scholarly journals High Intensity Muscle Metaboreflex Activation Blunts Cardiopulmonary Baroreflex Control of Sympathetic Vasomotor Outflow

2018 ◽  
Vol 32 (S1) ◽  
Author(s):  
Keisho Katayama ◽  
Jasdeep Kaur ◽  
Benjamin E. Young ◽  
Thales C. Barbosa ◽  
Shigehiko Ogoh ◽  
...  
Keyword(s):  
High Intensity ◽  
Baroreflex Control ◽  
Muscle Metaboreflex ◽  
Cardiopulmonary Baroreflex

Muscle pump-induced inhibition of sympathetic vasomotor outflow during low-intensity leg cycling is attenuated by muscle metaboreflex activation

2020 ◽  
Vol 128 (1) ◽  
pp. 1-7
Author(s):  
Keisho Katayama ◽  
Thales C. Barbosa ◽  
Jasdeep Kaur ◽  
Benjamin E. Young ◽  
Damsara Nandadeva ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
High Intensity ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Muscle Metaboreflex ◽  
Muscle Pump ◽  
Low Intensity ◽  
Leg Cycling ◽  
Cardiopulmonary Baroreflex

Muscle sympathetic nerve activity (MSNA) decreases during leg cycling at low intensity because of muscle pump-induced increases in venous return and loading of the cardiopulmonary baroreceptors. However, MSNA increases during leg cycling when exercise is above moderate intensity or for a long duration, suggesting that the sympathoinhibitory effect of the cardiopulmonary baroreflex can be overridden by a powerful sympathoexcitatory drive, such as the skeletal muscle metaboreflex. Therefore, we tested the hypothesis that high-intensity muscle metaboreflex activation attenuates muscle pump-induced inhibition of MSNA during leg cycling. MSNA (left radial nerve) was recorded during graded isolation of the muscle metaboreflex in the forearm with postexercise ischemia (PEI) after low (PEI-L)- and high (PEI-H)-intensity isometric handgrip exercise (20% and 40% maximum voluntary contraction, respectively). Leg cycling (15–20 W) was performed alone and during each PEI trial (PEI-L+Cycling, PEI-H+Cycling). Cycling alone induced a significant decrease in MSNA burst frequency (BF) and total activity (TA). MSNA BF and TA also decreased when cycling was performed during PEI-L. However, the magnitude of decrease in MSNA during PEI-L+Cycling [∆BF: –19 ± 2% ( P < 0.001), ∆TA: –25 ± 4% ( P < 0.001); mean ± SE] was less than that during cycling alone [∆BF: –39 ± 5% ( P = 0.003), ∆TA: –45 ± 5% ( P = 0.002)]. More importantly, MSNA did not decrease during cycling with PEI-H [∆BF: –1 ± 2% ( P = 0.845), ∆TA: +2 ± 3% ( P = 0.959)]. These results suggest that muscle pump-induced inhibition of sympathetic vasomotor outflow during low-intensity leg cycling is attenuated by muscle metaboreflex activation in an intensity-dependent manner. NEW & NOTEWORTHY There are no available data concerning the interaction between the sympathoinhibitory effect of muscle pump-induced cardiopulmonary baroreflex loading during leg cycling and the sympathoexcitatory influence of the muscle metaboreflex. In this study, muscle metaboreflex activation attenuated the inhibition of muscle sympathetic nerve activity (MSNA) during leg cycling. This may explain, in part, the response of MSNA to graded-intensity dynamic exercise in which low-intensity leg cycling inhibits MSNA whereas high-intensity exercise elicits graded sympathoexcitation.

scholarly journals High-intensity muscle metaboreflex activation attenuates cardiopulmonary baroreflex-mediated inhibition of muscle sympathetic nerve activity

2018 ◽  
Vol 125 (3) ◽  
pp. 812-819 ◽  
Author(s):  
Keisho Katayama ◽  
Jasdeep Kaur ◽  
Benjamin E. Young ◽  
Thales C. Barbosa ◽  
Shigehiko Ogoh ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
High Intensity ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Moderate Intensity ◽  
Positive Pressure ◽  
Nerve Activity ◽  
Muscle Metaboreflex ◽  
Cardiopulmonary Baroreflex ◽  
Cardiopulmonary Baroreceptors

Previous studies have shown that muscle sympathetic nerve activity (MSNA) is reduced during low- and mild-intensity dynamic leg exercise. It has been suggested that such inhibition is mediated by loading of the cardiopulmonary baroreceptors and that this effect is overridden by muscle metaboreflex activation with higher-intensity exercise. However, limited data are available regarding the interaction between the cardiopulmonary baroreflex and the muscle metaboreflex. Therefore, we tested the hypothesis that cardiopulmonary baroreflex-mediated inhibition of MSNA is attenuated during high-intensity muscle metaboreflex activation. In nine young men, MSNA (right peroneal nerve), mean arterial pressure (MAP), and thoracic impedance were recorded. Graded isolation of muscle metaboreflex activation was achieved via postexercise ischemia (PEI) following low (PEI-L)-, moderate (PEI-M)-, and high (PEI-H)-intensity isometric handgrip performed at 20, 30, and 40% maximum voluntary contraction, respectively. Lower-body positive pressure (LBPP, +10 Torr) was applied at rest and during PEI, to load the cardiopulmonary baroreceptors. Handgrip exercise elicited intensity-dependent increases in MSNA and MAP that were maintained during PEI, indicating a graded muscle metaboreflex activation. LBPP at rest significantly decreased MSNA burst frequency (BF: −36.7 ± 4.7%, mean ± SE, P < 0.05), whereas MAP was unchanged. When LBPP was applied during PEI, MSNA BF decreased significantly at PEI-L (−40.0 ± 9.2%, P < 0.05) and PEI-M (−27.0 ± 6.3%, P < 0.05), but not at PEI-H (+1.9 ± 7.1%, P > 0.05). These results suggest that low- and moderate-intensity muscle metaboreflex activation does not modulate the inhibition of MSNA by cardiopulmonary baroreceptor loading, whereas high-intensity metaboreflex activation can override cardiopulmonary baroreflex-mediated inhibition of sympathetic vasomotor outflow. NEW & NOTEWORTHY The interaction between the sympathoinhibitory influence of cardiopulmonary baroreflex and sympathoexcitatory effect of skeletal muscle metaboreflex is not completely understood. In the current study, light- to moderate-intensity muscle metaboreflex activation did not modulate the suppression of muscle sympathetic nerve activity by cardiopulmonary baroreceptor loading, whereas high-intensity muscle metaboreflex activation attenuated the cardiopulmonary baroreflex-mediated inhibition of muscle sympathetic nerve activity. These results provide important information concerning the neural reflex mechanisms regulating sympathetic vasomotor outflow during exercise.

Reflex regulation of renal nerve activity in cardiac failure

1994 ◽  
Vol 266 (1) ◽  
pp. R27-R39 ◽  
Author(s):  
G. F. DiBona ◽  
L. L. Sawin
Keyword(s):  
Cardiac Index ◽  
Single Unit ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Central Portion ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Afferent Limb ◽  
Pressure Threshold ◽  
Cardiopulmonary Baroreflex

Efferent renal sympathetic nerve activity (ERSNA) is increased in the rat with low-cardiac-output congestive heart failure (CHF; myocardial infarction). Arterial and cardiopulmonary baroreflex control of ERSNA in CHF and control rats was examined. Cardiac index and arterial pressure were lower and total peripheral resistance index, left ventricular end-diastolic pressure, and heart-to-body weight ratio were higher in CHF than in control rats. Increases in left ventricular end diastolic pressure produced by intravenous volume loading failed to increase cardiac index in CHF rats as it did in control rats. Single-unit analysis of aortic baroreceptor nerve activity showed that CHF rats had higher pressure threshold, lower frequency at pressure threshold, and lower gain than control rats. Arterial baroreflex control of ERSNA was attenuated; this was due to diminished gain of the afferent limb while the gain of the central portion of the reflex was normal. Single-unit analysis of vagal nerve activity showed that CHF rats had higher pressure threshold, lower frequency at saturation, and lower gain than control rats. Cardiopulmonary baroreflex control of ERSNA was attenuated; this was due to diminished gain of the afferent limb while the gain of the central portion of the reflex was normal. In the CHF rat, arterial and cardiopulmonary baroreflex control of ERSNA is markedly attenuated because of abnormalities in the periphery at the level of the aortic and cardiopulmonary receptors, respectively, and not in the central nervous system.

Ontogeny of the arterial and cardiopulmonary baroreflex during fetal and postnatal life

1997 ◽  
Vol 273 (2) ◽  
pp. R457-R471 ◽  
Author(s):  
J. L. Segar
Keyword(s):  
Nervous System ◽  
Angiotensin Ii ◽  
Cardiovascular System ◽  
Cardiovascular Function ◽  
Postnatal Life ◽  
Fetal Life ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Autonomic Reflexes ◽  
Cardiopulmonary Baroreflex

The autonomic nervous system is intimately involved in regulating cardiovascular function. Sensing mechanisms dispersed throughout the circulation, including arterial baroreceptors, low pressure receptors, and chemosensitive receptors, continually evoke reflexes designed to maintain cardiovascular homeostasis. Although there is a growing body of knowledge regarding neural regulation of the adult cardiovascular system, characterization and understanding of these physiological systems during development is limited. This review highlights developmental changes in the arterial and cardiopulmonary baroreflex during fetal and postnatal life and contrasts the function of these responses with those seen in the adult. Baroreceptors are functional in the immature animal and reset toward higher pressure levels with maturation. In our ovine model, the sensitivity of the efferent limb of the baroreflex is greatest during fetal life and decreases with postnatal development. As in the adult, angiotensin II and arginine vasopressin interact with the sympathetic nervous system early during development to alter baroreflex control of the cardiovascular system. However, the extent to which these hormonal systems influence autonomic reflexes during the fetal and newborn period appears vastly different than in the adult. Endogenous angiotensin II significantly contributes to resetting of the arterial baroreflex early in life, whereas even high circulating levels of vasopressin have little effect on baroreflex function until adulthood. Finally, the ability of cardiopulmonary mechanoreceptors to regulate cardiovascular function is impaired early in development, in sharp contrast to the heightened sensitivity of the arterial baroreflex at this stage of maturation. The potential importance of these autonomic reflexes on cardiovascular function during the perinatal period is highlighted.

scholarly journals Dynamic cardiac output regulation at rest, during exercise, and muscle metaboreflex activation: impact of congestive heart failure

2012 ◽  
Vol 303 (7) ◽  
pp. R757-R768 ◽  
Author(s):  
Masashi Ichinose ◽  
Javier A. Sala-Mercado ◽  
Matthew Coutsos ◽  
ZhenHua Li ◽  
Tomoko K. Ichinose ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Dynamic Exercise ◽  
Moderate Exercise ◽  
Baroreflex Control ◽  
Ventricular Systolic Pressure ◽  
Muscle Metaboreflex ◽  
High Level

We tested whether mild and moderate dynamic exercise and muscle metaboreflex activation (MMA) affect dynamic baroreflex control of heart rate (HR) and cardiac output (CO), and the influence of stroke volume (SV) fluctuations on CO regulation in normal (N) and pacing-induced heart failure (HF) dogs by employing transfer function analyses of the relationships between spontaneous changes in left ventricular systolic pressure (LVSP) and HR, LVSP and CO, HR and CO, and SV and CO at low and high frequencies (Lo-F, 0.04–0.15 Hz; Hi-F, 0.15–0.6 Hz). In N dogs, both workloads significantly decreased the gains for LVSP-HR and LVSP-CO in Hi-F, whereas only moderate exercise also reduced the LVSP-CO gain in Lo-F. MMA during mild exercise further decreased the gains for LVSP-HR in both frequencies and for LVSP-CO in Lo-F. MMA during moderate exercise further reduced LVSP-HR gain in Lo-F. Coherence for HR-CO in Hi-F was decreased by exercise and MMA, whereas that in Lo-F was sustained at a high level (>0.8) in all settings. HF significantly decreased dynamic HR and CO regulation in all situations. In HF, the coherence for HR-CO in Lo-F decreased significantly in all settings; the coherence for SV-CO in Lo-F was significantly higher. We conclude that dynamic exercise and MMA reduces dynamic baroreflex control of HR and CO, and these are substantially impaired in HF. In N conditions, HR modulation plays a major role in CO regulation. In HF, influence of HR modulation wanes, and fluctuations of SV dominate in CO variations.

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