Effect of muscle metaboreflex activation on carotid-cardiac baroreflex function in humans

2008 ◽  
Vol 294 (5) ◽  
pp. H2296-H2304 ◽  
Author(s):  
James P. Fisher ◽  
Colin N. Young ◽  
Paul J. Fadel
Keyword(s):  
Blood Pressure ◽  
Maximum Voluntary Contraction ◽  
Voluntary Contraction ◽  
Isometric Handgrip ◽  
Response Curves ◽  
Baroreflex Control ◽  
Muscle Metaboreflex ◽  
Baroreflex Function ◽  
Carotid Baroreflex ◽  
Neck Pressure

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.

Exercise intensity influences cardiac baroreflex function at the onset of isometric exercise in humans

2007 ◽  
Vol 103 (3) ◽  
pp. 941-947 ◽  
Author(s):  
James P. Fisher ◽  
Shigehiko Ogoh ◽  
Colin N. Young ◽  
David M. Keller ◽  
Paul J. Fadel
Keyword(s):  
Blood Pressure ◽  
Exercise Intensity ◽  
Isometric Exercise ◽  
Voluntary Contraction ◽  
Isometric Handgrip ◽  
Baroreflex Control ◽  
Cardiac Responses ◽  
Carotid Baroreflex ◽  
Exercise Onset ◽  
Exercise In Humans

We sought to examine the influence of exercise intensity on carotid baroreflex (CBR) control of heart rate (HR) and mean arterial pressure (MAP) at the onset of exercise in humans. To accomplish this, eight subjects performed multiple 1-min bouts of isometric handgrip (HG) exercise at 15, 30, 45 and 60% maximal voluntary contraction (MVC), while breathing to a metronome set at eupneic frequency. Neck suction (NS) of −60 Torr was applied for 5 s at end expiration to stimulate the CBR at rest, at the onset of HG (<1 s), and after ∼40 s of HG. Beat-to-beat measurements of HR and MAP were recorded throughout. Cardiac responses to NS at onset of 15% (−12 ± 2 beats/min) and 30% (−10 ± 2 beats/min) MVC HG were similar to rest (−10 ± 1 beats/min). However, HR responses to NS were reduced at the onset of 45% and 60% MVC HG (−6 ± 2 and −4 ± 1 beats/min, respectively; P < 0.001). In contrast to HR, MAP responses to NS were not different from rest at exercise onset. Furthermore, both HR and MAP responses to NS applied at ∼40s of HG were similar to rest. In summary, CBR control of HR was transiently blunted at the immediate onset of high-intensity HG, whereas MAP responses were preserved demonstrating differential baroreflex control of HR and blood pressure at exercise onset. Collectively, these results suggest that carotid-cardiac baroreflex control is dynamically modulated throughout isometric exercise in humans, whereas carotid baroreflex regulation of blood pressure is well-maintained.

Abstract 266: Neural Circulatory Responses to Isolated Muscle Metaboreflex Activation in Postmenopausal Women

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Jody L Greaney ◽  
Evan L Matthews ◽  
Paul J Fadel ◽  
William B Farquhar ◽  
Megan M Wenner
Keyword(s):  
Blood Pressure ◽  
Postmenopausal Women ◽  
Young Women ◽  
Blood Pressure Response ◽  
Muscle Sympathetic Nerve Activity ◽  
Feedback Mechanism ◽  
Voluntary Contraction ◽  
Pressure Response ◽  
Isometric Handgrip ◽  
Muscle Metaboreflex

Understanding the neural circulatory responses to exercise in postmenopausal women (PMW) is important given their greater risk for developing hypertension. During exercise, blood pressure is controlled, in part, by the exercise pressor reflex, which is a feedback mechanism originating in skeletal muscle and compromised of mechanically and metabolically sensitive afferents. A recent study reported an enhanced blood pressure response during exercise in normotensive PMW due to greater muscle metaboreflex activation, but the mechanism(s) underlying these responses are unknown. Herein, we tested the hypothesis that metaboreflex activation elicits exaggerated sympathetic nervous system responses in PMW compared to young women, contributing to the enhanced blood pressure response during exercise. Methods: Blood pressure (BP, Finometer) and muscle sympathetic nerve activity (MSNA, peroneal microneurography) were continuously measured in 7 PMW (age 59±2 years; BMI 24±1 kg/m 2 ) and 7 young women (age 23±2 years; BMI 22±2 kg/m 2 ) during 2-minutes of isometric handgrip exercise performed at 30% of maximal voluntary contraction followed by 3-minutes of forearm ischemia (post-exercise ischemia, PEI) to isolate muscle metaboreflex activation. Results: Resting mean arterial pressure (MAP) was similar between PMW (85±3 mmHg) and young women (82±2 mmHg; P>0.05). During exercise, the increase in MAP was greater in PMW (Δ18±2mmHg) compared to young women (Δ 12±2 mmHg; P<0.05), and this was maintained during PEI (Δ13±1 mmHg PMW vs. Δ 6±1 mmHg young women; P<0.05). Resting MSNA was higher in PMW (24±4 bursts/min) compared to young women (9±3 bursts/min; P<0.05). Interestingly, the increase in MSNA during exercise was comparable between groups (P>0.05), whereas during PEI, the increase in MSNA was approximately 50% greater in PMW compared to young women (Δ13±2 burst/min PMW vs. 7±2 bursts/min young women; P<0.05). Conclusions: These preliminary data suggest that compared to young women, PMW exhibit an exaggerated MSNA response to isolated muscle metaboreflex activation.

scholarly journals Carotid baroreflex control of arterial blood pressure at rest and during dynamic exercise in aging humans

2010 ◽  
Vol 299 (5) ◽  
pp. R1241-R1247 ◽  
Author(s):  
James P. Fisher ◽  
Areum Kim ◽  
Colin N. Young ◽  
Paul J. Fadel
Keyword(s):  
Blood Pressure ◽  
Response Curve ◽  
Dynamic Exercise ◽  
Baroreflex Control ◽  
Stimulus Response ◽  
Arterial Blood ◽  
Carotid Baroreflex ◽  
Older Subjects ◽  
Maximal Gain ◽  
Neck Pressure

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.

Baroreflex responsiveness is maintained during isometric exercise in humans

1986 ◽  
Vol 61 (2) ◽  
pp. 797-803 ◽  
Author(s):  
T. J. Ebert
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Maximum Voluntary Contraction ◽  
Transmural Pressure ◽  
Handgrip Exercise ◽  
Isometric Handgrip ◽  
Baroreflex Control ◽  
Baroreflex Function ◽  
Isometric Handgrip Exercise

The simultaneous rise in heart rate and arterial pressure during isometric handgrip exercise suggests that arterial baroreflex control may be altered. We applied incremental intensities of neck suction and pressure to nine healthy young men to alter carotid sinus transmural pressure. Carotid stimuli were delivered during 1) supine control, 2) “anticipation” of beginning exercise, and 3) handgrip (20% of maximum voluntary contraction). Anticipation was a quiet period, immediately preceding the beginning of handgrip, when no muscular work was being performed. Compared with control, the R-R interval prolongation and mean arterial pressure decline provoked by carotid stimuli were decreased during the anticipation period. These data suggest that influences from higher central neural locations may alter baroreflex function. Furthermore, we derived stimulus-response curves relating carotid sinus transmural pressure to changes in R-R interval and mean arterial pressure. These curves were shifted during handgrip; however, calculated regression slopes were not changed from control. The data indicate that isometric handgrip exercise has a specific influence on human carotid baroreflex control of arterial pressure and heart period: baroreflex function curves are shifted rightward during handgrip, whereas baroreflex sensitivity is unchanged. Furthermore, central neural influences may be partially involved in these alterations.

Neural blockade during exercise augments central command's contribution to carotid baroreflex resetting

2001 ◽  
Vol 280 (4) ◽  
pp. H1635-H1644 ◽  
Author(s):  
R. G. Querry ◽  
S. A. Smith ◽  
M. Strømstad ◽  
K. Ide ◽  
P. B. Raven ◽  
...  
Keyword(s):  
Perceived Exertion ◽  
Voluntary Contraction ◽  
Control Force ◽  
Central Command ◽  
Response Curves ◽  
Neural Blockade ◽  
Stimulus Response ◽  
Carotid Baroreflex ◽  
Before And After ◽  
Neck Pressure

This investigation was designed to determine central command's role on carotid baroreflex (CBR) resetting during exercise. Nine volunteer subjects performed static and rhythmic handgrip exercise at 30 and 40% maximal voluntary contraction (MVC), respectively, before and after partial axillary neural blockade. Stimulus-response curves were developed using the neck pressure-neck suction technique and a rapid pulse train protocol (+40 to −80 Torr). Regional anesthesia resulted in a significant reduction in MVC. Heart rate (HR) and ratings of perceived exertion (RPE) were used as indexes of central command and were elevated during exercise at control force intensity after induced muscle weakness. The CBR function curves were reset vertically with a minimal lateral shift during control exercise and exhibited a further parallel resetting during exercise with neural blockade. The operating point was progressively reset to coincide with the centering point of the CBR curve. These data suggest that central command was a primary mechanism in the resetting of the CBR during exercise. However, it appeared that central command modulated the carotid-cardiac reflex proportionately more than the carotid-vasomotor reflex.

Muscle metaboreflex activation speeds the recovery of arterial blood pressure following acute hypotension in humans

2013 ◽  
Vol 304 (11) ◽  
pp. H1568-H1575 ◽  
Author(s):  
Masashi Ichinose ◽  
Kazuhito Watanabe ◽  
Naoto Fujii ◽  
Narihiko Kondo ◽  
Takeshi Nishiyasu
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Maximum Voluntary Contraction ◽  
Cardiovascular Responses ◽  
Arterial Baroreflex ◽  
Isometric Handgrip ◽  
Muscle Metaboreflex ◽  
Peripheral Vasoconstriction ◽  
Arterial Blood ◽  
Acute Hypotension

It has been suggested that the arterial baroreflex and muscle metaboreflex are both activated during heavy exercise and that they interact to modulate primary cardiovascular reflex responses. This proposed interaction and its consequences are not fully understood, however. The purpose of present study was to test our hypothesis that dynamic arterial baroreflex-mediated cardiovascular responses to acute systemic hypotension in humans are augmented when the muscle metaboreflex is active and that this results in a faster recovery of arterial blood pressure. Acute hypotension was induced nonpharmacologically in 12 healthy subjects by releasing bilateral thigh cuffs after 9 min of suprasystolic resting ischemia, with and without muscle metaboreflex activation via postexercise muscle ischemia (PEMI) after 1 min of isometric handgrip exercise at 50% maximum voluntary contraction. The thigh-cuff release evoked rapid reductions in mean arterial pressure (MAP) and increases in heart rate, cardiac output (Doppler), and total vascular conductance (TVC) under control conditions and during PEMI. The reductions in MAP from baseline were greater and the increases in TVC were smaller during PEMI than control. In addition, arterial baroreflex-mediated peripheral vasoconstriction was augmented during PEMI, as evidenced by a near doubling of the rate of recovery of MAP and TVC. These results show that when the muscle metaboreflex is activated in humans, arterial baroreflex-mediated peripheral vasoconstriction elicited in response to acute hypotension is augmented, which halves the time needed for MAP recovery. Such modulation of baroreflex function would be advantageous for maintaining an elevated arterial blood pressure during activation of the muscle metaboreflex.

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 ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Vascular Tone ◽  
Knee Extension ◽  
Vascular Conductance ◽  
Baroreflex Control ◽  
Carotid Baroreflex ◽  
Neck Pressure ◽  
Induced Changes ◽  
Knee Extension Exercise ◽  
Rest And Exercise

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.

scholarly journals Impaired carotid baroreflex control of arterial blood pressure in multiple sclerosis

2016 ◽  
Vol 116 (1) ◽  
pp. 81-87 ◽  
Author(s):  
Mu Huang ◽  
Dustin R. Allen ◽  
David M. Keller ◽  
Paul J. Fadel ◽  
Elliot M. Frohman ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Blood Pressure ◽  
Heart Rate ◽  
Cardiovascular Responses ◽  
Vascular Conductance ◽  
Baroreflex Control ◽  
Arterial Blood ◽  
Carotid Baroreflex ◽  
Relapsing Remitting ◽  
Neck Pressure

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.

Muscle metaboreflex modulates the arterial baroreflex dynamic effects on peripheral vascular conductance in humans

2005 ◽  
Vol 288 (4) ◽  
pp. H1532-H1538 ◽  
Author(s):  
Masashi Ichinose ◽  
Takeshi Nishiyasu
Keyword(s):  
Dynamic Effect ◽  
Voluntary Contraction ◽  
Dynamic Responses ◽  
Arterial Baroreflex ◽  
Peripheral Vascular ◽  
Vascular Conductance ◽  
Muscle Metaboreflex ◽  
Arterial Blood ◽  
Carotid Baroreflex ◽  
Neck Pressure

We aimed to investigate the interaction between the arterial baroreflex and muscle metaboreflex [as reflected by alterations in the dynamic responses shown by leg blood flow (LBF: by the ultrasound Doppler method), leg vascular conductance (LVC), mean arterial blood pressure (MAP), and heart rate (HR)] in humans. In 12 healthy subjects (10 men and 2 women), who performed sustained 1-min handgrip exercise at 50% maximal voluntary contraction followed immediately by an imposed postexercise muscle ischemia (PEMI), 5-s periods of neck pressure (NP; 50 mmHg) or neck suction (NS; −60 mmHg) were used to evaluate carotid baroreflex function both at rest (Con) and during PEMI. First, the decreases in LVC and LBF and the augmentation of MAP elicited by NP were all greater during PEMI than in Con (ΔLVC, −1.2 ± 0.2 vs. −1.9 ± 0.2 ml·min−1·mmHg−1; ΔLBF, −97.3 ± 11.2 vs. −177.0 ± 21.8 ml/min; ΔMAP, 6.7 ± 1.2 vs. 11.5 ± 1.4 mmHg, Con vs. PEMI; each P < 0.05). Second, in Con, NS significantly increased both LVC and LBF (ΔLVC, 0.9 ± 0.2 ml·min−1·mmHg−1; ΔLBF, 46.6 ± 9.8 ml/min; significant change from baseline: each P < 0.05), and, whereas during PEMI no significant increases in LVC and LBF occurred during NS itself (ΔLVC, 0.2 ± 0.1 ml·min−1·mmHg−1; ΔLBF, 10.8 ± 9.6 ml/min; each P > 0.05), a decrease was evident in each parameters at 5 s after the cessation of NS. Third, during PEMI, the decrease in MAP elicited by NS was smaller (ΔMAP, −8.4 ± 1.0 vs. −5.8 ± 0.4 mmHg, Con vs. PEMI; P < 0.05), and it recovered to its initial level more quickly after NS (vs. Con). Finally, however, the HR responses to NS and NP were not different between PEMI and Con. These results suggest that during muscle metaboreflex activation in humans, the arterial baroreflex dynamic effect on peripheral vascular conductance is modulated, as exemplified by 1) an augmentation of the NP-induced LVC decrease, and 2) a loss of the NS-induced LVC increase.

Cardiovascular responses to forearm muscle metaboreflex activation during hypercapnia in humans

2015 ◽  
Vol 309 (1) ◽  
pp. R43-R50 ◽  
Author(s):  
Stephane Delliaux ◽  
Masashi Ichinose ◽  
Kazuhito Watanabe ◽  
Naoto Fujii ◽  
Takeshi Nishiyasu
Keyword(s):  
Maximum Voluntary Contraction ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Voluntary Contraction ◽  
Isometric Handgrip ◽  
Experimental Conditions ◽  
Muscle Metaboreflex ◽  
Healthy Humans ◽  
Forearm Muscle ◽  
Inhibitory Interactions

We characterized the cardiovascular responses to forearm muscle metaboreflex activation during hypercapnia. Ten healthy males participated under three experimental conditions: 1) hypercapnia (HCA, PetCO2: +10 mmHg, by inhalation of a CO2-enriched gas mixture); 2) muscle metaboreflex activation (MMA, by 5 min of local circulatory occlusion after 1 min of 50% maximum voluntary contraction isometric handgrip under normocapnia); and 3) HCA+MMA. We measured mean arterial pressure (MAP), heart rate (HR), and cardiac output (CO); calculated stroke volume (SV), and total peripheral resistance (TPR); and evaluated myocardial oxygen consumption (MV̇o2) and cardiac work (CW) noninvasively. MAP increased in the three experimental conditions but HCA+MMA led to the highest MAP, CO, and HR. Moreover, HCA+MMA increased SV and was associated with the highest MV̇o2 and CW. HCA and MMA exhibited inhibitory interactions with MAP, HR, TPR, MV̇o2, and CW, increases of which were smaller during HCA+MMA than the sum of the increases during HCA and MMA alone (MAP: +28 ± 2 vs. +34 ± 2 mmHg, P < 0.001; HR: +15 ± 2 vs. +22 ± 3 bpm, P < 0.01; TPR: +1.1 ± 1.4 vs. +3.0 ± 1.5 mmHg·l·min−1, P < 0.05; MV̇o2: +50.25 ± 4.74 vs. +59.48 ± 5.37 mmHg·min−1·10−2, P < 0.01; CW: +59.10 ± 7.52 vs. +63.67 ± 7.71 ml mmHg·min−1·10−4, P < 0.05). Oppositely, HCA and MMA interactions were linearly additive for CO (+2.3 ± 0.4 l/min) and SV (+13 ± 4 ml). We showed that muscle metaboreflex and hypercapnia interact in healthy humans, reducing vasoconstriction but enhancing SV.

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