Carotid baroreflex control of leg vascular conductance at rest and during exercise

2003 ◽  
Vol 94 (2) ◽  
pp. 542-548 ◽  
Author(s):  
David M. Keller ◽  
Wendy L. Wasmund ◽  
D. Walter Wray ◽  
Shigehiko Ogoh ◽  
Paul J. Fadel ◽  
...  

We sought to test the hypothesis that the carotid baroreflex (CBR) alters mean leg blood flow (LBF) and leg vascular conductance (LVC) at rest and during exercise. In seven men and one woman, 25 ± 2 (SE) yr of age, CBR control of LBF and LVC was determined at rest and during steady-state one-legged knee extension exercise at ∼65% peak O2 uptake. The application of 5-s pulses of +40 Torr neck pressure and −60 Torr neck suction significantly altered mean arterial pressure (MAP) and LVC both at rest and during exercise. CBR-mediated changes in MAP were similar between rest and exercise ( P > 0.05). However, CBR-mediated decreases in LVC (%change) to neck pressure were attenuated in the exercising leg (16.4 ± 1.6%) compared with rest (33 ± 2.1%) and the nonexercising leg (23.7 ± 1.9%) ( P < 0.01). These data suggest CBR control of blood pressure is partially mediated by changes in leg vascular tone both at rest and during exercise. Furthermore, despite alterations in CBR-induced changes in LVC during exercise, CBR control of blood pressure was well maintained.

2016 ◽  
Vol 116 (1) ◽  
pp. 81-87 ◽  
Author(s):  
Mu Huang ◽  
Dustin R. Allen ◽  
David M. Keller ◽  
Paul J. Fadel ◽  
Elliot M. Frohman ◽  
...  

Multiple sclerosis (MS), a progressive neurological disease, can lead to impairments in the autonomic control of cardiovascular function. We tested the hypothesis that individuals with relapsing-remitting MS ( n = 10; 7 females, 3 males; 13 ± 4 yr from diagnosis) exhibit impaired carotid baroreflex control of blood pressure and heart rate compared with sex, age, and body weight-matched healthy individuals (CON: n = 10; 7 females, 3 males). At rest, 5-s trials of neck pressure (NP; +40 Torr) and neck suction (NS; −60 Torr) were applied to simulate carotid hypotension and hypertension, respectively, while mean arterial pressure (MAP; finger photoplethysmography), heart rate (HR), cardiac output (CO; Modelflow), and total vascular conductance (TVC) were continuously measured. In response to NP, there was a blunted increase in peak MAP responses (MS: 5 ± 2 mmHg) in individuals with MS compared with healthy controls (CON: 9 ± 3 mmHg; P = 0.005), whereas peak HR responses were not different between groups. At the peak MAP response to NP, individuals with MS demonstrated an attenuated decrease in TVC (MS, −10 ± 4% baseline vs. CON, −15 ± 4% baseline, P = 0.012), whereas changes in CO were similar between groups. Following NS, all cardiovascular responses (i.e., nadir MAP and HR and percent changes in CO and TVC) were not different between MS and CON groups. These data suggest that individuals with MS have impaired carotid baroreflex control of blood pressure via a blunted vascular conductance response resulting in a diminished ability to increase MAP in response to a hypotensive challenge.


2011 ◽  
Vol 301 (6) ◽  
pp. H2454-H2465 ◽  
Author(s):  
Areum Kim ◽  
Shekhar H. Deo ◽  
Lauro C. Vianna ◽  
George M. Balanos ◽  
Doreen Hartwich ◽  
...  

It is presently unknown whether there are sex differences in the magnitude of blood pressure (BP) responses to baroreceptor perturbation or if the relative contribution of cardiac output (CO) and total vascular conductance (TVC) to baroreflex-mediated changes in BP differs in young women and men. Since sympathetic vasoconstrictor tone is attenuated in women, we hypothesized that carotid baroreflex-mediated BP responses would be attenuated in women by virtue of a blunted vascular response (i.e., an attenuated TVC response). BP, heart rate (HR), and stroke volume were continuously recorded during the application of 5-s pulses of neck pressure (NP; carotid hypotension) and neck suction (NS; carotid hypertension) ranging from +40 to −80 Torr in women ( n = 20, 21 ± 0.5 yr) and men ( n = 20, 21 ± 0.4 yr). CO and TVC were calculated on a beat-to-beat basis. Women demonstrated greater depressor responses to NS (e.g., −60 Torr, −17 ± 1%baseline in women vs. −11 ± 1%baseline in men, P < 0.05), which were driven by augmented decreases in HR that, in turn, contributed to larger reductions in CO (−60 Torr, −15 ± 2%baseline in women vs. −6 ± 2%baseline in men, P < 0.05). In contrast, pressor responses to NP were similar in women and men (e.g., +40 Torr, +14 ± 2%baseline in women vs. +10 ± 1%baseline in men, P > 0.05), with TVC being the primary mediating factor in both groups. Our findings indicate that sex differences in the baroreflex control of BP are evident during carotid hypertension but not carotid hypotension. Furthermore, in contrast to our hypothesis, young women exhibited greater BP responses to carotid hypertension by virtue of a greater cardiac responsiveness.


2010 ◽  
Vol 299 (5) ◽  
pp. R1241-R1247 ◽  
Author(s):  
James P. Fisher ◽  
Areum Kim ◽  
Colin N. Young ◽  
Paul J. Fadel

The arterial baroreflex is fundamental for evoking and maintaining appropriate cardiovascular adjustments to exercise. We sought to investigate how aging influences carotid baroreflex regulation of blood pressure (BP) during dynamic exercise. BP and heart rate (HR) were continuously recorded at rest and during leg cycling performed at 50% HR reserve in 15 young (22 ± 1 yr) and 11 older (61 ± 2 yr) healthy subjects. Five-second pulses of neck pressure and neck suction from +40 to −80 Torr were applied to determine the full carotid baroreflex stimulus response curve and examine baroreflex resetting during exercise. Although the maximal gain of the modeled stimulus response curve was similar in both groups at rest and during exercise, in older subjects the operating point (OP) was located further away from the centering point (CP) and toward the reflex threshold, both at rest (OP minus CP; −10 ± 3 older vs. 0 ± 2 young mmHg, P < 0.05) and during exercise (OP minus CP; −10 ± 2 older vs. 1 ± 3 young mmHg, P < 0.05). In agreement, older subjects demonstrated a reduced BP response to neck pressure (simulated carotid hypotension) and a greater BP response to neck suction (simulated carotid hypertension). In addition, the magnitude of the upward and rightward resetting of the carotid baroreflex-BP stimulus response curve with exercise was ∼40% greater in older individuals. These data indicate that despite a maintained maximal gain, the ability of the carotid baroreflex to defend against a hypotensive challenge is reduced, whereas responses to hypertensive stimuli are greater with advanced age, both at rest and during exercise.


2012 ◽  
Vol 302 (3) ◽  
pp. H864-H871 ◽  
Author(s):  
Takeshi Nishiyasu ◽  
Rina Tsukamoto ◽  
Katsuhito Kawai ◽  
Keiji Hayashi ◽  
Shunsaku Koga ◽  
...  

Our aim was to test the hypothesis that apnea-induced hemodynamic responses during dynamic exercise in humans differ between those who show strong bradycardia and those who show only mild bradycardia. After apnea-induced changes in heart rate (HR) were evaluated during dynamic exercise, 23 healthy subjects were selected and divided into a large response group (L group; n = 11) and a small response group (S group; n = 12). While subjects performed a two-legged dynamic knee extension exercise at a work load that increased HR by 30 beats/min, apnea-induced changes in HR, cardiac output (CO), mean arterial pressure (MAP), arterial O2 saturation (SaO2), forearm blood flow (FBF), and leg blood flow (LBF) were measured. During apnea, HR in the L group (54 ± 2 beats/min) was lower than in the S group (92 ± 3 beats/min, P < 0.05). CO, SaO2, FBF, LBF, forearm vascular conductance (FVC), leg vascular conductance (LVC), and total vascular conductance (TVC) were all reduced, and MAP was increased in both groups, although the changes in CO, TVC, LBF, LVC, and MAP were larger in the L group than in the S group ( P < 0.05). Moreover, there were significant positive linear relationships between the reduction in HR and the reductions in TVC, LVC, and FVC. We conclude that individuals who show greater apnea-induced bradycardia during exercise also show greater vasoconstriction in both active and inactive muscle regions.


2014 ◽  
Vol 306 (10) ◽  
pp. H1417-H1425 ◽  
Author(s):  
Daniel P. Credeur ◽  
Seth W. Holwerda ◽  
Leryn J. Boyle ◽  
Lauro C. Vianna ◽  
Areum K. Jensen ◽  
...  

Recent work suggests that β-adrenergic vasodilation offsets α-adrenergic vasoconstriction in young women, but this effect is lost after menopause. Given these age-related vascular changes, we tested the hypothesis that older women would exhibit a greater change in vascular conductance following baroreflex perturbation compared with young women. In 10 young (21 ± 1 yr) and 10 older (62 ± 2 yr) women, mean arterial pressure (MAP; Finometer), heart rate (HR), cardiac output (CO; Modelflow), total vascular conductance (TVC), and leg vascular conductance (LVC, duplex-Doppler ultrasound) were continuously measured in response to 5-s pulses of neck suction (NS; −60 Torr) and neck pressure (NP; +40 Torr) to simulate carotid hypertension and hypotension, respectively. Following NS, decreases in MAP were similar between groups; however, MAP peak response latency was slower in older women ( P < 0.05). Moreover, at the time of peak MAP, increases in LVC (young, −11.5 ± 3.9%LVC vs. older, +19.1 ± 7.0%LVC; P < 0.05) and TVC were greater in older women, whereas young women exhibited larger decreases in HR and CO (young, −10 ± 3% CO vs. older, +0.8 ± 2% CO; P < 0.05). Following NP, increases in MAP were blunted (young, +14 ± 1 mmHg vs. older, +8 ± 1 mmHg; P < 0.05) in older women, whereas MAP response latencies were similar. Interestingly, decreases in LVC and TVC were similar between groups, but HR and CO (young, +7.0 ± 2% CO vs. older, −4.0 ± 2% CO; P < 0.05) responses were attenuated in older women. These findings suggest that older women have greater reliance on vascular conductance to modulate MAP via carotid baroreflex, whereas young women rely more on cardiac responsiveness. Furthermore, older women demonstrate a blunted ability to increase MAP to hypotensive stimuli.


2008 ◽  
Vol 294 (5) ◽  
pp. H2296-H2304 ◽  
Author(s):  
James P. Fisher ◽  
Colin N. Young ◽  
Paul J. Fadel

Whether the activation of metabolically sensitive skeletal muscle afferents (i.e., muscle metaboreflex) influences cardiac baroreflex responsiveness remains incompletely understood. A potential explanation for contrasting findings of previous reports may be related to differences in the magnitude of muscle metaboreflex activation utilized. Therefore, the present study was designed to investigate the influence of graded intensities of muscle metaboreflex activation on cardiac baroreflex function. In eight healthy subjects (24 ± 1 yr), the graded isolation of the muscle metaboreflex was achieved by post-exercise ischemia (PEI) following moderate- (PEI-M) and high- (PEI-H) intensity isometric handgrip performed at 35% and 45% maximum voluntary contraction, respectively. Beat-to-beat heart rate (HR) and blood pressure were measured continuously. Rapid pulse trains of neck pressure and neck suction (+40 to −80 Torr) were applied to derive carotid baroreflex stimulus-response curves. Mean blood pressure increased significantly from rest during PEI-M (+13 ± 3 mmHg) and was further augmented during PEI-H (+26 ± 4 mmHg), indicating graded metaboreflex activation. However, the operating point gain and maximal gain (−0.51 ± 0.09, −0.48 ± 0.13, and −0.49 ± 0.12 beats·min−1·mmHg−1 for rest; PEI-M and PEI-H) of the carotid-cardiac baroreflex function curve were unchanged from rest during PEI-M and PEI-H ( P > 0.05 vs. rest). Furthermore, the carotid-cardiac baroreflex function curve was progressively reset rightward from rest to PEI-M to PEI-H, with no upward resetting. These findings suggest that the muscle metaboreflex contributes to the resetting of the carotid baroreflex control of HR; however, it would appear not to influence carotid-cardiac baroreflex responsiveness in humans, even with high-intensity activation during PEI.


2006 ◽  
Vol 572 (3) ◽  
pp. 869-880 ◽  
Author(s):  
James P. Fisher ◽  
Shigehiko Ogoh ◽  
Ellen A. Dawson ◽  
Paul J. Fadel ◽  
Niels H. Secher ◽  
...  

2005 ◽  
Vol 83 (5) ◽  
pp. 439-446 ◽  
Author(s):  
Deborah D O'Leary ◽  
Craig D Steinback ◽  
Angela D Cechetto ◽  
Blaine T Foell ◽  
Jane C Topolovec ◽  
...  

Previous evidence indicates that sensitivity of the baroreflex cardiovagal and sympathetic arms is dissociated. In addition, pharmacologic assessment of baroreflex sensitivity (BRS) has revealed that cardiovagal, but not sympathetic, BRS is greater when blood pressure is increasing versus falling. The origin of this hysteresis is unknown. In this study, carotid artery distensibility and absolute distension (diameter) were assessed to test the hypothesis that vessel mechanics in barosensitive regions affect the BRS of cardiovagal, but not sympathetic, outflow. R-R interval (i.e. time between successive R waves), finger arterial blood pressure, muscle sympathetic nerve activity, and carotid artery dimensions (B-mode imaging) were measured during sequential infusions of sodium nitroprusside (SNP) and phenylephrine (PHE). Systolic and diastolic common carotid artery diameters and pulse pressure were recorded to calculate distensibility of this vessel under each drug condition. Cardiovagal BRS was greater when blood pressure was increasing versus decreasing (p < 0.01). Sympathetic BRS was not affected by direction of pressure change. Distensibility did not differ between SNP and PHE injections. However, compared with SNP, infusion of PHE resulted in larger absolute systolic and diastolic carotid diameters (p < 0.001). Therefore, cardiovagal reflex hysteresis was related to drug-induced changes in common carotid artery diameter but not distensibility. The lack of sympathetic hysteresis in this model suggests a relative insensitivity of this baroreflex component to carotid artery dimensions and provides a possible mechanism for the dissociation between cardiovagal and sympathetic BRS.Key words: Oxford method, baroreflex hysteresis, cardiovagal, MSNA, distensibility.


1987 ◽  
Vol 114 (4) ◽  
pp. 765-772 ◽  
Author(s):  
Jan Staessen ◽  
Roberto Fiocchi ◽  
Robert Fagard ◽  
Peter Hespel ◽  
Antoon Amery

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