. Maximal cutaneous vasodilation was achieved by heating the arm in a water-spray device for 45 min and assessed using venous occlusion plethysmography. Forearm vascular conductance (FVC) was calculated as forearm blood flow divided by mean arterial pressure. Repeated forearm heating did not increase plateau percent maximal CVC (CVCmax) responses to local heating (89 ± 3 vs. 89 ± 2% CVCmax, P = 0.19), 1 mM ACh (43 ± 9 vs. 53 ± 7% CVCmax, P = 0.76), or 10 mM ACh (61 ± 9 vs. 85 ± 7% CVCmax, P = 0.37, by 2-way repeated-measures ANOVA). There was a main effect of time at 10 mM ACh ( P = 0.03). Maximal FVC remained unchanged (0.12 ± 0.02 vs. 0.14 ± 0.02 FVC, P = 0.30). No differences were observed in the control arm. Ten days of repeated forearm heating in recreationally active young adults did not improve the microvascular responsiveness to ACh or local heating. NEW & NOTEWORTHY We show for the first time that 10 days of repeated forearm heating is not sufficient to improve cutaneous vascular responsiveness in recreationally active young adults. In addition, this is the first study to investigate cutaneous cholinergic sensitivity and forearm blood flow following repeated local heat exposure. Our data add to the limited studies regarding repeated local heating of the cutaneous vasculature.


1999 ◽  
Vol 86 (5) ◽  
pp. 1676-1686 ◽  
Author(s):  
Carla M. Thomas ◽  
Jane M. Pierzga ◽  
W. Larry Kenney

To determine the effect and underlying mechanisms of exercise training and the influence of age on the skin blood flow (SkBF) response to exercise in a hot environment, 22 young (Y; 18–30 yr) and 21 older (O; 61–78 yr) men were assigned to 16 wk of aerobic (A; YA, n = 8; OA, n = 11), resistance (R; YR, n = 7; OR, n = 3), or no training (C; YC, n = 7; OC, n = 7). Before and after treatment, subjects exercised at 60% of maximum oxygen consumption (V˙o 2 max) on a cycle ergometer for 60 min at 36°C. Cutaneous vascular conductance, defined as SkBF divided by mean arterial pressure, was monitored at control (vasoconstriction intact) and bretylium-treated (vasoconstriction blocked) sites on the forearm using laser-Doppler flowmetry. Forearm vascular conductance was calculated as forearm blood flow (venous occlusion plethysmography) divided by mean arterial pressure. Esophageal and skin temperatures were recorded. Only aerobic training (functionally defined a priori as a 5% or greater increase inV˙o 2 max) produced a decrease in the mean body temperature threshold for increasing forearm vascular conductance (36.89 ± 0.08 to 36.63 ± 0.08°C, P < 0.003) and cutaneous vascular conductance (36.91 ± 0.08 to 36.65 ± 0.08°C, P < 0.004). Similar thresholds between control and bretylium-treated sites indicated that the decrease was mediated through the active vasodilator system. This shift was more pronounced in the older men who presented greater training-induced increases in V˙o 2 maxthan did the young men (22 and 9%, respectively). In summary, older men improved their SkBF response to exercise-heat stress through the effect of aerobic training on the cutaneous vasodilator system.



2010 ◽  
Vol 109 (6) ◽  
pp. 1736-1743 ◽  
Author(s):  
Santiago Lorenzo ◽  
Christopher T. Minson

The aim of this study was to explore heat acclimation effects on cutaneous vascular responses and sweating to local ACh infusions and local heating. We also sought to examine whether heat acclimation altered maximal skin blood flow. ACh (1, 10, and 100 mM) was infused in 20 highly trained cyclists via microdialysis before and after a 10-day heat acclimation program [two 45-min exercise bouts at 50% maximal O2 uptake (V̇o2max) in 40°C ( n = 12)] or control conditions [two 45-min exercise bouts at 50% V̇o2max in 13°C ( n = 8)]. Skin blood flow was monitored via laser-Doppler flowmetry (LDF), and cutaneous vascular conductance (CVC) was calculated as LDF ÷ mean arterial pressure. Sweat rate was measured by resistance hygrometry. Maximal brachial artery blood flow (forearm blood flow) was obtained by heating the contralateral forearm in a water spray device and measured by Doppler ultrasound. Heat acclimation increased %CVCmax responses to 1, 10, and 100 mM ACh (43.5 ± 3.4 vs. 52.6 ± 2.6% CVCmax, 67.7 ± 3.4 vs. 78.0 ± 3.0% CVCmax, and 81.0 ± 3.8 vs. 88.5 ± 1.1% CVCmax, respectively, all P < 0.05). Maximal forearm blood flow remained unchanged after heat acclimation (290.9 ± 12.7 vs. 269.9 ± 23.6 ml/min). The experimental group showed significant increases in sweating responses to 10 and 100 mM ACh (0.21 ± 0.03 vs. 0.31 ± 0.03 mg·cm−2·min−1 and 0.45 ± 0.05 vs. 0.67 ± 0.06 mg·cm−2·min−1, respectively, all P < 0.05), but not to 1 mM ACh (0.13 ± 0.02 vs. 0.18 ± 0.02 mg·cm−2·min−1, P = 0.147). No differences in any of the variables were found in the control group. Heat acclimation in highly trained subjects induced local adaptations within the skin microcirculation and sweat gland apparatus. Furthermore, maximal skin blood flow was not altered by heat acclimation, demonstrating that the observed changes were attributable to improvement in cutaneous vascular function and not to structural changes that limit maximal vasodilator capacity.



Circulation ◽  
2021 ◽  
Vol 143 (Suppl_1) ◽  
Author(s):  
Megan C Nelson ◽  
Madeline P Casanova ◽  
Jennavere R Ball ◽  
Rachel D Midence ◽  
Timothy R Johnson ◽  
...  

Introduction: A single bout of uninterrupted sitting impairs vascular function in the legs, which may be due to reductions in blood flow and shear stress. Participating in regular moderate-to-vigorous physical activity (MVPA) has been identified as an effective approach for improving vascular function, and recent evidence suggests meeting the physical activity (PA) guidelines may attenuate some of the negative health outcomes associated with excessive sedentary behavior; however, it is not well understood how meeting the PA guidelines may influence the acute response to sitting. Our aim was to investigate the effects of 3 h of uninterrupted sitting on hemodynamics and vascular and inflammatory biomarkers in physically inactive and active adults. Hypothesis: We hypothesized active adults would experience less detrimental physiological changes after sitting compared to inactive adults. Methods: Eleven inactive (mean±SD, age: 47.1±8.9 y, body fat: 33.1±8.5%; 78.5% women) and 16 active adults (age: 46.1±8.9 y, body fat: 25.2±7.2%; 31.1% women) completed 3 h of uninterrupted sitting. Adults self-reported their PA with the International PA Questionnaire. Adults engaging in ≥150 min·wk -1 were classified as active and <150 min·wk -1 , inactive. Hemodynamic variables, and superficial femoral artery (SFA) diameter and blood velocity were measured each hour over 3 h of sitting. Mean arterial pressure, blood flow and shear rate were calculated. Serum vascular and inflammatory biomarkers were measured pre and post sitting. Linear mixed-effects modeling was used to assess changes in dependent variables over time and between inactive and active adults, controlling for sex. Results: Inactive and active adults self-reported 7.3±7.1 and 93.3±64.8 min·d -1 of MVPA, respectively. Endothelin-1 (baseline: 8.3±13.4 pg/mL, post: 81.1±103.0 pg/mL; p<0.001) and interleukin-6 (baseline: 0.08±0.06 pg/mL, post: 0.11±0.11 pg/mL; p=0.03) increased post sitting compared to baseline in all adults, regardless of PA status. Systolic blood pressure, mean arterial pressure, calf circumference, and SFA diameter, blood velocity, and mean blood flow decreased over time in both groups (p<0.05 for all). There was an interaction effect for mean shear rate (p=0.008); inactive adults experienced a decline over 3 h of sitting (baseline: 76.1±48.2 s -1 ; 1 h: 55.0±27.4 s -1 ; 2 h: 45.3±24.2 s -1 ; 3 h: 40.8±25.5 s -1 ) while active participants demonstrated no change (baseline: 36.6±21.4 s -1 ; 1 h: 28.1±21.4 s -1 ; 2 h: 26.1±20.9 s -1 ; 3 h: 23.8±19.5 s -1 ). Inactive adults also had a higher oscillatory shear index compared to active adults (p<0.001). Conclusion: Uninterrupted sitting induced unfavorable changes regardless of PA status; however, active adults demonstrated a more favorable shear profile. Meeting PA guidelines may attenuate some unfavorable changes within the vasculature associated with prolonged sitting.



2007 ◽  
Vol 102 (3) ◽  
pp. 890-895 ◽  
Author(s):  
Kerrie L. Moreau ◽  
Ashley R. DePaulis ◽  
Kathleen M. Gavin ◽  
Douglas R. Seals

Basal whole leg blood flow and vascular conductance are reduced in estrogen-deficient postmenopausal compared with premenopausal women. The underlying mechanisms are unknown, but oxidative stress could be involved. We studied 9 premenopausal [23 ± 1 yr (mean ± SE)] and 20 estrogen-deficient postmenopausal (55 ± 1 yr) healthy women. During baseline control, oxidized low-density lipoprotein (LDL), a marker of oxidative stress, was 50% greater in the postmenopausal women ( P < 0.001). Basal whole leg blood flow (duplex ultrasound of femoral artery) was 34% lower in the postmenopausal women because of a 38% lower leg vascular conductance ( P < 0.0001); mean arterial pressure was not different. Intravenous administration of a supraphysiological dose of the antioxidant ascorbic acid increased leg blood flow by 15% in the postmenopausal women as a result of an increase in leg vascular conductance (both P < 0.001), but it did not affect leg blood flow in premenopausal controls or mean arterial pressure in either group. In the pooled subjects, the changes in leg blood flow and leg vascular conductance with ascorbic acid were related to baseline plasma oxidized LDL ( r = 0.46 and 0.53, P < 0.01) and waist-to-hip ratio and total body fat ( r = 0.41–0.44, all P < 0.05). Our results are consistent with the hypothesis that oxidative stress contributes to chronic leg vasoconstriction and reduced basal whole leg blood flow in estrogen-deficient postmenopausal women. This oxidative stress-related suppression of leg vascular conductance and blood flow may be linked in part to increased total and abdominal adiposity.



1992 ◽  
Vol 73 (4) ◽  
pp. 1232-1237 ◽  
Author(s):  
C. G. Tankersley ◽  
D. H. Zappe ◽  
T. G. Meister ◽  
W. L. Kenney

Elevated body core temperature stimulates cutaneous vasodilation, which can be modified by nonthermal factors. To test whether hypohydration affects forearm vascular conductance discretely from relative alterations in heart rate (HR), eight trained cyclists exercised progressively for 20 min each at 60, 120, and 180 W [approximately 22, 37, and 55% of maximal cycling O2 consumption (VO2peak), respectively] in a warm humid environment (dry bulb temperature 30 degrees C; wet bulb temperature 24 degrees C). Esophageal temperature and forearm blood flow were measured every 30 s, and mean arterial pressure and HR were measured at rest and during each exercise intensity (minutes 15, 35, and 55). In the hypovolemic (HP) compared with the euvolemic (EU) state, blood volume was contracted by 24-h fluid restriction an average of 510 ml, and this difference was sustained throughout exercise. The esophageal temperature and HR responses were similar between EU and HP states at 60 and 120 W but were significantly (P < 0.05) higher in HP by the end of 180 W. In contrast, the forearm blood flow response was significantly (P < 0.05) depressed during exercise at 120 and 180 W in HP, whereas mean arterial pressure remained similar between conditions. When body core temperature is elevated in a hypohydrated state, forearm vascular conductance is reduced at exercise intensities of approximately 37% VO2peak, which is independent of relative changes in HR. These findings are consistent with the notion that during exercise an attenuated cutaneous vasodilation is elicited by alterations in regionalized sympathetic outflow, which is unaccompanied by activation of cardiac pacemaker cells.



2003 ◽  
Vol 284 (1) ◽  
pp. R233-R244 ◽  
Author(s):  
Gabriela A. Eppel ◽  
Göran Bergström ◽  
Warwick P. Anderson ◽  
Roger G. Evans

We examined the extent of renal medullary blood flow (MBF) autoregulation in pentobarbital-anesthetized rabbits. Two methods for altering renal arterial pressure (RAP) were compared: the conventional method of graded suprarenal aortic occlusion and an extracorporeal circuit that allows RAP to be increased above systemic arterial pressure. Changes in MBF were estimated by laser-Doppler flowmetry, which appears to predominantly reflect erythrocyte velocity, rather than flow, in the kidney. We compared responses using a dual-fiber needle probe held in place by a micromanipulator, with responses from a single-fiber probe anchored to the renal capsule, to test whether RAP-induced changes in kidney volume confound medullary laser-Doppler flux (MLDF) measurements. MLDF responses were similar for both probe types and both methods for altering RAP. MLDF changed little as RAP was altered from 50 to ≥170 mmHg (24 ± 22% change). Within the same RAP range, RBF increased by 296 ± 48%. Urine flow and sodium excretion also increased with increasing RAP. Thus pressure diuresis/natriuresis proceeds in the absence of measurable increases in medullary erythrocyte velocity estimated by laser-Doppler flowmetry. These data do not, however, exclude the possibility that MBF is increased with increasing RAP in this model, because vasa recta recruitment may occur.



2007 ◽  
Vol 293 (5) ◽  
pp. H3187-H3192 ◽  
Author(s):  
Gary J. Hodges ◽  
Wojciech A. Kosiba ◽  
Kun Zhao ◽  
Guy E. Alvarez ◽  
John M. Johnson

Previous work showed that local cooling (LC) attenuates the vasoconstrictor response to whole body cooling (WBC). We tested the extent to which this attenuation was due to the decreased baseline skin blood flow following LC. In eight subjects, skin blood flow was assessed using laser-Doppler flowmetry (LDF). Cutaneous vascular conductance (CVC) was expressed as LDF divided by blood pressure. Subjects were dressed in water-perfused suits to control WBC. Four forearm sites were prepared with microdialysis fibers, local heating/cooling probe holders, and laser-Doppler probes. Three sites were locally cooled from 34 to 28°C, reducing CVC to 45.9 ± 3.9, 42 ± 3.9, and 44.5 ± 4.8% of baseline ( P < 0.05 vs. baseline; P > 0.05 among sites). At two sites, CVC was restored to precooling baseline levels with sodium nitroprusside (SNP) or isoproterenol (Iso), increasing CVC to 106.4 ± 12.4 and 98.9 ± 10.1% of baseline, respectively ( P > 0.05 vs. precooling). Whole body skin temperature, apart from the area of blood flow measurement, was reduced from 34 to 31°C. Relative to the original baseline, CVC decreased ( P < 0.05) by 44.9 ± 2.8 (control), 11.3 ± 2.4 (LC only), 29 ± 3.7 (SNP), and 45.8 ± 8.7% (Iso). The reductions at LC only and SNP sites were less than at control or Iso sites ( P < 0.05); the responses at those latter sites were not different ( P > 0.05), suggesting that the baseline change in CVC with LC is important in the attenuation of reflex vasoconstrictor responses to WBC.





1994 ◽  
Vol 76 (5) ◽  
pp. 2047-2053 ◽  
Author(s):  
N. M. Dietz ◽  
J. M. Rivera ◽  
D. O. Warner ◽  
M. J. Joyner

The neurotransmitter responsible for neurogenic vasodilation in human skin during body heating is unknown. We sought to determine whether the vasodilating substance nitric oxide (NO) is involved in this phenomenon. Six subjects were heated for 50 min by use of a water-perfused suit while forearm blood flow (FBF) was measured with plethysmography and skin blood flow (SkBF) was measured by the laser-Doppler method in both arms. In one forearm, NG-monomethyl-L-arginine (L-NMMA), an NO synthase blocker, was infused into the brachial artery. Bolus doses of L-NMMA (< or = 4 mg/min) for 5 min were given to blunt NO-mediated vasodilator responses to acetylcholine (ACh, 64 micrograms/min). A continuous infusion of L-NMMA (< or = 1.0 mg/min) was used during body heating to maintain NO synthase blockade. In the forearm receiving L-NMMA, FBF was 1.8 +/- 0.3 ml.100 ml-1.min-1 before drug infusion and rose to 9.5 +/- 1.3 ml.100 ml-1.min-1 with ACh. After L-NMMA infusion, FBF was 1.3 +/- 0.2 ml.100 ml-1.min-1 and rose to 2.6 +/- 0.4 ml.100 ml-1.min-1 with ACh (both P < 0.05 vs. pre-L-NMMA). Similar changes in SkBF were seen with ACh and L-NMMA, confirming that the drugs reached cutaneous vessels. With body heating, oral temperature increased by 1.2 degrees C, heart rate increased by 34 beats/min, and mean arterial pressure remained constant at approximately 75 mmHg. FBF in the treated forearm rose to 11.5 +/- 2.1 vs. 12.6 +/- 1.7 ml.100 ml-1.min-1 in the control forearm (P > 0.05, control vs. treated response).(ABSTRACT TRUNCATED AT 250 WORDS)



1998 ◽  
Vol 85 (1) ◽  
pp. 175-180 ◽  
Author(s):  
D. L. Kellogg ◽  
S. R. Morris ◽  
S. B. Rodriguez ◽  
Y. Liu ◽  
M. Grossmann ◽  
...  

During dynamic exercise in the heat, increases in skin blood flow are attenuated in hypertensive subjects when compared with normotensive subjects. We studied responses to passive heat stress (water-perfused suits) in eight hypertensive and eight normotensive subjects. Forearm blood flow was measured by venous-occlusion plethysmography, mean arterial pressure (MAP) was measured by Finapres, and forearm vascular conductance (FVC) was calculated. Bretylium tosylate (BT) iontophoresis was used to block active vasoconstriction in a small area of skin. Skin blood flow was indexed by laser-Doppler flowmetry at BT-treated and untreated sites, and cutaneous vascular conductance was calculated. In normothermia, FVC was lower in hypertensive than in normotensive subjects ( P < 0.01). During heat stress, FVC rose to similar levels in both groups ( P > 0.80); concurrent cutaneous vascular conductance increases were unaffected by BT treatment ( P > 0.60). MAP was greater in hypertensive than in normotensive subjects during normothermia ( P < 0.05, hypertensive vs. normotensive subjects). During hyperthermia, MAP fell in hypertensive subjects but showed no statistically significant change in normotensive subjects ( P < 0.05, hypertensive vs. normotensive subjects). The internal temperature at which vasodilation began did not differ between groups ( P> 0.80). FVC is reduced during normothermia in unmedicated hypertensive subjects; however, they respond to passive heat stress in a fashion no different from normotensive subjects.



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