scholarly journals The Effect of Being Aerobically Active vs. Inactive on Cutaneous Vascular Conductance during Local Heat Stress in an Older Population

2017 ◽  
Vol 8 ◽  
Author(s):  
Ulrike H. Mitchell ◽  
Samantha Burton ◽  
Christopher Gordon ◽  
Gary W. Mack
Keyword(s):  
Heat Stress ◽  
Local Heat ◽  
Vascular Conductance ◽  
Older Population ◽  
Cutaneous Vascular Conductance

scholarly journals Small reductions in skin temperature after onset of a simulated hemorrhagic challenge improve tolerance in exercise heat-stressed individuals

2018 ◽  
Vol 315 (3) ◽  
pp. R539-R546
Author(s):  
Claire E. Trotter ◽  
Faith K. Pizzey ◽  
Philip M. Batterson ◽  
Robert A. Jacobs ◽  
James Pearson
Keyword(s):  
Heat Stress ◽  
Mean Arterial Pressure ◽  
Skin Temperature ◽  
Healthy Subjects ◽  
Lower Body Negative Pressure ◽  
Stress Index ◽  
Lower Body ◽  
Vascular Conductance ◽  
Cumulative Stress ◽  
Cutaneous Vascular Conductance

We investigated whether small reductions in skin temperature 60 s after the onset of a simulated hemorrhagic challenge would improve tolerance to lower body negative pressure (LBNP) after exercise heat stress. Eleven healthy subjects completed two trials (High and Reduced). Subjects cycled at ~55% maximal oxygen uptake wearing a warm water-perfused suit until core temperatures increased by ~1.2°C before lying supine and undergoing LBNP to presyncope. LBNP tolerance was quantified as cumulative stress index (CSI; product of each LBNP level multiplied by time; mmHg·min). Skin temperature was similarly elevated from baseline before LBNP and remained elevated 60 s after the onset of LBNP in both High (37.72 ± 0.52°C) and Reduced (37.95 ± 0.54°C) trials (both P < 0.0001). At 60%CSI skin temperature remained elevated in the High trial (37.51 ± 0.56°C) but was reduced to 34.97 ± 0.72°C by the water-perfused suit in the Reduced trial ( P < 0.0001 between trials). Cutaneous vascular conductance was not different between trials [High: 1.57 ± 0.43 vs. Reduced: 1.39 ± 0.38 arbitrary units (AU)/mmHg; P = 0.367] before LBNP but decreased to 0.67 ± 0.19 AU/mmHg at 60%CSI in the Reduced trial while remaining unchanged in the High trial ( P = 0.002 between trials). CSI was higher in the Reduced (695 ± 386 mmHg·min) relative to the High (441 ± 290 mmHg·min; P = 0.023) trial. Mean arterial pressure was not different between trials at presyncope (High: 62 ± 10 vs. Reduced: 62 ± 9 mmHg; P = 0.958). Small reductions in skin temperature after the onset of a simulated hemorrhagic challenge improve LBNP tolerance after exercise heat stress. This may have important implications regarding treatment of an exercise heat-stressed individual (e.g., soldier) who has experienced a hemorrhagic injury.

Bradykinin does not mediate cutaneous active vasodilation during heat stress in humans

2002 ◽  
Vol 93 (4) ◽  
pp. 1215-1221 ◽  
Author(s):  
D. L. Kellogg ◽  
Y. Liu ◽  
K. McAllister ◽  
C. Friel ◽  
P. E. Pérgola
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Receptor Antagonist ◽  
Healthy Subjects ◽  
Ringer Solution ◽  
Vascular Conductance ◽  
Doppler Flowmetry ◽  
Hoe 140 ◽  
Control Body ◽  
Cutaneous Vascular Conductance

To test the hypothesis that bradykinin effects cutaneous active vasodilation during hyperthermia, we examined whether the increase in skin blood flow (SkBF) during heat stress was affected by blockade of bradykinin B2 receptors with the receptor antagonist HOE-140. Two adjacent sites on the forearm were instrumented with intradermal microdialysis probes for local delivery of drugs in eight healthy subjects. HOE-140 was dissolved in Ringer solution (40 μM) and perfused at one site, whereas the second site was perfused with Ringer alone. SkBF was monitored by laser-Doppler flowmetry (LDF) at both sites. Mean arterial pressure (MAP) was monitored from a finger, and cutaneous vascular conductance (CVC) was calculated (CVC = LDF/MAP). Water-perfused suits were used to control body temperature and evoke hyperthermia. After hyperthermia, both microdialysis sites were perfused with 28 mM nitroprusside to effect maximal vasodilation. During hyperthermia, CVC increased at HOE-140 (69 ± 2% maximal CVC, P < 0.01) and untreated sites (65 ± 2% maximal CVC, P < 0.01). These responses did not differ between sites ( P > 0.05). Because the bradykinin B2-receptor antagonist HOE-140 did not alter SkBF responses to heat stress, we conclude that bradykinin does not mediate cutaneous active vasodilation.

Effect of increasing central venous pressure during passive heating on skin blood flow

1999 ◽  
Vol 86 (2) ◽  
pp. 605-610 ◽  
Author(s):  
C. G. Crandall ◽  
B. D. Levine ◽  
R. A. Etzel
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Pressure Pulse ◽  
Venous Pressure ◽  
Saline Infusion ◽  
Whole Body ◽  
Passive Heating ◽  
Central Venous ◽  
Vascular Conductance ◽  
Cutaneous Vascular Conductance

Whole body heating in humans increases skin blood flow (SkBF) and decreases central venous pressure (CVP). This study sought to identify whether elevations in SkBF are augmented during passive heating if CVP is increased during the heat stress. Seven subjects were exposed to passive heating. Once SkBF was substantially elevated, 15 ml/kg warm saline were rapidly infused intravenously. Whole body heating significantly increased cutaneous vascular conductance and decreased CVP from 7.7 ± 0.6 to 4.9 ± 0.5 mmHg ( P < 0.05). Saline infusion returned CVP to pre-heat-stress pressures (7.9 ± 0.6 mmHg; P > 0.05) and significantly increased cutaneous vascular conductance relative to the period before saline administration. Moreover, saline infusion did not alter mean arterial pressure, pulse pressure, or esophageal temperature (all P > 0.05). To serve as a volume control, 15 ml/kg saline were rapidly infused intravenously in normothermic subjects. Saline infusion increased CVP ( P < 0.05) without affecting mean arterial pressure, pulse pressure, or cutaneous vascular conductance (all P > 0.05). These data suggest that cardiopulmonary baroreceptor unloading during passive heating may attenuate the elevation in SkBF in humans, whereas loading cardiopulmonary baroreceptors in normothermia has no effect on SkBF.

scholarly journals Nitric oxide and cutaneous active vasodilation during heat stress in humans

1998 ◽  
Vol 85 (3) ◽  
pp. 824-829 ◽  
Author(s):  
D. L. Kellogg ◽  
C. G. Crandall ◽  
Y. Liu ◽  
N. Charkoudian ◽  
J. M. Johnson
Keyword(s):  
Nitric Oxide ◽  
Heat Stress ◽  
Laser Doppler Flowmetry ◽  
Sweat Rate ◽  
Ringer Solution ◽  
No Synthase ◽  
Laser Doppler ◽  
Vascular Conductance ◽  
Doppler Flowmetry ◽  
Cutaneous Vascular Conductance

Whether nitric oxide (NO) is involved in cutaneous active vasodilation during hyperthermia in humans is unclear. We tested for a role of NO in this process during heat stress (water-perfused suits) in seven healthy subjects. Two forearm sites were instrumented with intradermal microdialysis probes. One site was perfused with the NO synthase inhibitor N G-nitro-l-arginine methyl ester (l-NAME) dissolved in Ringer solution to abolish NO production. The other site was perfused with Ringer solution only. At those sites, skin blood flow (laser-Doppler flowmetry) and sweat rate were simultaneously and continuously monitored. Cutaneous vascular conductance, calculated from laser-Doppler flowmetry and mean arterial pressure, was normalized to maximal levels as achieved by perfusion with the NO donor nitroprusside through the microdialysis probes. Under normothermic conditions,l-NAME did not significantly reduce cutaneous vascular conductance. During hyperthermia, with skin temperature held at 38–38.5°C, internal temperature rose from 36.66 ± 0.10 to 37.34 ± 0.06°C ( P < 0.01). Cutaneous vascular conductance at untreated sites increased from 12 ± 2 to 44 ± 5% of maximum, but only rose from 13 ± 2 to 30 ± 5% of maximum at l-NAME-treated sites ( P < 0.05 between sites) during heat stress. l-NAME had no effect on sweat rate ( P > 0.05). Thus cutaneous active vasodilation requires functional NO synthase to achieve full expression.

Effects of obesity and mild hypohydration on local sweating and cutaneous vascular responses during passive heat stress in females

2016 ◽  
Vol 41 (8) ◽  
pp. 879-887 ◽  
Author(s):  
Nicole E. Moyen ◽  
Jenna M. Burchfield ◽  
Cory L. Butts ◽  
Jordan M. Glenn ◽  
Matthew A. Tucker ◽  
...  
Keyword(s):  
Heat Stress ◽  
Steady State ◽  
Body Fat ◽  
Urine Specific Gravity ◽  
Fluid Restriction ◽  
Vascular Conductance ◽  
Mean Body Temperature ◽  
Doppler Flowmetry ◽  
Vascular Responses ◽  
Cutaneous Vascular Conductance

The purpose of this study was to evaluate the effect of obesity and mild hypohydration on local sweating (LSR) and cutaneous vascular conductance (CVC) responses during passive heat stress in females. Thirteen obese (age, 24 ± 4 years; 45.4% ± 5.2% body fat) and 12 nonobese (age, 22 ± 2 years; 25.1% ± 3.9% body fat) females were passively heated (1.0 °C rectal temperature increase) while either euhydrated (EUHY) or mildly hypohydrated (HYPO; via fluid restriction). Chest and forearm LSR (ventilated capsule) and CVC (Laser Doppler flowmetry) onset, sensitivity, and plateau/steady state were recorded as mean body temperature increased (ΔTb). Participants began trials EUHY (urine specific gravity, Usg = 1.009 ± 0.006) or HYPO (Usg = 1.025 ± 0.004; p < 0.05), and remained EUHY or HYPO. Independent of obesity, HYPO decreased sweat sensitivity at the chest (HYPO = 0.79 ± 0.35, EUHY = 0.95 ± 0.39 Δmg·min−1·cm−2/°C ΔTb) and forearm (HYPO = 0.82 ± 0.39, EUHY = 1.06 ± 0.34 Δmg·min−1·cm−2/°C ΔTb); forearm LSR plateau was also decreased (HYPO = 0.66 ± 0.19, EUHY = 0.78 ± 0.23 mg·min−1·cm−2; all p < 0.05). Overall, obese females had lower chest-sweat sensitivity (0.72 ± 0.35 vs. 1.01 ± 0.33 Δmg·min−1·cm−2/°C ΔTb) and plateau (0.55 ± 0.27 vs. 0.80 ± 0.25 mg·min−1·cm−2; p < 0.05). While hypohydrated, obese females had a lower chest LSR (p < 0.05) versus nonobese females midway (0.45 ± 0.26 vs. 0.73 ± 0.23 mg·min−1·cm−2) and at the end (0.53 ± 0.27 vs. 0.81 ± 0.24 mg·min−1·cm−2) of heating. Furthermore, HYPO (relative to the EUHY trials) led to a greater decrease in CVC sensitivity in obese (–28 ± 27 Δ% maximal CVC/°C ΔTb) versus nonobese females (+9.2 ± 33 Δ% maximal CVC/°C ΔTb; p < 0.05). In conclusion, mild hypohydration impairs females’ sweating responses during passive heat stress, and this effect is exacerbated when obese.

Cholinergic mechanisms of cutaneous active vasodilation during heat stress in cystic fibrosis

2007 ◽  
Vol 103 (3) ◽  
pp. 963-968 ◽  
Author(s):  
D. L. Kellogg ◽  
G. J. Hodges ◽  
C. R. Orozco ◽  
T. M. Phillips ◽  
J. L. Zhao ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Heat Stress ◽  
Receptor Sensitivity ◽  
Ach Release ◽  
Vascular Conductance ◽  
Cholinergic Mechanisms ◽  
Doppler Flowmetry ◽  
Site Specific ◽  
Cutaneous Vasodilation ◽  
Cutaneous Vascular Conductance

To test the hypothesis that cutaneous active vasodilation in heat stress is mediated by a redundant cholinergic cotransmitter system, we examined the effects of atropine on skin blood flow (SkBF) increases during heat stress in persons with (CF) and without cystic fibrosis (non-CF). Vasoactive intestinal peptide (VIP) has been implicated as a mediator of cutaneous vasodilation in heat stress. VIP-containing cutaneous neurons are sparse in CF, yet SkBF increases during heat stress are normal. In CF, augmented ACh release or muscarinic receptor sensitivity could compensate for decreased VIP; if so, active vasodilation would be attenuated by atropine in CF relative to non-CF. Atropine was administered into skin by iontophoresis in seven CF and seven matched non-CF subjects. SkBF was monitored by laser-Doppler flowmetry (LDF) at atropine treated and untreated sites. Blood pressure [mean arterial pressure (MAP)] was monitored (Finapres), and cutaneous vascular conductance was calculated (CVC = LDF/MAP). The protocol began with a normothermic period followed by a 3-min cold stress and 30–45 min of heat stress. Finally, LDF sites were warmed to 42°C to effect maximal vasodilation. CVC was normalized to its site-specific maximum. During heat stress, CVC increased in both CF and non-CF ( P < 0.01). CVC increases were attenuated by atropine in both groups ( P < 0.01); however, the responses did not differ between groups ( P = 0.99). We conclude that in CF there is not greater dependence on redundant cholinergic mechanisms for cutaneous active vasodilation than in non-CF.

Thermoregulatory reflexes and cutaneous active vasodilation during heat stress in hypertensive humans

1998 ◽  
Vol 85 (1) ◽  
pp. 175-180 ◽  
Author(s):  
D. L. Kellogg ◽  
S. R. Morris ◽  
S. B. Rodriguez ◽  
Y. Liu ◽  
M. Grossmann ◽  
...  
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Skin Blood Flow ◽  
Forearm Blood Flow ◽  
Venous Occlusion ◽  
Vascular Conductance ◽  
Doppler Flowmetry ◽  
Forearm Vascular Conductance ◽  
Normotensive Subjects ◽  
Cutaneous Vascular Conductance

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.

scholarly journals Diurnal variation in cutaneous vasodilator and vasoconstrictor systems during heat stress

2001 ◽  
Vol 281 (2) ◽  
pp. R591-R595 ◽  
Author(s):  
Ken Aoki ◽  
Dan P. Stephens ◽  
John M. Johnson
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Diurnal Variation ◽  
Skin Blood Flow ◽  
Whole Body ◽  
Noninvasive Blood Pressure ◽  
Vascular Conductance ◽  
Doppler Flowmetry ◽  
Cutaneous Vasodilation ◽  
Cutaneous Vascular Conductance

It is not clear whether the diurnal variation in the cutaneous circulatory response to heat stress is via the noradrenergic vasoconstrictor system or the nonadrenergic active vasodilator system. We conducted whole body heating experiments in eight male subjects at 0630 (AM) and 1630 (PM). Skin blood flow was monitored by laser-Doppler flowmetry at control sites and at sites pretreated with bretylium (BT) to block noradrenergic vasoconstriction. Noninvasive blood pressure was used to calculate cutaneous vascular conductance. The sublingual temperature (Tor) threshold for cutaneous vasodilation was significantly higher in PM at control and at BT-treated sites (both P < 0.01), suggesting the diurnal shift in threshold depends on the active vasodilator system. The slope of cutaneous vascular conductance as a percentage of its maximum with respect to Tor was significantly lower in AM at control sites only. Also, in the AM, the slope at control sites was significantly lower than that at BT-treated sites ( P < 0.05), suggesting that the diurnal change in the sensitivity of cutaneous vasodilation depends on vasoconstrictor system function. Overall, the diurnal variation in the reflex control of skin blood flow during heat stress involves both vasoconstrictor and active vasodilator systems.

Modification of cutaneous vasodilator response to heat stress by daytime exogenous melatonin administration

2006 ◽  
Vol 291 (3) ◽  
pp. R619-R624 ◽  
Author(s):  
Ken Aoki ◽  
Dan P. Stephens ◽  
Kun Zhao ◽  
Wojciech A. Kosiba ◽  
John M. Johnson
Keyword(s):  
Heat Stress ◽  
Random Order ◽  
Vascular Conductance ◽  
Exogenous Melatonin ◽  
Shift Control ◽  
Melatonin Administration ◽  
Relationship Of ◽  
The Relationship ◽  
Cutaneous Vascular Conductance ◽  
Male Subjects

In humans, the nocturnal fall in internal temperature is associated with increased endogenous melatonin and with a shift in the thermoregulatory control of skin blood flow (SkBF), suggesting a role for melatonin in the control of SkBF. The purpose of this study was to test whether daytime exogenous melatonin would shift control of SkBF to lower internal temperatures during heat stress, as is seen at night. Healthy male subjects ( n = 8) underwent body heating with melatonin administration (Mel) or without (control), in random order at least 1 wk apart. SkBF was monitored at sites pretreated with bretylium to block vasoconstrictor nerve function and at untreated sites. Cutaneous vascular conductance, calculated from SkBF and arterial pressure, sweating rate (SR), and heart rate (HR) were monitored. Skin temperature was elevated to 38°C for 35–50 min. Baseline esophageal temperature (Tes) was lower in Mel than in control ( P < 0.01). The Tes threshold for cutaneous vasodilation and the slope of cutaneous vascular conductance with respect to Tes were also lower in Mel at both untreated and bretylium-treated sites ( P < 0.05). The Tes threshold for the onset of sweating and the Tes for a standard HR were reduced in Mel. The slope of the relationship of HR, but not SR, to Tes was lower in Mel ( P < 0.05). These findings suggest that melatonin affects the thermoregulatory control of SkBF during hyperthermia via the cutaneous active vasodilator system. Because control of SR and HR are also modified, a central action of melatonin is suggested.

scholarly journals Combined heat and mental stress alters neurovascular control in humans

2010 ◽  
Vol 109 (6) ◽  
pp. 1880-1886 ◽  
Author(s):  
Jenna C. Klein ◽  
Craig G. Crandall ◽  
R. Matthew Brothers ◽  
Jason R. Carter
Keyword(s):  
Heart Rate ◽  
Heat Stress ◽  
Mental Stress ◽  
Muscle Sympathetic Nerve Activity ◽  
Thermal Conditions ◽  
Venous Occlusion ◽  
Vascular Conductance ◽  
Vascular Responses ◽  
Time Condition ◽  
Forearm Skin

This study examined the effect of combined heat and mental stress on neurovascular control. We hypothesized that muscle sympathetic nerve activity (MSNA) and forearm vascular responses to mental stress would be augmented during heat stress. Thirteen subjects performed 5 min of mental stress during normothermia (Tcore; 37 ± 0°C) and heat stress (38 ± 0°C). Heart rate, mean arterial pressure (MAP), MSNA, forearm vascular conductance (FVC; venous occlusion plethysmography), and forearm skin vascular conductance (SkVCf; via laser-Doppler) were analyzed. Heat stress increased heart rate, MSNA, SkVCf, and FVC at rest but did not change MAP. Mental stress increased MSNA and MAP during both thermal conditions; however, the increase in MAP during heat stress was blunted, whereas the increase in MSNA was accentuated, compared with normothermia (time × condition; P < 0.05 for both). Mental stress decreased SkVCf during heat stress but not during normothermia (time × condition, P < 0.01). Mental stress elicited similar increases in heart rate and FVC during both conditions. In one subject combined heat and mental stress induced presyncope coupled with atypical blood pressure and cutaneous vascular responses. In conclusion, these findings indicate that mental stress elicits a blunted increase of MAP during heat stress, despite greater increases in total MSNA and cutaneous vasoconstriction. The neurovascular responses to combined heat and mental stress may be clinically relevant to individuals frequently exposed to mentally demanding tasks in hyperthermic environmental conditions (i.e., soldiers, firefighters, and athletes).

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