scholarly journals Post-exercise Body Cooling: Skin Blood Flow, Venous Pooling, and Orthostatic Intolerance

2021 ◽  
Vol 3 ◽  
Author(s):  
Afton D. Seeley ◽  
Gabrielle E. W. Giersch ◽  
Nisha Charkoudian

Athletes and certain occupations (e.g., military, firefighters) must navigate unique heat challenges as they perform physical tasks during prolonged heat stress, at times while wearing protective clothing that hinders heat dissipation. Such environments and activities elicit physiological adjustments that prioritize thermoregulatory skin perfusion at the expense of arterial blood pressure and may result in decreases in cerebral blood flow. High levels of skin blood flow combined with an upright body position augment venous pooling and transcapillary fluid shifts in the lower extremities. Combined with sweat-driven reductions in plasma volume, these cardiovascular alterations result in levels of cardiac output that do not meet requirements for brain blood flow, which can lead to orthostatic intolerance and occasionally syncope. Skin surface cooling countermeasures appear to be a promising means of improving orthostatic tolerance via autonomic mechanisms. Increases in transduction of sympathetic activity into vascular resistance, and an increased baroreflex set-point have been shown to be induced by surface cooling implemented after passive heating and other arterial pressure challenges. Considering the further contribution of exercise thermogenesis to orthostatic intolerance risk, our goal in this review is to provide an overview of post-exercise cooling strategies as they are capable of improving autonomic control of the circulation to optimize orthostatic tolerance. We aim to synthesize both basic and applied physiology knowledge available regarding real-world application of cooling strategies to reduce the likelihood of experiencing symptomatic orthostatic intolerance after exercise in the heat.

2002 ◽  
Vol 93 (1) ◽  
pp. 85-91 ◽  
Author(s):  
Thad E. Wilson ◽  
Jian Cui ◽  
Rong Zhang ◽  
Sarah Witkowski ◽  
Craig G. Crandall

Orthostatic tolerance is reduced in the heat-stressed human. The purpose of this project was to identify whether skin-surface cooling improves orthostatic tolerance. Nine subjects were exposed to 10 min of 60° head-up tilting in each of four conditions: normothermia (NT-tilt), heat stress (HT-tilt), normothermia plus skin-surface cooling 1 min before and throughout tilting (NT-tiltcool), and heat stress plus skin-surface cooling 1 min before and throughout tilting (HT-tiltcool). Heating and cooling were accomplished by perfusing 46 and 15°C water, respectively, though a tube-lined suit worn by each subject. During HT-tilt, four of nine subjects developed presyncopal symptoms resulting in the termination of the tilt test. In contrast, no subject experienced presyncopal symptoms during NT-tilt, NT-tiltcool, or HT-tiltcool. During the HT-tilt procedure, mean arterial blood pressure (MAP) and cerebral blood flow velocity (CBFV) decreased. However, during HT-tiltcool, MAP, total peripheral resistance, and CBFV were significantly greater relative to HT-tilt (all P< 0.01). No differences were observed in calculated cerebral vascular resistance between the four conditions. These data suggest that skin-surface cooling prevents the fall in CBFV during upright tilting and improves orthostatic tolerance, presumably via maintenance of MAP. Hence, skin-surface cooling may be a potent countermeasure to protect against orthostatic intolerance observed in heat-stressed humans.


2002 ◽  
Vol 93 (6) ◽  
pp. 1918-1924 ◽  
Author(s):  
Robert Carter ◽  
Thad E. Wilson ◽  
Donald E. Watenpaugh ◽  
Michael L. Smith ◽  
Craig G. Crandall

To identify the effects of exercise recovery mode on cutaneous vascular conductance (CVC) and sweat rate, eight healthy adults performed two 15-min bouts of upright cycle ergometry at 60% of maximal heart rate followed by either inactive or active (loadless pedaling) recovery. An index of CVC was calculated from the ratio of laser-Doppler flux to mean arterial pressure. CVC was then expressed as a percentage of maximum (%max) as determined from local heating. At 3 min postexercise, CVC was greater during active recovery (chest: 40 ± 3, forearm: 48 ± 3%max) compared with during inactive recovery (chest: 21 ± 2, forearm: 25 ± 4%max); all P < 0.05. Moreover, at the same time point sweat rate was greater during active recovery (chest: 0.47 ± 0.10, forearm: 0.46 ± 0.10 mg · cm−2 · min−1) compared with during inactive recovery (chest: 0.28 ± 0.10, forearm: 0.14 ± 0.20 mg · cm−2 · min−1); all P < 0.05. Mean arterial blood pressure, esophageal temperature, and skin temperature were not different between recovery modes. These data suggest that skin blood flow and sweat rate during recovery from exercise may be modulated by nonthermoregulatory mechanisms and that sustained elevations in skin blood flow and sweat rate during mild active recovery may be important for postexertional heat dissipation.


Author(s):  
Björn Wieslander ◽  
Joao Génio Ramos ◽  
Malin Ax ◽  
Johan Petersson ◽  
Martin Ugander

Abstract Background Body position can be optimized for pulmonary ventilation/perfusion matching during surgery and intensive care. However, positional effects upon distribution of pulmonary blood flow and vascular distensibility measured as the pulmonary blood volume variation have not been quantitatively characterized. In order to explore the potential clinical utility of body position as a modulator of pulmonary hemodynamics, we aimed to characterize gravitational effects upon distribution of pulmonary blood flow, pulmonary vascular distension, and pulmonary vascular distensibility. Methods Healthy subjects (n = 10) underwent phase contrast cardiovascular magnetic resonance (CMR) pulmonary artery and vein flow measurements in the supine, prone, and right/left lateral decubitus positions. For each lung, blood volume variation was calculated by subtracting venous from arterial flow per time frame. Results Body position did not change cardiac output (p = 0.84). There was no difference in blood flow between the superior and inferior pulmonary veins in the supine (p = 0.92) or prone body positions (p = 0.43). Compared to supine, pulmonary blood flow increased to the dependent lung in the lateral positions (16–33%, p = 0.002 for both). Venous but not arterial cross-sectional vessel area increased in both lungs when dependent compared to when non-dependent in the lateral positions (22–27%, p ≤ 0.01 for both). In contrast, compared to supine, distensibility increased in the non-dependent lung in the lateral positions (68–113%, p = 0.002 for both). Conclusions CMR demonstrates that in the lateral position, there is a shift in blood flow distribution, and venous but not arterial blood volume, from the non-dependent to the dependent lung. The non-dependent lung has a sizable pulmonary vascular distensibility reserve, possibly related to left atrial pressure. These results support the physiological basis for positioning patients with unilateral pulmonary pathology with the “good lung down” in the context of intensive care. Future studies are warranted to evaluate the diagnostic potential of these physiological insights into pulmonary hemodynamics, particularly in the context of non-invasively characterizing pulmonary hypertension.


2014 ◽  
Vol 116 (6) ◽  
pp. 645-653 ◽  
Author(s):  
Aaron A. Phillips ◽  
Andrei V. Krassioukov ◽  
Philip N. Ainslie ◽  
Darren E. R. Warburton

Individuals with spinal cord injury (SCI) above the T6 spinal segment suffer from orthostatic intolerance. How cerebral blood flow (CBF) responds to orthostatic challenges in SCI is poorly understood. Furthermore, it is unclear how interventions meant to improve orthostatic tolerance in SCI influence CBF. This study aimed to examine 1) the acute regional CBF responses to rapid changes in blood pressure (BP) during orthostatic stress in individuals with SCI and able-bodied (AB) individuals; and 2) the effect of midodrine (alpha1-agonist) on orthostatic tolerance and CBF regulation in SCI. Ten individuals with SCI >T6, and 10 age- and sex-matched AB controls had beat-by-beat BP and middle and posterior cerebral artery blood velocity (MCAv, PCAv, respectively) recorded during a progressive tilt-test to quantify the acute CBF response and orthostatic tolerance. Dynamic MCAv and PCAv to BP relationships were evaluated continuously in the time domain and frequency domain (via transfer function analysis). The SCI group was tested again after administration of 10 mg midodrine to elevate BP. Coherence (i.e., linearity) was elevated in SCI between BP-MCAv and BP-PCAv by 35% and 22%, respectively, compared with AB, whereas SCI BP-PCAv gain (i.e., magnitudinal relationship) was reduced 30% compared with AB (all P < 0.05). The acute (i.e., 0–30 s after tilt) MCAv and PCAv responses were similar between groups. In individuals with SCI, midodrine led to improved PCAv responses 30–60 s following tilt (10 ± 3% vs. 4 ± 2% decline; P < 0.05), and a 59% improvement in orthostatic tolerance ( P < 0.01). The vertebrobasilar region may be particularly susceptible to hypoperfusion in SCI, leading to increased orthostatic intolerance.


2006 ◽  
Vol 291 (5) ◽  
pp. R1443-R1448 ◽  
Author(s):  
Thad E. Wilson ◽  
Jian Cui ◽  
Rong Zhang ◽  
Craig G. Crandall

Orthostatic tolerance is reduced in the heat-stressed human. This study tested the following hypotheses: 1) whole body heat stress reduces cerebral blood velocity (CBV) and increases cerebral vascular resistance (CVR); and 2) reductions in CBV and increases in CVR in response to an orthostatic challenge will be greater while subjects are heat stressed. Fifteen subjects were instrumented for measurements of CBV (transcranial ultrasonography), mean arterial blood pressure (MAP), heart rate, and internal temperature. Whole body heating increased both internal temperature (36.4 ± 0.1 to 37.3 ± 0.1° C) and heart rate (59 ± 3 to 90 ± 3 beats/min); P < 0.001. Whole body heating also reduced CBV (62 ± 3 to 53 ± 2 cm/s) primarily via an elevation in CVR (1.35 ± 0.06 to 1.63 ± 0.07 mmHg · cm−1 · s); P < 0.001. A subset of subjects ( n = 8) were exposed to lower-body negative pressure (LBNP 10, 20, 30, 40 mmHg) in both normothermic and heat-stressed conditions. During normothermia, LBNP of 30 mmHg (highest level of LBNP achieved by the majority of subjects in both thermal conditions) did not significantly alter CBV, CVR, or MAP. During whole body heating, this LBNP decreased MAP (81 ± 2 to 75 ± 3 mmHg), decreased CBV (50 ± 4 to 39 ± 1 cm/s), and increased CVR (1.67 ± 0.17 to 1.92 ± 0.12 mmHg · cm−1 · s); P < 0.05. These data indicate that heat stress decreases CBV, and the reduction in CBV for a given orthostatic challenge is greater during heat stress. These outcomes reduce the reserve to buffer further decreases in cerebral perfusion before presyncope. Increases in CVR during whole body heating, coupled with even greater increases in CVR during orthostasis and heat stress, likely contribute to orthostatic intolerance.


2004 ◽  
Vol 287 (5) ◽  
pp. R1230-R1234 ◽  
Author(s):  
Thad E. Wilson ◽  
Kevin D. Monahan ◽  
Daniel S. Short ◽  
Chester A. Ray

To test the hypothesis that cutaneous vasoconstrictor responsiveness to exogenous norepinephrine is reduced in older compared with young subjects, dose-response relations between norepinephrine and skin blood flow were established. Seven doses of norepinephrine (1·10−8 to 10−2 log M) were perfused (2 μl/min) intradermally (4 min/dose) using cutaneous microdialysis (2 probes/subject). To account for possible differences in endogenous norepinephrine between groups, one microdialysis probe was perfused with bretylium tosylate to locally block noradrenergic vesicle release before establishing the norepinephrine dose-response relations. Skin blood flow was indexed via laser-Doppler flowmetry directly over both microdialysis probe sites and is expressed as cutaneous vascular conductance (laser-Doppler flux/mean arterial blood pressure). Local skin temperature was maintained at 34°C at both sites throughout the protocol. Dose-response relation between norepinephrine and cutaneous vascular conductance was similar between control and bretylium-pretreated sites in young subjects (EC50 = −5.18 ± 0.27 and −5.03 ± 0.27 log M, respectively). In contrast, the dose-response relation was significantly shifted to the right (i.e., a higher dose of norepinephrine was needed to produce the same vasoconstrictor response) in the bretylium-pretreated site in older subjects (EC50 = −5.46 ± 0.23 and −4.53 ± 0.23 log M, respectively). Significant increases in EC50 were observed in older compared with young subjects at the bretylium-pretreated but not the control sites. These data indicate that cutaneous vasoconstrictor responsiveness is decreased in older subjects when endogenous release of norepinephrine is antagonized. Furthermore, these findings suggest that differences in presynaptic norepinephrine release between older and younger subjects are profound enough to affect dose-response relations between norepinephrine and cutaneous vascular conductance.


1983 ◽  
Vol 65 (3) ◽  
pp. 247-253 ◽  
Author(s):  
O. J. Hartling ◽  
J. Trap-Jensen

1. The pre- and post-junctional α-adrenoceptor blocking agent, phentolamine, was given by intravenous infusion to eight healthy volunteers during rest, forearm exercise and post-exercise. 2. Phentolamine produced a sustained increase in heart rate. The diastolic blood pressure decreased slightly whereas systolic and mean blood pressures remained unchanged. Phentolamine caused a marked increase in the forearm blood flow and a decrease in vascular resistance at rest and post-exercise, but did not influence the blood flow or vascular resistance in the exercising forearm. 3. There was a small increase in arterial blood glucose concentration, and a decrease in blood alanine concentration during drug infusion. Blood lactate was not affected by phentolamine. The arterial concentrations of free fatty acids and glycerol increased, and the concentration of triglycerides decreased during phentolamine infusion. 4. Forearm exchange of glucose, lactate, alanine, glycerol, free fatty acids, triglycerides and forearm oxygen consumption were not changed significantly. 5. These findings corroborate the concept that α-adrenoceptor induced vasoconstriction plays a subordinate role in exercising skeletal muscle. All of the metabolic findings might be explained as secondary to an increased noradrenaline release during phentolamine infusion.


2018 ◽  
Vol 1 (96) ◽  
Author(s):  
Julius Dovydaitis ◽  
Albinas Grūnovas

Background.  In  most  studies  on  cardiovascular  system,  testing  of  subjects  was  performed  in  a  horizontal position. With the change of the body position, certain functional changes occur in the cardiovascular system. The aim of this study was to analyze the effect of electrical muscle stimulation (EMS) on arterial and venous blood flows.Methods. Eighteen athletes aged 19–23 performed two sessions of tests in horizontal and sitting positions. Changes in arterial and venous blood flows were recorded before and after EMS. In each session two occlusions were performed. In the horizontal position, the initial occlusion pressure of 20 mmHg was applied and as the balance in arterial and venous blood flow rates was reached, the additional pressure of 20 mmHg (40  mmHg in total). In the sitting position, the occlusion pressure of 40 and 20 mmHg was applied respectively (60 mmHg in total). In both sessions EMS was performed using the electrical stimulator Mioritm 021.Results. In both horizontal and vertical positions, the effect of EMS on arterial blood flow, venous reserve capacity and venous elasticity was insignificant. Arterial and venous blood flows was affected significantly by the change of the body position. In the sitting position, arterial blood flow was significantly (p < .05) lower compared to the horizontal position. Similar results were recorded in venous reserve capacity.Conclusion.  The  study  suggests  that  blood  flow  in  the  calf  muscles  is  affected  by  the  body  position  and hydrostatic pressure; arterial blood flow increases in the horizontal body position.Keywords:  electrical muscle stimulation (EMS), arterial blood flow, venous reserve capacity, venous elasticity


2012 ◽  
Vol 302 (2) ◽  
pp. H489-H497 ◽  
Author(s):  
Sung-Moon Jeong ◽  
Shigeki Shibata ◽  
Benjamin D. Levine ◽  
Rong Zhang

This study tested the hypothesis that reduction in cerebral blood flow (CBF) during orthostatic stress after bed rest can be ameliorated with volume loading, exercise, or both. Transcranial Doppler was used to measure changes in CBF velocity during lower body negative pressure (LBNP) before and after an 18-day bed rest in 33 healthy subjects. Subjects were assigned into four groups with similar age and sex: 1) supine cycling during bed rest (Exercise group; n = 7), 2) volume loading with Dextran infusion after bed rest to restore reduced left ventricular filling pressure (Dextran group; n = 7), 3) exercise combined with volume loading to prevent orthostatic intolerance (Ex-Dex group; n = 7), and 4) a control group ( n = 12). LBNP tolerance was measured using a cumulative stress index (CSI). After bed rest, CBF velocity was reduced at a lower level of LBNP in the Control group, and the magnitude of reduction was greater in the Ex-Dex group. However, reduction in orthostatic tolerance was prevented in the Ex-Dex group. Notably, volume loading alone prevented greater reductions in CBF velocity after bed rest, but CSI was reduced still by 25%. Finally, decreases in CBF velocity during LBNP were correlated with reduction in cardiac output under all conditions ( r2 = 0.86; P = < 0.001). Taken together, these findings demonstrate that volume loading alone can ameliorate reductions in CBF during LBNP. However, the lack of associations between changes in CBF velocity and orthostatic tolerance suggests that reductions in CBF during LBNP under steady-state conditions by itself are unlikely to be a primary factor leading to orthostatic intolerance.


1990 ◽  
Vol 68 (4) ◽  
pp. 1453-1457 ◽  
Author(s):  
M. J. Joyner ◽  
R. L. Lennon ◽  
D. J. Wedel ◽  
S. H. Rose ◽  
J. T. Shepherd

The purpose of this study was to examine the effects of the increased sympathetic activity elicited by the upright posture on blood flow to exercising human forearm muscles. Six subjects performed light and heavy rhythmic forearm exercise. Trials were conducted with the subjects supine and standing. Forearm blood flow (FBF, plethysmography) and skin blood flow (laser Doppler) were measured during brief pauses in the contractions. Arterial blood pressure and heart rate were also measured. During the first 6 min of light exercise, blood flow was similar in the supine and standing positions (approximately 15 ml.min-1.100 ml-1); from minutes 7 to 20 FBF was approximately 3-7 ml.min-1.100 ml-1 less in the standing position (P less than 0.05). When 5 min of heavy exercise immediately followed the light exercise, FBF was approximately 30-35 ml.min-1.100 ml-1 in the supine position. These values were approximately 8-12 ml.min-1.100 ml-1 greater than those observed in the upright position (P less than 0.05). When light exercise did not precede 8 min of heavy exercise, the blood flow at the end of minute 1 was similar in the supine and standing positions but was approximately 6-9 ml.min-1.100 ml-1 lower in the standing position during minutes 2-8. Heart rate was always approximately 10-20 beats higher in the upright position (P less than 0.05). Forearm skin blood flow and mean arterial pressure were similar in the two positions, indicating that the changes in FBF resulted from differences in the caliber of the resistance vessels in the forearm muscles.(ABSTRACT TRUNCATED AT 250 WORDS)


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