scholarly journals Muscle metaboreflex-induced central blood volume mobilization in heart failure

2019 ◽  
Vol 316 (5) ◽  
pp. H1047-H1052 ◽  
Author(s):  
Donal S. O’Leary ◽  
Danielle Senador ◽  
Robert A. Augustyniak
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Cardiac Output ◽  
Blood Volume ◽  
Systolic Heart Failure ◽  
Normal Subjects ◽  
Dynamic Exercise ◽  
Central Blood Volume ◽  
Ventricular Contractility ◽  
Muscle Metaboreflex

Underperfusion of active skeletal muscle causes metabolites to accumulate and stimulate group III and IV skeletal muscle afferents, which triggers a powerful pressor response termed the muscle metaboreflex. Muscle metaboreflex activation (MMA) during submaximal dynamic exercise in healthy individuals increases arterial pressure mainly via substantial increases in cardiac output (CO). The increases in CO occur via the combination of tachycardia and increased ventricular contractility. Importantly, MMA also elicits substantial central blood volume mobilization, which allows the ventricular responses to sustain the increases in CO. Otherwise preload would fall and the increases in CO could not be maintained. In subjects with systolic heart failure (HF), the ability to increase CO during exercise and MMA is markedly reduced, which has been attributed to impaired ventricular contractility. Whether the ability to maintain preload during MMA in HF is preserved is unknown. Using a conscious chronically instrumented canine model, we observed that MMA in HF is able to raise central blood volume similarly as in normal subjects. Therefore, the loss of the ability to raise CO during MMA in HF is not because of the loss of the ability to mobilize blood volume centrally. NEW & NOTEWORTHY In normal subjects during dynamic exercise muscle metaboreflex activation elicits large increases in cardiac output that occur via increases in heart rate, ventricular contractility, and, importantly, marked central blood volume mobilization that acts to maintain ventricular preload, thereby allowing the changes in cardiac function to maintain the increases in cardiac output. In subjects with heart failure, the ability to raise cardiac output during muscle metaboreflex activation is impaired. We investigated whether this is because of the inability to maintain ventricular preload. We found that this reflex is still able to elicit large increases in central blood volume, and therefore the limited ability to raise cardiac output likely stems from ventricular dysfunction and not the ability to maintain preload.

Heart failure alters the strength and mechanisms of arterial baroreflex pressor responses during dynamic exercise

2004 ◽  
Vol 287 (4) ◽  
pp. H1682-H1688 ◽  
Author(s):  
Jong-Kyung Kim ◽  
Robert A. Augustyniak ◽  
Javier A. Sala-Mercado ◽  
Robert L. Hammond ◽  
Eric J. Ansorge ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Cardiac Output ◽  
Pressor Response ◽  
Normal Subjects ◽  
Dynamic Exercise ◽  
Arterial Baroreflex ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid ◽  
Before And After

Arterial baroreflex function is well preserved during dynamic exercise in normal subjects. In subjects with heart failure (HF), arterial baroreflex ability to regulate blood pressure is impaired at rest. However, whether exercise modifies the strength and mechanisms of baroreflex responses in HF is unknown. Therefore, we investigated the relative roles of cardiac output and peripheral vasoconstriction in eliciting the pressor response to bilateral carotid occlusion (BCO) in conscious, chronically instrumented dogs at rest and during treadmill exercise ranging from mild to heavy workloads. Experiments were performed in the same animals before and after rapid ventricular pacing-induced HF. At rest, the pressor response to BCO was significantly attenuated in HF (33.3 ± 1.2 vs. 18.7 ± 2.7 mmHg), and this difference persisted during exercise in part due to lower cardiac output responses in HF. However, both before and after the induction of HF, the contribution of vasoconstriction in active skeletal muscle toward the pressor response became progressively greater as workload increased. We conclude that, although there is an impaired ability of the baroreflex to regulate arterial pressure at rest and during exercise in HF, vasoconstriction in active skeletal muscle becomes progressively more important in mediating the baroreflex pressor response as workload increases with a pattern similar to that observed in normal subjects.

scholarly journals Muscle metaboreflex-induced coronary vasoconstriction limits ventricular contractility during dynamic exercise in heart failure

2013 ◽  
Vol 304 (7) ◽  
pp. H1029-H1037 ◽  
Author(s):  
Matthew Coutsos ◽  
Javier A. Sala-Mercado ◽  
Masashi Ichinose ◽  
ZhenHua Li ◽  
Elizabeth J. Dawe ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Left Ventricular ◽  
Dynamic Exercise ◽  
Adrenergic Blockade ◽  
Ventricular Contractility ◽  
Cardiac Work ◽  
Muscle Metaboreflex ◽  
Coronary Vasoconstriction ◽  
Before And After

Muscle metaboreflex activation (MMA) during dynamic exercise increases cardiac work and myocardial O2 demand via increases in heart rate, ventricular contractility, and afterload. This increase in cardiac work should lead to metabolic coronary vasodilation; however, no change in coronary vascular conductance occurs. This indicates that the MMA-induced increase in sympathetic activity to the heart, which raises heart rate, ventricular contractility, and cardiac output, also elicits coronary vasoconstriction. In heart failure, cardiac output does not increase with MMA presumably due to impaired ability to improve left ventricular contractility. In this setting actual coronary vasoconstriction is observed. We tested whether this coronary vasoconstriction could explain, in part, the reduced ability to increase cardiac performance during MMA. In conscious, chronically instrumented dogs before and after pacing-induced heart failure, MMA responses during mild exercise were observed before and after α1-adrenergic blockade (prazosin 20–50 μg/kg). During MMA, the increases in coronary vascular conductance, coronary blood flow, maximal rate of left ventricular pressure change, and cardiac output were significantly greater after α1-adrenergic blockade. We conclude that in subjects with heart failure, coronary vasoconstriction during MMA limits the ability to increase left ventricular contractility.

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.

Vascular capacitance and cardiac output in pacing-induced canine models of acute and chronic heart failure

1995 ◽  
Vol 73 (11) ◽  
pp. 1641-1650 ◽  
Author(s):  
Richard Ian Ogilvie ◽  
Danuta Zborowska-Sluis
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Chronic Heart Failure ◽  
Blood Volume ◽  
Central Blood Volume ◽  
Ventricular Pacing ◽  
Volume Loading ◽  
Total Blood ◽  
Volume Load ◽  
Vascular Capacitance

The relationship between stressed and total blood volume, total vascular capacitance, central blood volume, cardiac output (CO), and pulmonary capillary wedge pressure (Ppcw) was investigated in pacing-induced acute and chronic heart failure. Acute heart failure was induced in anesthetized splenectomized dogs by a volume load (20 mL/kg over 10 min) during rapid right ventricular pacing at 250 beats/min (RRVP) for 60 min. Chronic heart failure was induced by continuous RRVP for 2–6 weeks (average 24 ± 2 days). Total vascular compliance and capacitance were calculated from the mean circulatory filling pressure (Pmcf) during transient circulatory arrest after acetylcholine at three different circulating volumes. Stressed blood volume was calculated as a product of compliance and Pmcf, with the total blood volume measured by a dye dilution. Central blood volume (CBV) and CO were measured by thermodilution. Central (heart and lung) vascular capacitance was estimated from the plot of Ppcw against CBV. Acute volume loading without RRVP increased capacitance and CO, whereas after volume loading with RRVP, capacitance and CO were unaltered from baseline. Chronic RRVP reduced capacitance and CO. All interventions, volume ± RRVP or chronic RRVP, increased stressed and central blood volumes and Ppcw. Acute or chronic RRVP reduced central vascular capacitance. Cardiac output was increased when stressed and unstressed blood volumes increased proportionately as during volume loading alone. When CO was reduced and Ppcw increased, as during chronic RRVP or acute RRVP plus a volume load, stressed blood volume was increased and unstressed blood volume was decreased. Thus, interventions that reduced CO and increased Ppcw also increased stressed and reduced unstressed blood volume and total vascular capacitance.Key words: vascular capacitance, vascular compliance, central blood volume, rapid ventricular pacing, dogs, heart failure.

scholarly journals Muscle metaboreflex-induced increases in effective arterial elastance: effect of heart failure

2020 ◽  
Vol 319 (1) ◽  
pp. R1-R10 ◽  
Author(s):  
Joseph Mannozzi ◽  
Jasdeep Kaur ◽  
Marty D. Spranger ◽  
Mohamed-Hussein Al-Hassan ◽  
Beruk Lessanework ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Dynamic Exercise ◽  
Stroke Work ◽  
Arterial Elastance ◽  
Muscle Metaboreflex ◽  
Effective Arterial Elastance

Dynamic exercise elicits robust increases in sympathetic activity in part due to muscle metaboreflex activation (MMA), a pressor response triggered by activation of skeletal muscle afferents. MMA during dynamic exercise increases arterial pressure by increasing cardiac output via increases in heart rate, ventricular contractility, and central blood volume mobilization. In heart failure, ventricular function is compromised, and MMA elicits peripheral vasoconstriction. Ventricular-vascular coupling reflects the efficiency of energy transfer from the left ventricle to the systemic circulation and is calculated as the ratio of effective arterial elastance ( Ea) to left ventricular maximal elastance ( Emax). The effect of MMA on Ea in normal subjects is unknown. Furthermore, whether muscle metaboreflex control of Ea is altered in heart failure has not been investigated. We utilized two previously published methods of evaluating Ea [end-systolic pressure/stroke volume ( EaPV)] and [heart rate × vascular resistance ( EaZ)] during rest, mild treadmill exercise, and MMA (induced via partial reductions in hindlimb blood flow imposed during exercise) in chronically instrumented conscious canines before and after induction of heart failure via rapid ventricular pacing. In healthy animals, MMA elicits significant increases in effective arterial elastance and stroke work that likely maintains ventricular-vascular coupling. In heart failure, Ea is high, and MMA-induced increases are exaggerated, which further exacerbates the already uncoupled ventricular-vascular relationship, which likely contributes to the impaired ability to raise stroke work and cardiac output during exercise in heart failure.

Heart failure attenuates muscle metaboreflex control of ventricular contractility during dynamic exercise

2007 ◽  
Vol 292 (5) ◽  
pp. H2159-H2166 ◽  
Author(s):  
Javier A. Sala-Mercado ◽  
Robert L. Hammond ◽  
Jong-Kyung Kim ◽  
Phillip J. McDonald ◽  
Larry W. Stephenson ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pressor Response ◽  
Left Ventricular ◽  
Dynamic Exercise ◽  
Stroke Work ◽  
Moderate Exercise ◽  
Ventricular Contractility ◽  
Loop Analysis ◽  
Muscle Metaboreflex ◽  
Before And After

Underperfusion of active skeletal muscle elicits a reflex pressor response termed the muscle metaboreflex (MMR). In normal dogs during mild exercise, MMR activation causes large increases in cardiac output (CO) and mean arterial pressure (MAP); however, in heart failure (HF) although MAP increases, the rise in CO is virtually abolished, which may be due to an impaired ability to increase left ventricular contractility (LVC). The objective of the present study was to determine whether the increases in LVC seen with MMR activation during dynamic exercise in normal animals are abolished in HF. Conscious dogs were chronically instrumented to measure CO, MAP, and left ventricular (LV) pressure and volume. LVC was calculated from pressure-volume loop analysis [LV maximal elastance ( Emax) and preload-recruitable stroke work (PRSW)] at rest and during mild and moderate exercise under free-flow conditions and with MMR activation (via partial occlusion of hindlimb blood flow) before and after rapid ventricular pacing-induced HF. In control experiments, MMR activation at both workloads [mild exercise (3.2 km/h) and moderate exercise (6.4 km/h at 10% grade)] significantly increased CO, Emax, and PRSW. In contrast, after HF was induced, CO, Emax, and PRSW were significantly lower at rest. Although CO increased significantly from rest to exercise, Emax and PRSW did not change. In addition, MMR activation caused no significant change in CO, Emax, or PRSW at either workload. We conclude that MMR causes large increases in LVC in normal animals but that this ability is abolished in HF.

scholarly journals Heart failure abolishes muscle metaboreflex induced increases in left ventricular contractility during moderate dynamic exercise

2007 ◽  
Vol 21 (6) ◽  
Author(s):  
Javier A. Sala‐Mercado ◽  
Robert L. Hammond ◽  
Jong‐Kyung Kim ◽  
Phillip J. McDonald ◽  
Larry W. Stephenson ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricular ◽  
Dynamic Exercise ◽  
Ventricular Contractility ◽  
Left Ventricular Contractility ◽  
Muscle Metaboreflex

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

2010 ◽  
Vol 298 (1) ◽  
pp. H245-H250 ◽  
Author(s):  
Masashi J. Ichinose ◽  
Javier A. Sala-Mercado ◽  
Matthew Coutsos ◽  
ZhenHua Li ◽  
Tomoko K. Ichinose ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Maximal Exercise ◽  
Pressor Response ◽  
Superior Vena ◽  
Normal Subjects ◽  
Dynamic Exercise ◽  
Muscle Metaboreflex ◽  
Peripheral Vasoconstriction ◽  
Co Reduction

Muscle metaboreflex activation during submaximal dynamic exercise in normal subjects elicits a pressor response primarily due to increased cardiac output (CO). However, when the ability to increase CO is limited, such as in heart failure or during maximal exercise, the muscle metaboreflex-induced increases in arterial pressure occur via peripheral vasoconstriction. How the mechanisms of this pressor response are altered is unknown. We tested the hypothesis that this change in metaboreflex function is dependent on the level of CO. The muscle metaboreflex was activated in dogs during mild dynamic exercise (3.2 km/h) via a partial reduction of hindlimb blood flow. Muscle metaboreflex activation increased CO and arterial pressure, whereas vascular conductance of all areas other than the hindlimbs did not change. CO was then reduced to the same level observed during exercise before the muscle metaboreflex activation via partial occlusion of the inferior and superior vena cavae. Arterial pressure dropped rapidly with the reduction in CO but, subsequently, nearly completely recovered. With the removal of the muscle metaboreflex-induced rise in CO, substantial peripheral vasoconstriction occurred that maintained arterial pressure at the same levels as before CO reduction. Therefore, the muscle metaboreflex function is nearly instantaneously shifted from increased CO to increased vasoconstriction when the muscle metaboreflex-induced rise in CO is removed. We conclude that whether vasoconstriction occurs with muscle metaboreflex depends on whether CO rises.

scholarly journals Muscle Metaboreflex Control of Coronary Blood Flow and Ventricular Contractility During Dynamic Exercise in Heart Failure

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Matthew Coutsos ◽  
Javier Sala‐Mercado ◽  
Masashi Ichinose ◽  
Zhen Hua Li ◽  
Donal O'Leary
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Coronary Blood Flow ◽  
Dynamic Exercise ◽  
Ventricular Contractility ◽  
Muscle Metaboreflex

Spontaneous baroreflex control of cardiac output during dynamic exercise, muscle metaboreflex activation, and heart failure

2008 ◽  
Vol 294 (3) ◽  
pp. H1310-H1316 ◽  
Author(s):  
Masashi Ichinose ◽  
Javier A. Sala-Mercado ◽  
Donal S. O'Leary ◽  
Robert L. Hammond ◽  
Matthew Coutsos ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Dynamic Exercise ◽  
Baroreflex Control ◽  
Ventricular Systolic Pressure ◽  
Muscle Metaboreflex ◽  
Before And After ◽  
Spontaneous Baroreflex

We have previously shown that spontaneous baroreflex-induced changes in heart rate (HR) do not always translate into changes in cardiac output (CO) at rest. We have also shown that heart failure (HF) decreases this linkage between changes in HR and CO. Whether dynamic exercise and muscle metaboreflex activation (via imposed reductions in hindlimb blood flow) further alter this translation in normal and HF conditions is unknown. We examined these questions using conscious, chronically instrumented dogs before and after pacing-induced HF during mild and moderate dynamic exercise with and without muscle metaboreflex activation. We measured left ventricular systolic pressure (LVSP), CO, and HR and analyzed the spontaneous HR-LVSP and CO-LVSP relationships. In normal animals, mild exercise significantly decreased HR-LVSP (−3.08 ± 0.5 vs. −5.14 ± 0.6 beats·min−1·mmHg−1; P < 0.05) and CO-LVSP (−134.74 ± 24.5 vs. −208.6 ± 22.2 ml·min−1·mmHg−1; P < 0.05). Moderate exercise further decreased both and, in addition, significantly reduced HR-CO translation (25.9 ± 2.8% vs. 52.3 ± 4.2%; P < 0.05). Muscle metaboreflex activation at both workloads decreased HR-LVSP, whereas it had no significant effect on CO-LVSP and the HR-CO translation. HF significantly decreased HR-LVSP, CO-LVSP, and the HR-CO translation in all situations. We conclude that spontaneous baroreflex HR responses do not always cause changes in CO during exercise. Moreover, muscle metaboreflex activation during mild and moderate dynamic exercise reduces this coupling. In addition, in HF the HR-CO translation also significantly decreases during both workloads and decreases even further with muscle metaboreflex activation.

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