The Postexercise Increase in the Threshold for Cutaneous Vasodilation and Sweating is Not Observed With Extended Recovery

2005 ◽  
Vol 30 (1) ◽  
pp. 113-121 ◽  
Author(s):  
Glen P. Kenny ◽  
W. Shane Journeay
Keyword(s):  
Heat Stress ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
No Reduction ◽  
Treadmill Running ◽  
Whole Body ◽  
Exercise Recovery ◽  
Mean Skin Temperature ◽  
Cutaneous Vasodilation ◽  
Postexercise Hypotension

The following study was conducted to evaluate the hypothesis that an increase in the postexercise onset threshold for cutaneous vasodilation (ThVD) and sweating (ThSW) would not be observed upon the restoration of baseline mean arterial pressure (MAP). Subjects remained either seated resting for 15 min or performed 15 min of treadmill running at 70% [Formula: see text]peak followed by either 20- (short) or 60-min (extended) recovery. At the end of each recovery protocol (20 and 60 min) a water perfusion suit was then used to increase mean skin temperature until ThVD and ThSW was noted. Exercise resulted in an increase in ThVD and ThSW of 0.24 ± 0.03 and 0.24 ± 0.02 °C, respectively, above no-exercise for the short recovery (p < 0.05). No increase was measured for the extended recovery. Postexercise MAP was significantly reduced prior to whole-body warming for the short recovery whereas no reduction was measured for the extended recovery. The increase in ThVD and ThSW, measured during the early stages of recovery, is reversed with the reestablishment of baseline MAP. Key words: postexercise hypotension, exercise recovery, baroreceptors, heat stress

scholarly journals Carotid baroreflex control of heart rate is enhanced, while control of mean arterial pressure is preserved during whole body heat stress in young healthy men

2016 ◽  
Vol 311 (4) ◽  
pp. R735-R741 ◽  
Author(s):  
Davor Krnjajic ◽  
Dustin R. Allen ◽  
Cory L. Butts ◽  
David M. Keller
Keyword(s):  
Heart Rate ◽  
Heat Stress ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Whole Body ◽  
Chamber Pressure ◽  
Carotid Baroreflex ◽  
Whole Body Heat Stress ◽  
Neck Pressure ◽  
Body Heat

Whole body heat stress (WBH) results in numerous cardiovascular alterations that ultimately reduce orthostatic tolerance. While impaired carotid baroreflex (CBR) function during WBH has been reported as a potential reason for this decrement, study design considerations may limit interpretation of previous findings. We sought to test the hypothesis that CBR function is unaltered during WBH. CBR function was assessed in 10 healthy male subjects (age: 26 ± 3; height: 185 ± 7 cm; weight: 82 ± 10 kg; BMI: 24 ± 3 kg/m2; means ± SD) using 5-s trials of neck pressure (+45, +30, and +15 Torr) and neck suction (−20, −40, −60, and −80 Torr) during normothermia (NT) and passive WBH (Δ core temp ∼1°C). Analyses of stimulus response curves (four-parameter logistic model) for CBR control of heart rate (CBR-HR) and mean arterial pressure (CBR-MAP), as well as separate two-way ANOVA of the hypotensive and hypertensive stimuli (factor 1: thermal condition, factor 2: chamber pressure), were performed. For CBR-HR, maximal gain was increased during WBH (−0.73 ± 0.11) compared with NT (−0.39 ± 0.04, mean ± SE, P = 0.03). In addition, the CBR-HR responding range was increased during WBH (33 ± 5) compared with NT (19 ± 2 bpm, P = 0.03). Separate analysis of hypertensive stimulation revealed enhanced HR responses during WBH at −40, −60, and −80 Torr (condition × chamber pressure interaction, P = 0.049) compared with NT. For CBR-MAP, both logistic analysis and separate two-way ANOVA revealed no differences during WBH. Therefore, in response to passive WBH, CBR control of heart rate (enhanced) and arterial pressure (no change) is well preserved.

Effect of exercise intensity on the postexercise sweating threshold

2003 ◽  
Vol 95 (6) ◽  
pp. 2355-2360 ◽  
Author(s):  
Glen P. Kenny ◽  
Julien Périard ◽  
W. Shane Journeay ◽  
Ronald J. Sigal ◽  
Francis D. Reardon
Keyword(s):  
Core Temperature ◽  
Exercise Intensity ◽  
Sweat Rate ◽  
Treadmill Running ◽  
Peak Oxygen Consumption ◽  
Whole Body ◽  
Exercise Recovery ◽  
Postexercise Hypotension ◽  
Intensity Of Exercise ◽  
Sweating Threshold

The hypothesis that the magnitude of the postexercise onset threshold for sweating is increased by the intensity of exercise was tested in eight subjects. Esophageal temperature was monitored as an index of core temperature while sweat rate was measured by using a ventilated capsule placed on the upper back. Subjects remained seated resting for 15 min (no exercise) or performed 15 min of treadmill running at either 55, 70, or 85% of peak oxygen consumption (V̇o2 peak) followed by a 20-min seated recovery. Subjects then donned a liquid-conditioned suit used to regulate mean skin temperature. The suit was first perfused with 20°C water to control and stabilize skin and core temperature before whole body heating. Subsequently, the skin was heated (∼4.0°C/h) until sweating occurred. Exercise resulted in an increase in the onset threshold for sweating of 0.11 ± 0.02, 0.23 ± 0.01, and 0.33 ± 0.02°C above that measured for the no-exercise resting values ( P < 0.05) for the 55, 70, and 85% of V̇o2 peak exercise conditions, respectively. We did note that there was a greater postexercise hypotension as a function of exercise intensity as measured at the end of the 20-min exercise recovery. Thus it is plausible that the increase in postexercise threshold may be related to postexercise hypotension. It is concluded that the sweating response during upright recovery is significantly modified by exercise intensity and may likely be influenced by the nonthermal baroreceptor reflex adjustments postexercise.

Sympathetic nonnoradrenergic cutaneous vasoconstriction in women is associated with reproductive hormone status

2002 ◽  
Vol 282 (1) ◽  
pp. H264-H272 ◽  
Author(s):  
Dan P. Stephens ◽  
Lee Ann T. Bennett ◽  
Ken Aoki ◽  
Wojciech A. Kosiba ◽  
Nisha Charkoudian ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Contraceptive Use ◽  
Intradermal Injection ◽  
Reproductive Hormones ◽  
Whole Body ◽  
Reproductive Hormone ◽  
Doppler Flowmetry ◽  
Hormone Status ◽  
Cutaneous Vasoconstriction

We tested whether a nonnoradrenergic component of reflex vasoconstriction of skin blood flow (SkBF) is sensitive to female reproductive hormones. Six women taking oral contraceptives underwent whole-body cooling during high-hormone (HH) and low-hormone (LH) phases of oral contraceptive use. SkBF was monitored by laser Doppler flowmetry (LDF) at sites treated by intradermal injection of yohimbine-propranolol (5 mM and 1 mM; YOPR) to block the effects of norepinephrine (NE) or at saline (Sal) control sites. Mean arterial pressure (MAP) was measured with the use of the Penaz method. Cutaneous vascular conductance (CVC = LDF/mean arterial pressure) was expressed as a percentage of baseline. Whole body skin temperature was decreased from 34 to 31°C in HH and LH. In both HH and LH, CVC at Sal-treated sites was reduced during cooling (CVC = 53.1 ± 8.6% and 54.4 ± 4.2%, both P < 0.05). In HH, CVC at YOPR sites was reduced during cooling (78.8 ± 3.6%, P < 0.05). In contrast, CVC at YOPR sites was not reduced significantly during cooling in LH (CVC = 95.9 ± 2.8%, P > 0.05). Across phases, CVC at YOPR sites during cooling was significantly different ( P < 0.05). After cooling, the effects of NE at YOPR sites were completely blocked. These data indicate that a nonnoradrenergic mechanism of reflex cutaneous vasoconstriction is present in women and is associated with reproductive hormone status.

scholarly journals Roles of nitric oxide synthase isoforms in cutaneous vasodilation induced by local warming of the skin and whole body heat stress in humans

2009 ◽  
Vol 107 (5) ◽  
pp. 1438-1444 ◽  
Author(s):  
Dean L. Kellogg ◽  
Joan L. Zhao ◽  
Yubo Wu
Keyword(s):  
Nitric Oxide ◽  
Heat Stress ◽  
No Synthase ◽  
Whole Body ◽  
Doppler Flowmetry ◽  
Vasodilator Response ◽  
Cutaneous Vasodilation ◽  
Forearm Skin ◽  
Whole Body Heat Stress ◽  
Body Heat

Nitric oxide (NO) participates in the cutaneous vasodilation caused by increased local skin temperature (Tloc) and whole body heat stress in humans. In forearm skin, endothelial NO synthase (eNOS) participates in vasodilation due to elevated Tloc and neuronal NO synthase (nNOS) participates in vasodilation due to heat stress. To explore the relative roles and interactions of these isoforms, we examined the effects of a relatively specific eNOS inhibitor, Nω-amino-l-arginine (LNAA), and a specific nNOS inhibitor, Nω-propyl-l-arginine (NPLA), both separately and in combination, on skin blood flow (SkBF) responses to increased Tloc and heat stress in two protocols. In each protocol, SkBF was monitored by laser-Doppler flowmetry (LDF) and mean arterial pressure (MAP) by Finapres. Cutaneous vascular conductance (CVC) was calculated (CVC = LDF/MAP). Intradermal microdialysis was used to treat one site with 5 mM LNAA, another with 5 mM NPLA, a third with combined 5 mM LNAA and 5 mM NPLA (Mix), and a fourth site with Ringer only. In protocol 1, Tloc was controlled with combined LDF/local heating units. Tloc was increased from 34°C to 41.5°C to cause local vasodilation. In protocol 2, after a period of normothermia, whole body heat stress was induced (water-perfused suits). At the end of each protocol, all sites were perfused with 58 mM nitroprusside to effect maximal vasodilation for data normalization. In protocol 1, at Tloc = 34°C, CVC did not differ between sites ( P > 0.05). LNAA and Mix attenuated CVC increases at Tloc = 41.5°C to similar extents ( P < 0.05, LNAA or Mix vs. untreated or NPLA). In protocol 2, in normothermia, CVC did not differ between sites ( P > 0.05). During heat stress, NPLA and Mix attenuated CVC increases to similar extents, but no significant attenuation occurred with LNAA ( P < 0.05, NPLA or Mix vs. untreated or LNAA). In forearm skin, eNOS mediates the vasodilator response to increased Tloc and nNOS mediates the vasodilator response to heat stress. The two isoforms do not appear to interact during either response.

Forearm cutaneous vascular and sudomotor responses to whole body passive heat stress in young smokers

2015 ◽  
Vol 309 (1) ◽  
pp. R36-R42 ◽  
Author(s):  
Nicole E. Moyen ◽  
Hannah M. Anderson ◽  
Jenna M. Burchfield ◽  
Matthew A. Tucker ◽  
Melina A. Gonzalez ◽  
...  
Keyword(s):  
Heat Stress ◽  
Sweat Gland ◽  
Sweat Rate ◽  
Whole Body ◽  
Mean Body Temperature ◽  
Doppler Flowmetry ◽  
Cutaneous Vasodilation ◽  
Local Sweat Rate ◽  
Vasomotor Activity ◽  
Young Smokers

The purpose of this study was to compare smokers and nonsmokers' sudomotor and cutaneous vascular responses to whole body passive heat stress. Nine regularly smoking (SMK: 29 ± 9 yr; 10 ± 6 cigarettes/day) and 13 nonsmoking (N-SMK: 27 ± 8 yr) males were passively heated until core temperature (TC) increased 1.5°C from baseline. Forearm local sweat rate (LSR) via ventilated capsule, sweat gland activation (SGA), sweat gland output (SGO), and cutaneous vasomotor activity via laser-Doppler flowmetry (CVC) were measured as mean body temperature increased (ΔTb) during passive heating using a water-perfused suit. Compared with N-SMK, SMK had a smaller ΔTb at the onset of sweating (0.52 ± 0.19 vs. 0.35 ± 0.14°C, respectively; P = 0.03) and cutaneous vasodilation (0.61 ± 0.21 vs. 0.31 ± 0.12°C, respectively; P < 0.01). Increases in LSR and CVC per °C ΔTb (i.e., sensitivity) were similar in N-SMK and SMK (LSR: 0.63 ± 0.21 vs. 0.60 ± 0.40 Δmg/cm2/min/°C ΔTb, respectively, P = 0.81; CVC: 82.5 ± 46.2 vs. 58.9 ± 23.3 Δ%max/°C ΔTb, respectively; P = 0.19). However, the plateau in LSR during whole body heating was higher in N-SMK vs. SMK (1.00 ± 0.13 vs. 0.79 ± 0.26 mg·cm−2·min−1; P = 0.03), which was likely a result of higher SGO (8.94 ± 3.99 vs. 5.94 ± 3.49 μg·gland−1·min−1, respectively; P = 0.08) and not number of SGA (104 ± 7 vs. 121 ± 9 glands/cm2, respectively; P = 0.58). During whole body passive heat stress, smokers had an earlier onset for forearm sweating and cutaneous vasodilation, but a lower local sweat rate that was likely due to lower sweat output per gland. These data provide insight into local (i.e., forearm) thermoregulatory responses of young smokers during uncompensatory whole body passive heat stress.

Arterial baroreflex modulation of heat-induced vasodilation in the rabbit ear

1997 ◽  
Vol 83 (6) ◽  
pp. 2091-2097 ◽  
Author(s):  
Kathy L. Ryan ◽  
W. Fred Taylor ◽  
Vernon S. Bishop
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Whole Body ◽  
Arterial Baroreflex ◽  
Animal Group ◽  
Arterial Baroreceptors ◽  
Mechanical Unloading ◽  
Rabbit Ear ◽  
Cardiac Afferents ◽  
Plateau Level

Ryan, Kathy L., W. Fred Taylor, and Vernon S. Bishop.Arterial baroreflex modulation of heat-induced vasodilation in the rabbit ear. J. Appl. Physiol. 83(6): 2091–2097, 1997.—The purpose of this study was to determine whether nonthermal baroreflexes arising from cardiopulmonary and/or arterial baroreceptors modulate rabbit ear blood flow (EBF) during hyperthermia. Intact and sinoaortic-denervated (SAD) rabbits were chronically instrumented with a Doppler ultrasonic flow probe for measurement of EBF velocity (kHz). During whole body heating in conscious rabbits, EBF and ear vascular conductance (EVC) increased as core temperature increased until maximal plateau levels of EBF and EVC were reached. The maximal plateau level of EVC attained during heat stress was lower in SAD than in intact rabbits. Subsequent intrapericardial administration of procaine at maximal EBF blocked cardiac afferents but did not alter EVC in either animal group. In a second experiment, ramp decreases in mean arterial pressure were produced by vena caval occlusion at maximal EBF. In intact rabbits, EBF and EVC decreased linearly as mean arterial pressure fell, but EBF and EVC did not decrease during vena caval occlusion in SAD rabbits. Thus neither pharmacological nor mechanical unloading of cardiac baroreceptors results in reflex vasoconstriction in the heat-stressed rabbit ear. However, baroreflexes arising from arterial baroreceptors may modulate EBF in heat-stressed rabbits.

Intermittent sequential pneumatic compression does not enhance whole-body heat loss in elderly adults during extreme heat exposure

2019 ◽  
Vol 44 (12) ◽  
pp. 1383-1386
Author(s):  
Andrew W. D’Souza ◽  
Sean R. Notley ◽  
Robert D. Meade ◽  
Glen P. Kenny
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Heat Loss ◽  
Lower Limb ◽  
Vascular Function ◽  
Heat Exposure ◽  
Extreme Heat ◽  
Whole Body ◽  
Elderly Adults ◽  
Body Heat

Lower-limb intermittent sequential pneumatic compression (ISPC) improves circulation and vascular function in elderly adults. We evaluated the hypothesis that ISPC would also augment whole-body heat loss (WBHL) in elderly adults (aged 69 ± 4 years) resting in extreme heat (40 °C). While ISPC increased mean arterial pressure (91 ± 9 mm Hg) relative to no-ISPC (83 ± 5 mm Hg; P = 0.013) at the end of the exposure, no influence on WBHL was observed (81 ± 7 and 86 ± 11 W for ISPC and no-ISPC, respectively, P = 0.310). Novelty When assessed in elderly adults during an extreme heat exposure, intermittent sequential pneumatic compression augmented mean arterial pressure but did not enhance whole-body heat loss.

scholarly journals Tyrosine kinase inhibitors modulate the ventilatory response to hypoxia in the conscious rat

1999 ◽  
Vol 87 (1) ◽  
pp. 363-369 ◽  
Author(s):  
Marc A. Czapla ◽  
Narong Simakajornboon ◽  
Gregory A. Holt ◽  
David Gozal
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Brain Stem ◽  
Tyrosine Phosphorylation ◽  
Minute Ventilation ◽  
Whole Body ◽  
Control Mechanisms ◽  
Conscious Rat ◽  
Adult Rats

Tyrosine kinases (TKs) exert multiple regulatory roles in neuronal activity and synaptic plasticity and could be involved in modulation of cardiovascular and respiratory control mechanisms within the dorsocaudal brain stem. To study this issue, the cardioventilatory responses to 1-μl microinjection within the dorsocaudal brain stem of either vehicle (Veh), the inactive TK inhibitor analog tyrphostin A1 (A1; 1 mM), or the active TK inhibitors genistein (Gen; 10 mM) and tyrphostin A25 (A25; 1 mM) were assessed by whole body plethysmography in unrestrained Sprague-Dawley adult rats. No changes in minute ventilation, heart rate, or mean arterial pressure occurred with Veh, A1, Gen, or A25 during room air breathing ( P not significant). However, Gen and A25 attenuated the peak hypoxic ventilatory responses (HVR) to 10% O2( P < 0.006 vs. Veh), whereas A1 did not modify HVR ( P not significant). HVR reductions by Gen and A25 were primarily due to diminished respiratory frequency enhancements ( P< 0.002). No changes in heart rate or mean arterial pressure responses occurred during hypoxia with TK inhibition. In addition, increases in tyrosine phosphorylation of the NR2A/B subunits, but not of the NR2C subunit, of the N-methyl-d-aspartate receptor occurred at 5, 30, and 60 min of hypoxia in the dorsocaudal brain stem and returned to baseline values at 120 min. We conclude that hypoxia induces tyrosine phosphorylation of the N-methyl-d-aspartate glutamate receptor, and TK inhibition within the dorsocaudal brain stem attenuates components of HVR in conscious rats.

scholarly journals Modelflow underestimates cardiac output in heat-stressed individuals

2011 ◽  
Vol 300 (2) ◽  
pp. R486-R491 ◽  
Author(s):  
Manabu Shibasaki ◽  
Thad E. Wilson ◽  
Morten Bundgaard-Nielsen ◽  
Thomas Seifert ◽  
Niels H. Secher ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Heat Stress ◽  
Arterial Pressure ◽  
Lower Body Negative Pressure ◽  
Whole Body ◽  
Arterial Cannulation ◽  
Artery Cannulation ◽  
Whole Body Heat Stress ◽  
Acute Changes ◽  
Body Heat

An estimation of cardiac output can be obtained from arterial pressure waveforms using the Modelflow method. However, whether the assumptions associated with Modelflow calculations are accurate during whole body heating is unknown. This project tested the hypothesis that cardiac output obtained via Modelflow accurately tracks thermodilution-derived cardiac outputs during whole body heat stress. Acute changes of cardiac output were accomplished via lower-body negative pressure (LBNP) during normothermic and heat-stressed conditions. In nine healthy normotensive subjects, arterial pressure was measured via brachial artery cannulation and the volume-clamp method of the Finometer. Cardiac output was estimated from both pressure waveforms using the Modeflow method. In normothermic conditions, cardiac outputs estimated via Modelflow (arterial cannulation: 6.1 ± 1.0 l/min; Finometer 6.3 ± 1.3 l/min) were similar with cardiac outputs measured by thermodilution (6.4 ± 0.8 l/min). The subsequent reduction in cardiac output during LBNP was also similar among these methods. Whole body heat stress elevated internal temperature from 36.6 ± 0.3 to 37.8 ± 0.4°C and increased cardiac output from 6.4 ± 0.8 to 10.9 ± 2.0 l/min when evaluated with thermodilution ( P < 0.001). However, the increase in cardiac output estimated from the Modelflow method for both arterial cannulation (2.3 ± 1.1 l/min) and Finometer (1.5 ± 1.2 l/min) was attenuated compared with thermodilution (4.5 ± 1.4 l/min, both P < 0.01). Finally, the reduction in cardiac output during LBNP while heat stressed was significantly attenuated for both Modelflow methods (cannulation: −1.8 ± 1.2 l/min, Finometer: −1.5 ± 0.9 l/min) compared with thermodilution (−3.8 ± 1.19 l/min). These results demonstrate that the Modelflow method, regardless of Finometer or direct arterial waveforms, underestimates cardiac output during heat stress and during subsequent reductions in cardiac output via LBNP.

Is postexercise hypotension related to excess postexercise oxygen consumption through changes in leg blood flow?

2005 ◽  
Vol 98 (4) ◽  
pp. 1463-1468 ◽  
Author(s):  
Jay T. Williams ◽  
Mollie P. Pricher ◽  
John R. Halliwill
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Muscle Blood Flow ◽  
Causal Link ◽  
Skeletal Muscle Blood Flow ◽  
Leg Blood Flow ◽  
Postexercise Hypotension

After a single bout of aerobic exercise, oxygen consumption remains elevated above preexercise levels [excess postexercise oxygen consumption (EPOC)]. Similarly, skeletal muscle blood flow remains elevated for an extended period of time. This results in a postexercise hypotension. The purpose of this study was to explore the possibility of a causal link between EPOC, postexercise hypotension, and postexercise elevations in skeletal muscle blood flow by comparing the magnitude and duration of these postexercise phenomena. Sixteen healthy, normotensive, moderately active subjects (7 men and 9 woman, age 20–31 yr) were studied before and through 135 min after a 60-min bout of upright cycling at 60% of peak oxygen consumption. Resting and recovery V̇o2 were measured with a custom-built dilution hood and mass spectrometer-based metabolic system. Mean arterial pressure was measured via an automated blood pressure cuff, and femoral blood flow was measured using ultrasound. During the first hour postexercise, V̇o2 was increased by 11 ± 2%, leg blood flow was increased by 51 ± 18%, leg vascular conductance was increased by 56 ± 19%, and mean arterial pressure was decreased by 2.2 ± 1.0 mmHg (all P < 0.05 vs. preexercise). At the end of the protocol, V̇o2 remained elevated by 4 ± 2% ( P < 0.05), whereas leg blood flow, leg vascular conductance, and mean arterial pressure returned to preexercise levels (all P > 0.7 vs. preexercise). Taken together, these data demonstrate that EPOC and the elevations in skeletal muscle blood flow underlying postexercise hypotension do not share a common time course. This suggests that there is no causal link between these two postexercise phenomena.

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