Reflex control of the cutaneous circulation during passive body core heating in humans

2000 ◽  
Vol 88 (5) ◽  
pp. 1756-1764 ◽  
Author(s):  
Jochen K. Peters ◽  
Takeshi Nishiyasu ◽  
Gary W. Mack
Keyword(s):  
Blood Pressure ◽  
Heat Stress ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Laser Doppler ◽  
Vascular Conductance ◽  
Arterial Blood ◽  
Body Core ◽  
Doppler Techniques ◽  
The Impact

The impact of body core heating on the interaction between the cutaneous and central circulation during blood pressure challenges was examined in eight adults. Subjects were exposed to −10 to −90 mmHg lower body negative pressure (LBNP) in thermoneutral conditions and −10 to −60 mmHg LBNP during heat stress. We measured forearm vascular conductance (FVC; ml ⋅ min−1 ⋅ 100 ml−1 ⋅ mmHg−1) by plethysmography; cutaneous vascular conductance (CVC) by laser-Doppler techniques; and central venous pressure, arterial blood pressure, and cardiac output by impedance cardiography. Heat stress increased FVC from 5.7 ± 0.9 to 18.8 ± 1.3 conductance units (CU) and CVC from 0.21 ± 0.07 to 1.02 ± 0.20 CU. The FVC-CVP relationship was linear over the entire range of LBNP and was shifted upward during heat stress with a slope increase from 0.46 ± 0.10 to 1.57 ± 0.3 CU/mmHg CVP ( P < 0.05). Resting CVP was lower during heat stress (6.3 ± 0.6 vs. 7.7 ± 0.6 mmHg; P < 0.05) but fell to similar levels during LBNP as in normothermic conditions. Data analysis indicates an increased capacity, but not sensitivity, of peripheral baroreflex responses during heat stress. Laser-Doppler techniques detected thermoregulatory responses in the skin, but no significant change in CVC occurred during mild-to-moderate LBNP. Interestingly, very high levels of LBNP produced cutaneous vasodilation in some subjects.

Cardiopulmonary baroreceptor control of muscle sympathetic nerve activity in heat-stressed humans

1999 ◽  
Vol 277 (6) ◽  
pp. H2348-H2352 ◽  
Author(s):  
C. G. Crandall ◽  
R. A. Etzel ◽  
D. B. Farr
Keyword(s):  
Blood Pressure ◽  
Heat Stress ◽  
Arterial Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Whole Body ◽  
Nerve Activity ◽  
Arterial Blood

Whole body heating decreases central venous pressure (CVP) while increasing muscle sympathetic nerve activity (MSNA). In normothermia, similar decreases in CVP elevate MSNA, presumably via cardiopulmonary baroreceptor unloading. The purpose of this project was to identify whether increases in MSNA during whole body heating could be attributed to cardiopulmonary baroreceptor unloading coincident with the thermal challenge. Seven subjects were exposed to whole body heating while sublingual temperature, skin blood flow, heart rate, arterial blood pressure, and MSNA were monitored. During the heat stress, 15 ml/kg warmed saline was infused intravenously over 7–10 min to increase CVP and load the cardiopulmonary baroreceptors. We reported previously that this amount of saline was sufficient to return CVP to pre-heat stress levels. Whole body heating increased MSNA from 25 ± 3 to 39 ± 3 bursts/min ( P < 0.05). Central blood volume expansion via rapid saline infusion did not significantly decrease MSNA (44 ± 4 bursts/min, P > 0.05 relative to heat stress period) and did not alter mean arterial blood pressure (MAP) or pulse pressure. To identify whether arterial baroreceptor loading decreases MSNA during heat stress, in a separate protocol MAP was elevated via steady-state infusion of phenylephrine during whole body heating. Increasing MAP from 82 ± 3 to 93 ± 4 mmHg ( P < 0.05) caused MSNA to decrease from 36 ± 3 to 15 ± 4 bursts/min ( P < 0.05). These data suggest that cardiopulmonary baroreceptor unloading during passive heating is not the primary mechanism resulting in elevations in MSNA. Moreover, arterial baroreceptors remain capable of modulating MSNA during heat stress.

scholarly journals Heat-stress-induced changes in central venous pressure do not explain interindividual differences in orthostatic tolerance during heat stress

2011 ◽  
Vol 110 (5) ◽  
pp. 1283-1289 ◽  
Author(s):  
R. Matthew Brothers ◽  
David M. Keller ◽  
Jonathan E. Wingo ◽  
Matthew S. Ganio ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Heat Stress ◽  
Central Venous Pressure ◽  
Blood Pressure Control ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Pressure Control ◽  
Stress Index ◽  
Central Venous ◽  
The Difference

The extent to which heat stress compromises blood pressure control is variable among individuals, with some individuals becoming very intolerant to a hypotensive challenge, such as lower body negative pressure (LBNP) while heat stressed, while others are relatively tolerant. Heat stress itself reduces indexes of ventricular filling pressure, including central venous pressure, which may be reflective of reductions in tolerance in this thermal condition. This study tested the hypothesis that the magnitude of the reduction in central venous pressure in response to heat stress alone is related to the subsequent decrement in LBNP tolerance. In 19 subjects, central hypovolemia was imposed via LBNP to presyncope in both normothermic and heat-stress conditions. Tolerance to LBNP was quantified using a cumulative stress index (CSI), and the difference between normothermic CSI and heat-stress CSI was calculated for each individual. The eight individuals with the greatest CSI difference between normothermic and heat-stress tolerances (LargeDif), and the eight individuals with the smallest CSI difference (SmallDif), were grouped together. By design, the difference in CSI between thermal conditions was greater in the LargeDif group (969 vs. 382 mmHg × min; P < 0.001). Despite this profound difference in the effect of heat stress in decreasing LBNP tolerance between groups, coupled with no difference in the rise in core body temperatures to the heat stress (LargeDif, 1.4 ± 0.1°C vs. SmallDif, 1.4 ± 0.1°C; interaction P = 0.89), the reduction in central venous pressure during heat stress alone was similar between groups (LargeDif: 5.7 ± 1.9 mmHg vs. SmallDif: 5.2 ± 2.0 mmHg; interaction P = 0.85). Contrary to the proposed hypothesis, differences in blood pressure control during LBNP are not related to differences in the magnitude of the heat-stress-induced reductions in central venous pressure.

Cardiopulmonary baroreflex is reset during dynamic exercise

2006 ◽  
Vol 100 (1) ◽  
pp. 51-59 ◽  
Author(s):  
Shigehiko Ogoh ◽  
R. Matthew Brothers ◽  
Quinton Barnes ◽  
Wendy L. Eubank ◽  
Megan N. Hawkins ◽  
...  
Keyword(s):  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Peak Oxygen Uptake ◽  
Operating Point ◽  
Vascular Conductance ◽  
Arterial Blood ◽  
Significant Difference ◽  
Forearm Vascular Conductance ◽  
Cardiopulmonary Baroreflex ◽  
Cardiac Filling

The purpose of this study was to examine the hypothesis that the operating point of the cardiopulmonary baroreflex resets to the higher cardiac filling pressure of exercise associated with the increased cardiac filling volumes. Eight men (age 26 ± 1 yr; height 180 ± 3 cm; weight 86 ± 6 kg; means ± SE) participated in the present study. Lower body negative pressure (LBNP) was applied at 8 and 16 Torr to decrease central venous pressure (CVP) at rest and during steady-state leg cycling at 50% peak oxygen uptake (104 ± 20 W). Subsequently, two discrete infusions of 25% human serum albumin solution were administered until CVP was increased by 1.8 ± 0.6 and 2.4 ± 0.4 mmHg at rest and 2.9 ± 0.9 and 4.6 ± 0.9 mmHg during exercise. During all protocols, heart rate, arterial blood pressure, and CVP were recorded continuously. At each stage of LBNP or albumin infusion, forearm blood flow and cardiac output were measured. During exercise, forearm vascular conductance increased from 7.5 ± 0.5 to 8.7 ± 0.6 U ( P = 0.024) and total systemic vascular conductance from 7.2 ± 0.2 to 13.5 ± 0.9 l·min−1·mmHg−1 ( P < 0.001). However, there was no significant difference in the responses of both forearm vascular conductance and total systemic vascular conductance to LBNP and the infusion of albumin between rest and exercise. These data indicate that the cardiopulmonary baroreflex had been reset during exercise to the new operating point associated with the exercise-induced change in cardiac filling volume.

scholarly journals Effect of heat stress on cardiac output and systemic vascular conductance during simulated hemorrhage to presyncope in young men

2012 ◽  
Vol 302 (8) ◽  
pp. H1756-H1761 ◽  
Author(s):  
Matthew S. Ganio ◽  
Morten Overgaard ◽  
Thomas Seifert ◽  
Niels H. Secher ◽  
Pär I. Johansson ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Heat Stress ◽  
Blood Pressure Control ◽  
Lower Body Negative Pressure ◽  
Pressure Control ◽  
Vascular Conductance ◽  
Low Cardiac Output ◽  
Primary Mechanism ◽  
Simulated Hemorrhage

During moderate actual or simulated hemorrhage, as cardiac output decreases, reductions in systemic vascular conductance (SVC) maintain mean arterial pressure (MAP). Heat stress, however, compromises the control of MAP during simulated hemorrhage, and it remains unknown whether this response is due to a persistently high SVC and/or a low cardiac output. This study tested the hypothesis that an inadequate decrease in SVC is the primary contributing mechanism by which heat stress compromises blood pressure control during simulated hemorrhage. Simulated hemorrhage was imposed via lower body negative pressure (LBNP) to presyncope in 11 passively heat-stressed subjects (increase core temperature: 1.2 ± 0.2°C; means ± SD). Cardiac output was measured via thermodilution, and SVC was calculated while subjects were normothermic, heat stressed, and throughout subsequent LBNP. MAP was not changed by heat stress but was reduced to 45 ± 12 mmHg at the termination of LBNP. Heat stress increased cardiac output from 7.1 ± 1.1 to 11.7 ± 2.2 l/min ( P < 0.001) and increased SVC from 0.094 ± 0.018 to 0.163 ± 0.032 l·min−1·mmHg−1 ( P < 0.001). Although cardiac output at the onset of syncopal symptoms was 37 ± 16% lower relative to pre-LBNP, presyncope cardiac output (7.3 ± 2.0 l/min) was not different than normothermic values ( P = 0.46). SVC did not change throughout LBNP ( P > 0.05) and at presyncope was 0.168 ± 0.044 l·min−1·mmHg−1. These data indicate that in humans a cardiac output adequate to maintain MAP while normothermic is no longer adequate during a heat-stressed-simulated hemorrhage. The absence of a decrease in SVC at a time of profound reductions in MAP suggests that inadequate control of vascular conductance is a primary mechanism compromising blood pressure control during these conditions.

Mechanisms of blood pressure regulation that differ in men repeatedly exposed to high-G acceleration

2001 ◽  
Vol 280 (4) ◽  
pp. R947-R958 ◽  
Author(s):  
Victor A. Convertino
Keyword(s):  
Blood Pressure ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Blood Pressure Regulation ◽  
Control Group ◽  
Pressure Regulation ◽  
Total Blood ◽  
Trained Subjects ◽  
Arterial Blood ◽  
Baroreceptor Stimulation

The purpose of this study was to test the hypothesis that repeated exposure to high acceleration (G) would be associated with enhanced functions of specific mechanisms of blood pressure regulation. We measured heart rate (HR), stroke volume (SV), cardiac output (Q̊), mean arterial blood pressure, central venous pressure, forearm and leg vascular resistance, catecholamines, and changes in leg volume (%ΔLV) during various protocols of lower body negative pressure (LBNP), carotid stimulation, and infusions of adrenoreceptor agonists in 10 males after three training sessions on different days over a period of 5–7 days using a human centrifuge (G trained). These responses were compared with the same measurements in 10 males who were matched for height, weight, and fitness but did not undergo G training (controls). Compared with the control group, G-trained subjects demonstrated greater R-R interval response to equal carotid baroreceptor stimulation (7.3 ± 1.2 vs. 3.9 ± 0.4 ms/mmHg, P = 0.02), less vasoconstriction to equal low-pressure baroreceptor stimulation (−1.4 ± 0.2 vs. −2.6 ± 0.3 U/mmHg, P = 0.01), and higher HR (−1.2 ± 0.2 vs. −0.5 ± 0.1 beats · min−1 · mmHg−1, P = 0.01) and α-adrenoreceptor response (32.8 ± 3.4 vs. 19.5 ± 4.7 U/mmHg, P = 0.04) to equal dose of phenylephrine. During graded LBNP, G-trained subjects had less decline in Q̊ and SV, %ΔLV, and elevation in thoracic impedance. G-trained subjects also had greater total blood (6,497 ± 496 vs. 5,438 ± 228 ml, P = 0.07) and erythrocyte (3,110 ± 364 vs. 2,310 ± 96 ml, P = 0.06) volumes. These results support the hypothesis that exposure to repeated high G is associated with increased capacities of mechanisms that underlie blood pressure regulation.

scholarly journals Effects of heat stress on dynamic cerebral autoregulation during large fluctuations in arterial blood pressure

2009 ◽  
Vol 107 (6) ◽  
pp. 1722-1729 ◽  
Author(s):  
R. Matthew Brothers ◽  
Rong Zhang ◽  
Jonathan E. Wingo ◽  
Kimberly A. Hubing ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Heat Stress ◽  
Arterial Blood Pressure ◽  
Cerebral Autoregulation ◽  
Lower Body Negative Pressure ◽  
Low Frequency ◽  
Thermal Conditions ◽  
Very Low Frequency ◽  
Arterial Blood ◽  
Dynamic Cerebral Autoregulation

Impaired cerebral autoregulation during marked reductions in arterial blood pressure may contribute to heat stress-induced orthostatic intolerance. This study tested the hypothesis that passive heat stress attenuates dynamic cerebral autoregulation during pronounced swings in arterial blood pressure. Mean arterial blood pressure (MAP) and middle cerebral artery blood velocity were continuously recorded for ∼6 min during normothermia and heat stress (core body temperature = 36.9 ± 0.1°C and 38.0 ± 0.1°C, respectively, P < 0.001) in nine healthy individuals. Swings in MAP were induced by 70-mmHg oscillatory lower body negative pressure (OLBNP) during normothermia and at a sufficient lower body negative pressure to cause similar swings in MAP during heat stress. OLBNP was applied at a very low frequency (∼0.03 Hz, i.e., 15 s on-15 s off) and a low frequency (∼0.1 Hz, i.e., 5 s on-5 s off). For each thermal condition, transfer gain, phase, and coherence function were calculated at both frequencies of OLBNP. During very low-frequency OLBNP, transfer function gain was reduced by heat stress (0.55 ± 0.20 and 0.31 ± 0.07 cm·s−1·mmHg−1 during normothermia and heat stress, respectively, P = 0.02), which is reflective of improved cerebrovascular autoregulation. During low-frequency OLBNP, transfer function gain was similar between thermal conditions (1.19 ± 0.53 and 1.01 ± 0.20 cm·s−1·mmHg−1 during normothermia and heat stress, respectively, P = 0.32). Estimates of phase and coherence were similar between thermal conditions at both frequencies of OLBNP. Contrary to our hypothesis, dynamic cerebral autoregulation during large swings in arterial blood pressure during very low-frequency (i.e., 0.03 Hz) OLBNP is improved during heat stress, but it is unchanged during low-frequency (i.e., 0.1 Hz) OLBNP.

Effect of unilateral resistance training on arterial compliance in elderly men

2007 ◽  
Vol 32 (4) ◽  
pp. 670-676 ◽  
Author(s):  
Fleur Poelkens ◽  
Mark Rakobowchuk ◽  
Kirsten A. Burgomaster ◽  
Maria T.E. Hopman ◽  
Stuart M. Phillips ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Resistance Training ◽  
Arterial Compliance ◽  
Stiffness Index ◽  
Elderly Men ◽  
Arterial Diameter ◽  
Healthy Elderly ◽  
Arterial Blood ◽  
The Impact ◽  
Peak Blood

An increase in age coincides with a decrease in arterial compliance, which is related to a higher risk for cardiovascular accidents. Evidence regarding the effects of resistance training on arterial compliance is conflicting. Currently, little information is available about the effect of resistance training on arterial compliance in elderly men. We assessed the impact of 10 weeks of unilateral arm and leg resistance training on carotid, brachial, and femoral arterial compliance in 12 healthy elderly men (mean age ± SD, 71 ± 7 y). Arterial compliance was evaluated before, after 4 weeks, and after 10 weeks of unilateral resistance training by simultaneously measuring arterial diameter and blood pressure in each artery. There were no significant differences in arterial compliance or stiffness index in any of the arteries examined after 10 weeks of training. However, after 10 weeks of resistance training, resting heart rate decreased from 76 ± 4 beats/min to 61 ± 3 beats/min (p < 0.05), plasma glucose decreased from 6.0 ± 0.9 to 5.1 ± 0.9 mmol/L (mean ± SE) (p < 0.05), and carotid artery peak blood flow increased from 1831 mL/min to 2245 mL/min (p < 0.05). There were no significant changes in resting arterial blood pressure. Unilateral resistance training for 10 weeks does not alter peripheral and central arterial compliance elderly men.

scholarly journals Carotid and aortic baroreflexes of the rat: II. Open-loop frequency response and the blood pressure spectrum

2000 ◽  
Vol 279 (5) ◽  
pp. R1922-R1933 ◽  
Author(s):  
Barry R. Dworkin ◽  
Xiaorui Tang ◽  
Alan J. Snyder ◽  
Susan Dworkin
Keyword(s):  
Blood Pressure ◽  
Venous Pressure ◽  
Low Frequency ◽  
Noise Spectrum ◽  
Open Loop ◽  
Step Response ◽  
Algebraic Solution ◽  
Noise Power ◽  
Vascular Conductance ◽  
Aortic Depressor Nerve

To determine the relationship between blood pressure (BP) variability and the open-loop frequency domain transfer function (TF) of the baroreflexes, we measured the pre- and postsinoaortic denervation (SAD) spectra and the effects of periodic and step inputs to the aortic depressor nerve and isolated carotid sinus of central nervous system-intact, neuromuscular-blocked (NMB) rats. Similar to previous results in freely moving rats, SAD greatly increased very low frequency (VLF) (0.01–0.2 Hz) systolic blood pressure (SBP) noise power. Step response-frequency measurements for SBP; interbeat interval (IBI); venous pressure; mesenteric, femoral, and skin blood flow; and direct modulation analyses of SBP showed that only VLF variability could be substantially attenuated by an intact baroreflex. The −3-dB frequency for SBP is 0.035–0.056 Hz; femoral vascular conductance is similar to SBP, but mesenteric vascular conductance has a reliably lower and IBI has a reliably higher −3-dB point. The overall open-loop transportation lag, of which ≤0.1 s is neural, is ≈1.07 s. Constrained algebraic solution, over a range of frequencies, of the pre- and postSAD endogenous noise spectra and the independently determined relative frequency and absolute lag measurements was used to calculate the absolute gain for the open-loop TF. The average gain at 0.02 Hz, the frequency of maximum sensitivity, was 1.47 (95% confidence interval = ±0.48), which agrees well with estimates for the dog reversible sinus. We found that, in the NMB rat, the effects of SAD on the BP noise spectrum were accounted for by the open-loop properties of the baroreflex.

Maximal vascular leg conductance in trained and untrained men

1987 ◽  
Vol 62 (2) ◽  
pp. 606-610 ◽  
Author(s):  
P. G. Snell ◽  
W. H. Martin ◽  
J. C. Buckey ◽  
C. G. Blomqvist
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Oxygen Uptake ◽  
Maximal Oxygen Uptake ◽  
Reactive Hyperemia ◽  
Venous Occlusion ◽  
Vascular Conductance ◽  
Blood Flows ◽  
Arterial Blood ◽  
Sedentary Subjects

Lower leg blood flow and vascular conductance were studied and related to maximal oxygen uptake in 15 sedentary men (28.5 +/- 1.2 yr, mean +/- SE) and 11 endurance-trained men (30.5 +/- 2.0 yr). Blood flows were obtained at rest and during reactive hyperemia produced by ischemic exercise to fatigue. Vascular conductance was computed from blood flow measured by venous occlusion plethysmography, and mean arterial blood pressure was determined by auscultation of the brachial artery. Resting blood flow and mean arterial pressure were similar in both groups (combined mean, 3.0 ml X min-1 X 100 ml-1 and 88.2 mmHg). After ischemic exercise, blood flows were 29- and 19-fold higher (P less than 0.001) than rest in trained (83.3 +/- 3.8 ml X min-1 X 100 ml-1) and sedentary subjects (61.5 +/- 2.3 ml X min-1 X 100 ml-1), respectively. Blood pressure and heart rate were only slightly elevated in both groups. Maximal vascular conductance was significantly higher (P less than 0.001) in the trained compared with the sedentary subjects. The correlation coefficients for maximal oxygen uptake vs. vascular conductance were 0.81 (trained) and 0.45 (sedentary). These data suggest that physical training increases the capacity for vasodilation in active limbs and also enables the trained individual to utilize a larger fraction of maximal vascular conductance than the sedentary subject.

scholarly journals Spontaneous bursts of muscle sympathetic nerve activity decrease leg vascular conductance in resting humans

2013 ◽  
Vol 304 (5) ◽  
pp. H759-H766 ◽  
Author(s):  
Seth T. Fairfax ◽  
Jaume Padilla ◽  
Lauro C. Vianna ◽  
Michael J. Davis ◽  
Paul J. Fadel
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Burst Size ◽  
Muscle Sympathetic Nerve Activity ◽  
Common Femoral Artery ◽  
Vascular Conductance ◽  
Nerve Activity ◽  
Arterial Blood

Previous studies in humans attempting to assess sympathetic vascular transduction have related large reflex-mediated increases in muscle sympathetic nerve activity (MSNA) to associated changes in limb vascular resistance. However, such procedures do not provide insight into the ability of MSNA to dynamically control vascular tone on a beat-by-beat basis. Thus we examined the influence of spontaneous MSNA bursts on leg vascular conductance (LVC) and how variations in MSNA burst pattern (single vs. multiple bursts) and burst size may affect the magnitude of the LVC response. In 11 young men, arterial blood pressure, common femoral artery blood flow, and MSNA were continuously recorded during 20 min of supine rest. Signal averaging was used to characterize percent changes in LVC for 15 cardiac cycles following heartbeats associated with and without MSNA bursts. LVC significantly decreased following MSNA bursts, reaching a nadir during the 6th cardiac cycle (single bursts, −2.9 ± 1.1%; and multiple bursts, −11.0 ± 1.4%; both, P < 0.001). Individual MSNA burst amplitudes and the total amplitude of consecutive bursts were related to the magnitude of peak decreases in LVC. In contrast, cardiac cycles without MSNA bursts were associated with a significant increase in LVC (+3.1 ± 0.5%; P < 0.001). Total vascular conductance decreased in parallel with LVC also reaching a nadir around the peak rise in arterial blood pressure following an MSNA burst. Collectively, these data are the first to assess beat-by-beat sympathetic vascular transduction in resting humans, demonstrating robust and dynamic decreases in LVC following MSNA bursts, an effect that was absent for cardiac cycles without MSNA bursts.

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