Modulation of cardiac output alters the mechanisms of the muscle metaboreflex pressor response

Ichinose, Masashi; Sala‐Mercado, Javier A.; Coutsos, Matthew; Li, Zhenhua; Ichinose, Tomoko; Dawe, Elizabeth J.; O’Leary, Donal S.

doi:10.1152/ajpheart.00909.2009

Cited by 49 publications

(53 citation statements)

References 40 publications

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“…These substances can trigger cardiovascular reflexes (i.e., the so called "metaboreflex"), thereby activating the sympathetic nervous system, which in turn increases blood pressure to guarantee sufficient metabolite wash-out from the contracting muscle (19,39). In normal individuals, this task is accomplished with a complex hemodynamic response that encompasses complex interplay between myocardial performance, cardiac preload, afterload, and HR (3,6,9,13,14,24,33,40,51,56). Recent evidence suggests that, at least in healthy subjects, when the metaboreflex is activated by PEMI, a central role in the described metaboreflex-induced blood pressure response is played by the possibility to keep constant or to increase SV, thereby maintaining or increasing CO, since HR is not usually involved in the phenomenon (3, 9 -11, 25, 38).…”

Section: Discussionmentioning

confidence: 99%

“…MEAN BLOOD PRESSURE RESPONSE (MBP) to metaboreflex activation in healthy individuals is normally the consequence of increases in both systemic vascular resistance (SVR) and cardiac output (CO) (3,9,10,12,14,24,29,31,54,56). This response is achieved as the result of an elevation in sympathetic tone, which produces arteriolar constriction and enhancement in myocardial performance and in cardiac preload (18,35,39).…”

Section: The Main New Finding Of the Present Investigation Is That Obmentioning

confidence: 99%

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Differences in hemodynamic response to metaboreflex activation between obese patients with metabolic syndrome and healthy subjects with obese phenotype

Milia

Velluzzi

Roberto

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Patients suffering from obesity and metabolic syndrome (OMS) manifest a dysregulation in hemodynamic response during exercise, with an exaggerated systemic vascular increase. However, it is not clear whether this is the consequence of metabolic syndrome per se or whether it is due to concomitant obesity. The aim of the present investigation was to discover whether OMS and noncomplicated obesity resulted in different hemodynamic responses during the metaboreflex. Twelve metabolically healthy but obese subjects (MHO; 7 women), 13 OMS patients (5 women), and 12 normal age-matched controls (CTL; 6 women) took part in this study. All participants underwent a postexercise muscle ischemia protocol to evaluate the metaboreflex activity. Central hemodynamics were evaluated by impedance cardiography. The main result shows an exaggerated increase in systemic vascular resistance from baseline during the metaboreflex in the OMS patients as compared with the other groups (481.6 ± 180.3, -0.52 ± 177.6, and -60.5 ± 58.6 dynes·s(-1)·cm(-5) for the OMS, the MHO, and the CTL groups, respectively; P < 0.05). Moreover, the MHO subjects and the CTL group showed an increase in cardiac output during the metaboreflex (288.7 ± 325.8 and 703.8 ± 276.2 ml/m increase with respect to baseline), whereas this parameter tended to decrease in the OMS group (-350 ± 236.5 ml/m). However, the blood pressure response, which tended to be higher in the OMS patients, was not statistically different between groups. The results of the present investigation suggest that OMS patients have an exaggerated vasoconstriction in response to metaboreflex activation and that this fact is not due to obesity per se

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Section: Discussionmentioning

confidence: 99%

Section: The Main New Finding Of the Present Investigation Is That Obmentioning

confidence: 99%

Differences in hemodynamic response to metaboreflex activation between obese patients with metabolic syndrome and healthy subjects with obese phenotype

Milia

Velluzzi

Roberto

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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“…Although differences in the type of exercise and muscle mass used in the exercise could potentially affect the results, an alternative explanation for this inconsistency is that the components of the muscle metaboreflex-mediated pressor response vary widely among human subjects. Previous studies (25,26,30,67) have shown that activation of the muscle metaboreflex during submaximal treadmill exercise in dogs with reduced hindlimb blood flow elicits a pressor response mediated primarily by an increase in CO. However, the mechanism of the pressor response shifts to increased peripheral vasoconstriction when the ability to increase CO is limited, such as in heart failure or during maximal exercise (2,20).…”

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confidence: 99%

“…However, the mechanism of the pressor response shifts to increased peripheral vasoconstriction when the ability to increase CO is limited, such as in heart failure or during maximal exercise (2,20). In addition, that shift has also been observed when the normal rise in CO is either pharmacologically or mechanically removed (26,54). Based on these findings, it is conceivable that individuals with a small or no increase in CO during PEMI, and maybe even during isometric exercise, may show substantial peripheral vasoconstriction.…”

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confidence: 99%

Individual differences in cardiac and vascular components of the pressor response to isometric handgrip exercise in humans

Watanabe

Ichinose

Tahara

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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Watanabe K, Ichinose M, Tahara R, Nishiyasu T. Individual differences in cardiac and vascular components of the pressor response to isometric handgrip exercise in humans. Am J Physiol Heart Circ Physiol 306: H251-H260, 2014. First published November 8, 2013 doi:10.1152/ajpheart.00699.2013.-We tested the hypotheses that, in humans, changes in cardiac output (CO) and total peripheral vascular resistance (TPR) occurring in response to isometric handgrip exercise vary considerably among individuals and that those individual differences are related to differences in muscle metaboreflex and arterial baroreflex function. Thirty-nine healthy subjects performed a 1-min isometric handgrip exercise at 50% of maximal voluntary contraction. This was followed by a 4-min postexercise muscle ischemia (PEMI) period to selectively maintain activation of the muscle metaboreflex. All subjects showed increases in arterial pressure during exercise. Interindividual coefficients of variation (CVs) for the changes in CO and TPR between rest and exercise periods (CO: 95.1% and TPR: 87.8%) were more than twofold greater than CVs for changes in mean arterial pressure (39.7%). There was a negative correlation between CO and TPR responses during exercise (r ϭ Ϫ0.751, P Ͻ 0.01), but these CO and TPR responses correlated positively with the corresponding responses during PEMI (r ϭ 0.568 and 0.512, respectively, P Ͻ 0.01). The CO response during exercise did not correlate with PEMI-induced changes in an index of cardiac parasympathetic tone and cardiac baroreflex sensitivity. These findings demonstrate that the changes in CO and TPR that occur in response to isometric handgrip exercise vary considerably among individuals and that the two responses have an inverse relationship. They also suggest that individual differences in components of the pressor response are attributable in part to variations in muscle metaboreflex-mediated cardioaccelerator and vasoconstrictor responses. cardiac output; peripheral vascular resistance; muscle metaboreflex; arterial baroreflex DURING ISOMETRIC EXERCISE, arterial blood pressure, heart rate (HR), and sympathetic nerve activity all increase in association with increases in the intensity and duration of the exercise. This pressor response is governed mainly by neural mechanisms: central command (52) as well as a feedback system operating via afferent input from exercising skeletal muscle receptors (muscle metaboreflex and mechanoreflex) (40,41,51) and from arterial and cardiopulmonary baroreceptors (arterial and cardiopulmonary baroreflexes) (51, 52). While the increase in arterial pressure during isometric exercise is a well-established response, the responses of the components mediating the pressor response, cardiac output (CO) and total peripheral vascular resistance (TPR), remain controversial. In fact, previous studies have shown that, during isometric handgrip exercise in healthy humans, the pressor response occurs via an increase in CO (16,32,[34][35][36]57), an increase in TPR (6, 17), or both of those...

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“…All animals were accustomed to human handling before they were surgically instrumented in two different procedures (sternotomy and left flank abdominal surgery), as described in several previous studies (10,11,14). Briefly, using aseptic procedures, a midline sternotomy was performed, and a fully implantable telemetered blood pressure transducer (model no.…”

Section: Methodsmentioning

confidence: 99%

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

Ichinose

Sala‐Mercado

Coutsos

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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.2012.-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 (Ͼ0.8) 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. arterial baroreflex; exercise reflexes; pressor response; impaired cardiac performance BEAT-TO-BEAT CARDIAC OUTPUT (CO) varies considerably across successive heart beats, whereas the average level remains remarkably constant under basal conditions (21, 50). This likely involves control mechanisms operating at markedly different frequencies. Rapid baroreflex control of heart rate (HR) is thought to play a crucial role in dynamic CO regulation. Previous studies suggest that low-frequency (Lo-F: 0.04 -0.15 Hz) blood pressure fluctuations are buffered by the dynamic baroreflex control of HR (25, 28). However, we and others have observed that changes in HR do not necessarily elicit proportional changes in CO because stroke volume (SV) may also vary with the changes in ventricular filling time (17,34,48). Furthermore, transient increases in CO will lower ventricular filling pressure (and decreases in CO will raise filling pressure), thereby providing a self-limiting response (6,30,40). Furthermore, baroreflex control of HR may not functionally buffer high-frequency (Hi-F: above 0.15 Hz) blood pressure fluctuations (4,38,44). In this case, Hi-F variations of CO could facilitate blood pressure variability via a feedforward mechanism rather than buffer arterial pressure. In addition, it has been shown that in anesthetized rats, the blood pressure response to cardiac pacing induced high-frequency oscillation of CO is smaller than that to low-frequency oscillation of CO (41). To our knowledge, however, the dynam...

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Modulation of cardiac output alters the mechanisms of the muscle metaboreflex pressor response

Cited by 49 publications

References 40 publications

Differences in hemodynamic response to metaboreflex activation between obese patients with metabolic syndrome and healthy subjects with obese phenotype

Differences in hemodynamic response to metaboreflex activation between obese patients with metabolic syndrome and healthy subjects with obese phenotype

Individual differences in cardiac and vascular components of the pressor response to isometric handgrip exercise in humans

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

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