Cardiovascular responses to exercise and muscle metaboreflex activation during the recovery from pacing-induced heart failure

2006 ◽  
Vol 101 (1) ◽  
pp. 14-22 ◽  
Author(s):  
Robert A. Augustyniak ◽  
Eric J. Ansorge ◽  
Jong-Kyung Kim ◽  
Javier A. Sala-Mercado ◽  
Robert L. Hammond ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Treadmill Exercise ◽  
Cardiovascular Responses ◽  
Moderate Exercise ◽  
Muscle Metaboreflex ◽  
Blood Flows ◽  
Graded Exercise ◽  
Rapid Ventricular Pacing ◽  
Chronically Instrumented Dogs

Rapid recovery of resting hemodynamics from tachycardia- or arrhythmia-induced heart failure (HF) has been demonstrated in both humans and animals. However, little is known about cardiovascular responses to exercise in animals or about reflex control of the cardiovascular system during exercise while recovering from HF. Inasmuch as the reduced cardiac output (CO) during exercise in HF has been shown to lead to underperfusion of active skeletal muscle and tonic activation of the muscle metaboreflex, an improved CO during exercise in subjects recovering from HF may lead to higher skeletal muscle blood flows and to relief of this metabolic stimulus. We investigated cardiovascular responses to graded treadmill exercise and metaboreflex activation [evoked by imposed graded reductions in hindlimb blood flow (HLBF) during mild and moderate exercise] in chronically instrumented dogs during control, mild to moderate HF (induced by rapid ventricular pacing), and recovery from HF. Most hemodynamic responses to graded exercise returned to control within 24 h of disconnecting the pacemaker. After 2 wk of recovery, CO and HLBF at each workload were significantly higher than control. In addition, whereas the increase in CO that normally occurs with metaboreflex activation was markedly attenuated in HF, it completely returned in the recovery experiments. We conclude that cardiovascular responses to graded exercise during the recovery from pacing-induced HF return rapidly to near or above control and that the increased CO and HLBF in recovery likely relieved the metabolic stimulus and tonic metaboreflex activation that may have occurred during moderate exercise in HF.

Severe exercise alters the strength and mechanisms of the muscle metaboreflex

2001 ◽  
Vol 280 (4) ◽  
pp. H1645-H1652 ◽  
Author(s):  
Robert A. Augustyniak ◽  
Heidi L. Collins ◽  
Eric J. Ansorge ◽  
Noreen F. Rossi ◽  
Donal S. O'Leary
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Treadmill Exercise ◽  
Pressor Response ◽  
Increase Blood Flow ◽  
Moderate Exercise ◽  
Muscle Metaboreflex ◽  
Severe Exercise

Previous studies have shown that in dogs performing mild to moderate treadmill exercise, partial graded reductions in hindlimb blood flow cause active skeletal muscle to become ischemic and metabolites to accumulate thus evoking the muscle metaboreflex. This leads to a substantial reflex increase in mean arterial pressure (MAP) mediated almost solely via a rise in cardiac output (CO). However, during severe exercise CO is likely near maximal and thus metaboreflex-mediated increases in MAP may be attenuated. We therefore evoked the metaboreflex via partial graded reductions in hindlimb blood flow in seven dogs during mild, moderate, and severe treadmill exercise. During mild and moderate exercise there was a large rise in CO (1.5 ± 0.2 and 2.2 ± 0.3 l/min, respectively), whereas during severe exercise no significant increase in CO occurred. The rise in CO caused a marked pressor response that was significantly attenuated during severe exercise (26.3 ± 7.0, 33.2 ± 5.6, and 12.2 ± 4.8 mmHg, respectively). We conclude that during severe exercise the metaboreflex pressor response mechanisms are altered such that the ability of this reflex to increase CO is abolished, and reduced pressor response occurs only via peripheral vasoconstriction. This shift in mechanisms likely limits the effectiveness of the metaboreflex to increase blood flow to ischemic active skeletal muscle. Furthermore, because the metaboreflex is a flow-raising reflex and not a pressure-raising reflex, it may be most appropriate to describe the metaboreflex magnitude based on its ability to evoke a rise in CO and not a rise in MAP.

Mechanism of skeletal muscle underperfusion in a dog model of low-output heart failure

1986 ◽  
Vol 251 (2) ◽  
pp. H227-H235 ◽  
Author(s):  
J. R. Wilson ◽  
R. Falcone ◽  
N. Ferraro ◽  
J. Egler
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Treadmill Exercise ◽  
Gracilis Muscle ◽  
Pressure Gradients ◽  
Vascular Control ◽  
Rapid Ventricular Pacing ◽  
Arteriolar Vasodilation ◽  
Minimal Resistance ◽  
Induce Heart Failure

To investigate the mechanism responsible for underperfusion of working skeletal muscle in heart failure, we measured systemic and femoral bed hemodynamics during treadmill exercise and gracilis muscle resistance during contraction frequencies of 1-9 Hz in 8 dogs ventricularly paced at 260 beats/min for 3 wk to induce heart failure (HF) and in 9 control dogs. At peak treadmill exercise (4 mph, 10%), HF dogs had reduced cardiac outputs (control: 297 +/- 42 vs. HF: 212 +/- 16 ml X min-1 X kg-1) and femoral bed flows (control: 352 +/- 112 vs. HF: 229 +/- 95 ml/min) and elevated arterial lactates [control: 1.7 +/- 0.7 vs. HF: 4.1 +/- 0.7 mM (all P less than 0.04)], consistent with skeletal muscle underperfusion. This muscle underperfusion was associated with reduced mean arteriovenous pressure gradients [control: 119 +/- 12 vs. HF: 91 +/- 9 mmHg (P less than 0.001)] but with normal systemic vascular [control: 21 +/- 6 vs. HF: 23 +/- 5 U (P = NS)] and femoral bed resistances [control: 3.5 +/- 1.6 vs. HF: 4.4 +/- 2.3 X 10(2) U (P = NS)]. Both groups also had similar gracilis muscle minimal resistance during exercise (control: 2.0 +/- 1.1 vs. HF: 1.9 +/- 0.9 X 10(3) U/100 g) and following maximal vasodilation (control: 2.0 +/- 1.0 vs. HF: 2.1 +/- 1.0 X 10(3) U/100 g). These results suggest that 1) short-term rapid ventricular pacing in the dog produces a model of low output HF resembling HF in humans, and 2) skeletal muscle underperfusion in this model is due to a reduced muscle arteriovenous pressure gradient and not to impaired skeletal muscle arteriolar vasodilation.

Impaired muscle metaboreflex-induced increases in ventricular function in heart failure

2004 ◽  
Vol 287 (6) ◽  
pp. H2612-H2618 ◽  
Author(s):  
Donal S. O'Leary ◽  
Javier A. Sala-Mercado ◽  
Robert A. Augustyniak ◽  
Robert L. Hammond ◽  
Noreen F. Rossi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Ventricular Function ◽  
Treadmill Exercise ◽  
Venous Pressure ◽  
Adrenergic Blockade ◽  
Ventricular Pacing ◽  
Ventricular Contractility ◽  
Muscle Metaboreflex ◽  
Rapid Ventricular Pacing

We investigated to what extent heart failure alters the ability of the muscle metaboreflex to improve ventricular function. Dogs were chronically instrumented to monitor mean arterial pressure (MAP), cardiac output (CO), heart rate (HR), stroke volume (SV), and central venous pressure (CVP) at rest and during mild treadmill exercise (3.2 km/h) before and during reductions in hindlimb blood flow imposed to activate the muscle metaboreflex. These control experiments were repeated at constant heart rate (ventricular pacing 225 beats/min) and at constant heart rate coupled with a β-adrenergic blockade (atenolol, 2 mg/kg iv) in normal animals and in the same animals after the induction of heart failure (HF, induced via rapid ventricular pacing). In control experiments in normal animals, metaboreflex activation caused tachycardia with no change in SV, resulting in large increases in CO and MAP. At constant HR, large increases in CO still occurred via significant increases in SV. Inasmuch as CVP did not change in this setting and that β-adrenergic blockade abolished the reflex increase in SV at constant HR, this increase in SV likely reflects increased ventricular contractility. In contrast, after the induction of HF, much smaller increases in CO occurred with metaboreflex activation because, although increases in HR still occurred, SV decreased thereby limiting any increase in CO. At constant HR, no increase in CO occurred with metaboreflex activation even though CVP increased significantly. After β-adrenergic blockade, CO and SV decreased with metaboreflex activation. We conclude that in HF, the ability of the muscle metaboreflex to increase ventricular function via both increases in contractility as well as increases in filling pressure are markedly impaired.

Skeletal muscle vasodilation at the onset of exercise

1998 ◽  
Vol 85 (5) ◽  
pp. 1649-1654 ◽  
Author(s):  
John B. Buckwalter ◽  
Stephen B. Ruble ◽  
Patrick J. Mueller ◽  
Philip S. Clifford
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Muscarinic Receptors ◽  
Treadmill Exercise ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Iliac Arteries ◽  
Blood Flows ◽  
Peak Blood

The purpose of this study was to determine whether β-adrenergic or muscarinic receptors are involved in skeletal muscle vasodilation at the onset of exercise. Mongrel dogs ( n = 7) were instrumented with flow probes on both external iliac arteries and a catheter in one femoral artery. Propranolol (1 mg), atropine (500 μg), both drugs, or saline was infused intra-arterially immediately before treadmill exercise at 3 miles/h, 0% grade. Immediate and rapid increases in iliac blood flow occurred with initiation of exercise under all conditions. Peak blood flows were not significantly different among conditions (682 ± 35, 646 ± 49, 637 ± 68, and 705 ± 50 ml/min, respectively). Although the doses of antagonists employed had no effect on heart rate or systemic blood pressure, they were adequate to abolish agonist-induced increases in iliac blood flow. Because neither propranolol nor atropine affected iliac blood flow, we conclude that activation of β-adrenergic and muscarinic receptors is not essential for the rapid vasodilation in active skeletal muscle at the onset of exercise in dogs.

Attenuated arterial baroreflex buffering of muscle metaboreflex in heart failure

2005 ◽  
Vol 289 (6) ◽  
pp. H2416-H2423 ◽  
Author(s):  
Jong-Kyung Kim ◽  
Javier A. Sala-Mercado ◽  
Robert L. Hammond ◽  
Jaime Rodriguez ◽  
Tadeusz J. Scislo ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pressor Response ◽  
Dynamic Exercise ◽  
Arterial Baroreflex ◽  
Muscle Metaboreflex ◽  
Peripheral Vasoconstriction ◽  
Arterial Blood ◽  
Pressor Responses ◽  
Before And After ◽  
Chronically Instrumented Dogs

Previous studies have shown that heart failure (HF) or sinoaortic denervation (SAD) alters the strength and mechanisms of the muscle metaboreflex during dynamic exercise. However, it is still unknown to what extent SAD may modify the muscle metaboreflex in HF. Therefore, we quantified the contribution of cardiac output (CO) and peripheral vasoconstriction to metaboreflex-mediated increases in mean arterial blood pressure (MAP) in conscious, chronically instrumented dogs before and after induction of HF in both barointact and SAD conditions during mild and moderate exercise. The muscle metaboreflex was activated via partial reductions in hindlimb blood flow. After SAD, the metaboreflex pressor responses were significantly higher with respect to the barointact condition despite lower CO responses. The pressor response was significantly lower in HF after SAD but still higher than that of HF in the barointact condition. During control experiments in the barointact condition, total vascular conductance summed from all beds except the hindlimbs did not change with muscle metaboreflex activation, whereas in the SAD condition both before and after induction of HF significant vasoconstriction occurred. We conclude that SAD substantially increased the contribution of peripheral vasoconstriction to metaboreflex-induced increases in MAP, whereas in HF SAD did not markedly alter the patterns of the reflex responses, likely reflecting that in HF the ability of the arterial baroreflex to buffer metaboreflex responses is impaired.

scholarly journals Muscle metaboreflex-induced vasoconstriction in the ischemic active muscle is exaggerated in heart failure

2018 ◽  
Vol 314 (1) ◽  
pp. H11-H18 ◽  
Author(s):  
Jasdeep Kaur ◽  
Danielle Senador ◽  
Abhinav C. Krishnan ◽  
Hanna W. Hanna ◽  
Alberto Alvarez ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Exercise Intolerance ◽  
Adrenergic Blockade ◽  
Active Muscle ◽  
Muscle Metaboreflex ◽  
Peripheral Vasoconstriction ◽  
Ischemic Muscle

When oxygen delivery to active muscle is insufficient to meet the metabolic demand during exercise, metabolites accumulate and stimulate skeletal muscle afferents, inducing a reflex increase in blood pressure, termed the muscle metaboreflex. In healthy individuals, muscle metaboreflex activation (MMA) during submaximal exercise increases arterial pressure primarily via an increase in cardiac output (CO), as little peripheral vasoconstriction occurs. This increase in CO partially restores blood flow to ischemic muscle. However, we recently demonstrated that MMA induces sympathetic vasoconstriction in ischemic active muscle, limiting the ability of the metaboreflex to restore blood flow. In heart failure (HF), increases in CO are limited, and metaboreflex-induced pressor responses occur predominantly via peripheral vasoconstriction. In the present study, we tested the hypothesis that vasoconstriction of ischemic active muscle is exaggerated in HF. Changes in hindlimb vascular resistance [femoral arterial pressure ÷ hindlimb blood flow (HLBF)] were observed during MMA (via graded reductions in HLBF) during mild exercise with and without α1-adrenergic blockade (prazosin, 50 µg/kg) before and after induction of HF. In normal animals, initial HLBF reductions caused metabolic vasodilation, while reductions below the metaboreflex threshold elicited reflex vasoconstriction, in ischemic active skeletal muscle, which was abolished after α1-adrenergic blockade. Metaboreflex-induced vasoconstriction of ischemic active muscle was exaggerated after induction of HF. This heightened vasoconstriction impairs the ability of the metaboreflex to restore blood flow to ischemic muscle in HF and may contribute to the exercise intolerance observed in these patients. We conclude that sympathetically mediated vasoconstriction of ischemic active muscle during MMA is exaggerated in HF. NEW & NOTEWORTHY We found that muscle metaboreflex-induced vasoconstriction of the ischemic active skeletal muscle from which the reflex originates is exaggerated in heart failure. This results in heightened metaboreflex activation, which further amplifies the reflex-induced vasoconstriction of the ischemic active skeletal muscle and contributes to exercise intolerance in patients.

Muscle metaboreflex control of coronary blood flow

2002 ◽  
Vol 283 (2) ◽  
pp. H526-H532 ◽  
Author(s):  
Eric J. Ansorge ◽  
Sachin H. Shah ◽  
Robert A. Augustyniak ◽  
Noreen F. Rossi ◽  
Heidi L. Collins ◽  
...  
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Adrenergic Receptor ◽  
Sympathetic Nerve Activity ◽  
Treadmill Exercise ◽  
Cardiac Work ◽  
Nerve Activity ◽  
Muscle Metaboreflex ◽  
Severe Exercise ◽  
Chronically Instrumented Dogs

We investigated the effect of muscle metaboreflex activation on left circumflex coronary blood flow (CBF) and vascular conductance (CVC) in conscious, chronically instrumented dogs during treadmill exercise ranging from mild to severe workloads. Metaboreflex responses were also observed during mild exercise with constant heart rate (HR) of 225 beats/min and β1-adrenergic receptor blockade to attenuate the substantial reflex increases in cardiac work. The muscle metaboreflex was activated via graded partial occlusion of hindlimb blood flow. During mild exercise, with muscle metaboreflex activation, hindlimb ischemia elicited significant reflex increases in mean arterial pressure (MAP), HR, and cardiac output (CO) (+39.0 ± 5.2 mmHg, +29.9 ± 7.7 beats/min, and +2.0 ± 0.4 l/min, respectively; all changes, P < 0.05). CBF increased from 51.9 ± 4.3 to 88.5 ± 6.6 ml/min, ( P < 0.05), whereas no significant change in CVC occurred (0.56 ± 0.06 vs. 0.59 ± 0.05 ml · min−1 · mmHg−1; P > 0.05). Similar responses were observed during moderate exercise. In contrast, with metaboreflex activation during severe exercise, no further increases in CO or HR occurred, the increases in MAP and CBF were attenuated, and a significant reduction in CVC was observed (1.00 ± 0.12 vs. 0.90 ± 0.13 ml · min−1 · mmHg−1; P < 0.05). Similarly, when the metaboreflex was activated during mild exercise with the rise in cardiac work lessened (via constant HR and β1-blockade), no increase in CO occurred, the MAP and CBF responses were attenuated (+15.6 ± 4.5 mmHg, +8.3 ± 2 ml/min), and CVC significantly decreased from 0.63 ± 0.11 to 0.53 ± 0.10 ml · min−1 · mmHg−1. We conclude that the muscle metaboreflex induced increases in sympathetic nerve activity to the heart functionally vasoconstricts the coronary vasculature.

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.

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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