Arterial baroreflex alters strength and mechanisms of muscle metaboreflex during dynamic exercise

2005 ◽  
Vol 288 (3) ◽  
pp. H1374-H1380 ◽  
Author(s):  
Jong-Kyung Kim ◽  
Javier A. Sala-Mercado ◽  
Jaime Rodriguez ◽  
Tadeusz J. Scislo ◽  
Donal S. O'Leary
Keyword(s):  
Pressor Response ◽  
Dynamic Exercise ◽  
Arterial Baroreflex ◽  
Vascular Conductance ◽  
Muscle Metaboreflex ◽  
Peripheral Vasoconstriction ◽  
Major Mechanism ◽  
Pressor Responses ◽  
Before And After ◽  
Chronically Instrumented Dogs

Previous studies showed that the arterial baroreflex opposes the pressor response mediated by muscle metaboreflex activation during mild dynamic exercise. However, no studies have investigated the mechanisms contributing to metaboreflex-mediated pressor responses during dynamic exercise after arterial baroreceptor denervation. Therefore, we investigated the contribution of cardiac output (CO) and peripheral vasoconstriction in mediating the pressor response to graded reductions in hindlimb perfusion in conscious, chronically instrumented dogs before and after sinoaortic denervation (SAD) during mild and moderate exercise. In control experiments, the metaboreflex pressor responses were mediated via increases in CO. After SAD, the metaboreflex pressor responses were significantly greater and significantly smaller increases in CO occurred. During control experiments, nonischemic vascular conductance (NIVC) did not change with muscle metaboreflex activation, whereas after SAD NIVC significantly decreased with metaboreflex activation; thus SAD shifted the mechanisms of the muscle metaboreflex from mainly increases in CO to combined cardiac and peripheral vasoconstrictor responses. We conclude that the major mechanism by which the arterial baroreflex buffers the muscle metaboreflex is inhibition of metaboreflex-mediated peripheral vasoconstriction.

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 Role of cardiac output versus peripheral vasoconstriction in mediating muscle metaboreflex pressor responses: dynamic exercise versus postexercise muscle ischemia

2013 ◽  
Vol 304 (8) ◽  
pp. R657-R663 ◽  
Author(s):  
Marty D. Spranger ◽  
Javier A. Sala-Mercado ◽  
Matthew Coutsos ◽  
Jasdeep Kaur ◽  
Doug Stayer ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Pressor Response ◽  
Dynamic Exercise ◽  
Muscle Metaboreflex ◽  
Peripheral Vasoconstriction ◽  
Muscle Ischemia ◽  
Normal Individuals ◽  
Pressor Responses ◽  
Sustained Increase

Muscle metaboreflex activation (MMA) during submaximal dynamic exercise in normal individuals increases mean arterial pressure (MAP) via increases in cardiac output (CO) with little peripheral vasoconstriction. The rise in CO occurs primarily via increases in heart rate (HR) with maintained or slightly increased stroke volume. When the reflex is sustained during recovery (postexercise muscle ischemia, PEMI), HR declines yet MAP remains elevated. The role of CO in mediating the pressor response during PEMI is controversial. In seven chronically instrumented canines, steady-state values with MMA during mild exercise (3.2 km/h) were observed by reducing hindlimb blood flow by ∼60% for 3–5 min. MMA during exercise was followed by 60 s of PEMI. Control experiments consisted of normal exercise and recovery. MMA during exercise increased MAP, HR, and CO by 55.3 ± 4.9 mmHg, 42.5 ± 6.9 beats/min, and 2.5 ± 0.4 l/min, respectively. During sustained MMA via PEMI, MAP remained elevated and CO remained well above the normal recovery levels. Neither MMA during dynamic exercise nor during PEMI significantly affected peripheral vascular conductance. We conclude that the sustained increase in MAP during PEMI is driven by a sustained increase in CO not peripheral vasoconstriction.

scholarly journals Muscle metaboreflex activation during dynamic exercise evokes epinephrine release resulting in β2-mediated vasodilation

2015 ◽  
Vol 308 (5) ◽  
pp. H524-H529 ◽  
Author(s):  
Jasdeep Kaur ◽  
Marty D. Spranger ◽  
Robert L. Hammond ◽  
Abhinav C. Krishnan ◽  
Alberto Alvarez ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Dynamic Exercise ◽  
Hindlimb Ischemia ◽  
Plasma Epinephrine ◽  
Vascular Conductance ◽  
Peripheral Vasculature ◽  
Muscle Metaboreflex ◽  
Before And After ◽  
Arterial Plasma ◽  
Chronically Instrumented Dogs

Muscle metaboreflex-induced increases in mean arterial pressure (MAP) during submaximal dynamic exercise are mediated principally by increases in cardiac output. To what extent, if any, the peripheral vasculature contributes to this rise in MAP is debatable. In several studies, we observed that in response to muscle metaboreflex activation (MMA; induced by partial hindlimb ischemia) a small but significant increase in vascular conductance occurred within the nonischemic areas (calculated as cardiac output minus hindlimb blood flow and termed nonischemic vascular conductance; NIVC). We hypothesized that these increases in NIVC may stem from a metaboreflex-induced release of epinephrine, resulting in β2-mediated dilation. We measured NIVC and arterial plasma epinephrine levels in chronically instrumented dogs during rest, mild exercise (3.2 km/h), and MMA before and after β-blockade (propranolol; 2 mg/kg), α1-blockade (prazosin; 50 μg/kg), and α1 + β-blockade. Both epinephrine and NIVC increased significantly from exercise to MMA: 81.9 ± 18.6 to 141.3 ± 22.8 pg/ml and 33.8 ± 1.5 to 37.6 ± 1.6 ml·min−1·mmHg−1, respectively. These metaboreflex-induced increases in NIVC were abolished after β-blockade (27.6 ± 1.8 to 27.5 ± 1.7 ml·min−1·mmHg−1) and potentiated after α1-blockade (36.6 ± 2.0 to 49.7 ± 2.9 ml·min−1·mmHg−1), while α1 + β-blockade also abolished any vasodilation (33.7 ± 2.9 to 30.4 ± 1.9 ml·min−1·mmHg−1). We conclude that MMA during mild dynamic exercise induces epinephrine release causing β2-mediated vasodilation.

scholarly journals Attenuated muscle metaboreflex-induced pressor response during postexercise muscle ischemia in renovascular hypertension

2015 ◽  
Vol 308 (7) ◽  
pp. R650-R658 ◽  
Author(s):  
Marty D. Spranger ◽  
Jasdeep Kaur ◽  
Javier A. Sala-Mercado ◽  
Tiago M. Machado ◽  
Abhinav C. Krishnan ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Pressor Response ◽  
Dynamic Exercise ◽  
Hindlimb Ischemia ◽  
Muscle Metaboreflex ◽  
Muscle Ischemia ◽  
Normal Individuals ◽  
Before And After ◽  
Exercise Muscle ◽  
Sustained Increase

During dynamic exercise, muscle metaboreflex activation (MMA; induced via partial hindlimb ischemia) markedly increases mean arterial pressure (MAP), and MAP is sustained when the ischemia is maintained following the cessation of exercise (postexercise muscle ischemia, PEMI). We previously reported that the sustained pressor response during PEMI in normal individuals is driven by a sustained increase in cardiac output (CO) with no peripheral vasoconstriction. However, we have recently shown that the rise in CO with MMA is significantly blunted in hypertension (HTN). The mechanisms sustaining the pressor response during PEMI in HTN are unknown. In six chronically instrumented canines, hemodynamic responses were observed during rest, mild exercise (3.2 km/h), MMA, and PEMI in the same animals before and after the induction of HTN [Goldblatt two kidney, one clip (2K1C)]. In controls, MAP, CO and HR increased with MMA (+52 ± 6 mmHg, +2.1 ± 0.3 l/min, and +37 ± 7 beats per minute). After induction of HTN, MAP at rest increased from 97 ± 3 to 130 ± 4 mmHg, and the metaboreflex responses were markedly attenuated (+32 ± 5 mmHg, +0.6 ± 0.2 l/min, and +11 ± 3 bpm). During PEMI in HTN, HR and CO were not sustained, and MAP fell to normal recovery levels. We conclude that the attenuated metaboreflex-induced HR, CO, and MAP responses are not sustained during PEMI in HTN.

Muscle metaboreflex control of cardiac output and peripheral vasoconstriction exhibit different latencies

2000 ◽  
Vol 278 (2) ◽  
pp. H530-H537 ◽  
Author(s):  
Robert A. Augustyniak ◽  
Eric J. Ansorge ◽  
Donal S. O'Leary
Keyword(s):  
Cardiac Output ◽  
Vascular Occlusion ◽  
Systemic Arterial Pressure ◽  
Vascular Conductance ◽  
Muscle Metaboreflex ◽  
Peripheral Vasoconstriction ◽  
Pressor Responses ◽  
Vascular Beds ◽  
The Individual ◽  
Renal Vascular

Experiments were designed to determine 1) the mechanisms mediating metaboreflex-induced increases in systemic arterial pressure (SAP) in response to total vascular occlusion of hindlimb blood flow [e.g., increases in cardiac output (CO) vs. peripheral vasoconstriction] and 2) whether the individual mechanisms display differential latencies for the onset of the responses. Responses were observed in seven dogs performing steady-state treadmill exercise of mild and moderate workloads (3.2 km/h at 0% grade and 6.4 km/h at 10% grade). Differential latencies were exhibited among CO, nonischemic vascular conductance (NIVC; conductance to all nonischemic vascular beds), and renal vascular conductance (RVC), with peripheral vasoconstriction significantly preceding metaboreflex-mediated increases in CO. In addition, the latencies for SAP were not different from those for NIVC or RVC at either workload. During the lower workload there were small increases and then subsequent decreases in CO before the metaboreflex-induced increase in CO, which did contribute somewhat to the initial increases in SAP. However, the increases in CO mediated by the metaboreflex occurred significantly later than the initial increases in SAP. Therefore, we conclude that the substantial metaboreflex-mediated pressor responses that occur during the initial phase of total vascular occlusion during mild and moderate exercise are primarily caused by peripheral vasoconstriction.

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 Altered arterial baroreflex-muscle metaboreflex interaction in heart failure

2018 ◽  
Vol 315 (5) ◽  
pp. H1383-H1392 ◽  
Author(s):  
Jasdeep Kaur ◽  
Abhinav C. Krishnan ◽  
Danielle Senador ◽  
Alberto Alvarez ◽  
Hanna W. Hanna ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Ventricular Function ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Arterial Baroreflex ◽  
Active Muscle ◽  
Muscle Metaboreflex ◽  
Peripheral Vasoconstriction ◽  
Vascular Beds

Two powerful reflexes controlling cardiovascular function during exercise are the muscle metaboreflex and arterial baroreflex. In heart failure (HF), the strength and mechanisms of these reflexes are altered. Muscle metaboreflex activation (MMA) in normal subjects increases mean arterial pressure (MAP) primarily via increases in cardiac output (CO), whereas in HF the mechanism shifts to peripheral vasoconstriction. Baroreceptor unloading increases MAP via peripheral vasoconstriction, and this pressor response is blunted in HF. Baroreceptor unloading during MMA in normal animals elicits an enormous pressor response via combined increases in CO and peripheral vasoconstriction. The mode of interaction between these reflexes is intimately dependent on the parameter (e.g., MAP and CO) being investigated. The interaction between the two reflexes when activated simultaneously during dynamic exercise in HF is unknown. We activated the muscle metaboreflex in chronically instrumented dogs during mild exercise (via graded reductions in hindlimb blood flow) followed by baroreceptor unloading [via bilateral carotid occlusion (BCO)] before and after induction of HF. We hypothesized that BCO during MMA in HF would cause a smaller increase in MAP and a larger vasoconstriction of ischemic hindlimb vasculature, which would attenuate the restoration of blood flow to ischemic muscle observed in normal dogs. We observed that BCO during MMA in HF increases MAP by substantial vasoconstriction of all vascular beds, including ischemic active muscle, and that all cardiovascular responses, except ventricular function, exhibit occlusive interaction. We conclude that vasoconstriction of ischemic active skeletal muscle in response to baroreceptor unloading during MMA attenuates restoration of hindlimb blood flow. NEW & NOTEWORTHY We found that baroreceptor unloading during the muscle metaboreflex in heart failure results in occlusive interaction (except for ventricular function) with significant vasoconstriction of all vascular beds. In addition, restoration of blood flow to ischemic active muscle, via preferentially larger vasoconstriction of nonischemic beds, is significantly attenuated 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 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 Heart failure alters the strength and mechanisms of the muscle metaboreflex

2000 ◽  
Vol 278 (3) ◽  
pp. H818-H828 ◽  
Author(s):  
Robert L. Hammond ◽  
Robert A. Augustyniak ◽  
Noreen F. Rossi ◽  
Paul C. Churchill ◽  
Karen Lapanowski ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pressor Response ◽  
Vascular Occlusion ◽  
Strenuous Exercise ◽  
Aortic Blood Flow ◽  
Muscle Metaboreflex ◽  
Peripheral Vasoconstriction ◽  
Control Threshold ◽  
Before And After ◽  
Rapid Ventricular Pacing

We hypothesized that excessive sympathoactivation observed during strenuous exercise in subjects with heart failure (HF) may result from tonic activation of the muscle metaboreflex (MMR) via hypoperfusion of active skeletal muscle. We studied MMR responses in dogs during treadmill exercise by graded reduction of terminal aortic blood flow (TAQ) before and after induction of HF by rapid ventricular pacing. At a low workload, in both control and HF experiments, large decreases in TAQ were required to elicit the MMR pressor response. During control experiments, this pressor response resulted from increased cardiac output (CO), whereas in HF CO did not increase; thus the pressor response was solely due to peripheral vasoconstriction. In HF, MMR activation also induced higher plasma levels of vasopressin, norepinephrine (NE), and renin. At a higher workload, in control experiments any reduction of TAQ elicited MMR pressor responses. In HF, before any vascular occlusion, TAQ was already below MMR control threshold levels and reductions in TAQ again did not result in higher CO; thus SAP increased via peripheral vasoconstriction. NE rose markedly, indicating intense sympathetic activation. We conclude that in HF, the MMR is likely tonically active at moderate workloads and contributes to the tonic sympathoactivation.

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