Is the muscle metaboreflex important in control of blood flow to ischemic active skeletal muscle in dogs?

O’Leary, Donal S.; Sheriff, Don D.

doi:10.1152/ajpheart.1995.268.3.h980

Cited by 76 publications

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“…This suggests that humans rely on local vasodilator mechanisms, and not a reflex increase in pressure, to restore blood flow to hypoperfused contracting muscle. In contrast, there is overwhelming evidence that suggests a pressor response is essential in the restoration of blood flow to underperfused hindlimbs of exercising dogs (12,22,23,30,35). The discrepant findings between our series of studies in humans and those performed in dogs may simply be related to species differences.…”

Section: Restoration Of Flow Via Local Vasodilator Mechanismscontrasting

confidence: 57%

“…To investigate the role of PGs and NO on percent recovery of blood flow and conductance, one-way repeatedmeasures ANOVA were performed between drug conditions. To further explore the contribution of local vasodilatation to any restoration of flow, we analyzed balloon resistance and forearm vascular resistance and considered them individually and in series (4,5,23). Using systemic arterial pressure (SAP; Finometer), brachial artery pressure distal to the balloon (BAP; catheter), and brachial artery blood flow, we calculated the resistance of the balloon (SAP-BAP/ flow) and vascular resistance (BAP/flow).…”

Section: Data Analysis and Statisticsmentioning

confidence: 99%

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Prostaglandins do not contribute to the nitric oxide-mediated compensatory vasodilation in hypoperfused exercising muscle

Casey

Joyner

2011

American Journal of Physiology-Heart and Circulatory Physiology

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Casey DP, Joyner MJ. Prostaglandins do not contribute to the nitric oxide-mediated compensatory vasodilation in hypoperfused exercising muscle. Am J Physiol Heart Circ Physiol 301: H261-H268, 2011. First published May 2, 2011; doi:10.1152/ajpheart.00222.2011.-We tested the hypothesis that 1) prostaglandins (PGs) contribute to compensatory vasodilation in contracting human forearm subjected to acute hypoperfusion, and 2) the combined inhibition of PGs and nitric oxide would attenuate the compensatory vasodilation more than PG inhibition alone. In separate protocols, subjects performed forearm exercise (20% of maximum) during hypoperfusion evoked by intra-arterial balloon inflation. Each trial included baseline, exercise before inflation, exercise with inflation, and exercise after deflation. Forearm blood flow (FBF; ultrasound) and local (brachial artery) and systemic arterial pressure [mean arterial pressure (MAP); Finometer] were measured. In protocol 1 (n ϭ 8), exercise was repeated during cyclooxygenase (COX) inhibition (Ketorolac) alone and during Ke-In protocol 2 (n ϭ 8), exercise was repeated during L-NMMA alone and during L-NMMA-Ketorolac. Forearm vascular conductance (FVC; ml·min Ϫ1 · 100 mmHg Ϫ1 ) was calculated from FBF (ml/min) and local MAP (mmHg). The percent recovery in FVC during inflation was calculated as (steady-state inflation ϩ exercise value Ϫ nadir)/ [steady-state exercise (control) value Ϫ nadir] ϫ 100. In protocol 1, COX inhibition alone did not reduce the %FVC recovery compared with the control (no drug) trial (92 Ϯ 11 vs. 100 Ϯ 10%, P ϭ 0.83). However, combined COX-nitric oxide synthase (NOS) inhibition caused a substantial reduction in %FVC recovery (54 Ϯ 8%, P Ͻ 0.05 vs. Ketorolac alone). In protocol 2, the percent recovery in FVC was attenuated with NOS inhibition alone (69 Ϯ 9 vs. 107 Ϯ 10%, P Ͻ 0.01) but not attenuated further during combined NOS-COX inhibition (62 Ϯ 10%, P ϭ 0.74 vs. L-NMMA alone). Our data indicate that PGs are not obligatory to the compensatory dilation observed during forearm exercise with hypoperfusion.prostaglandins; blood flow; nitric oxide; vasodilation; exercise; hypoperfusion DURING ACUTE EXPERIMENTAL hypoperfusion, skeletal muscle blood flow is partially restored in the exercising forearm through local dilator mechanisms and/or a myogenic response (4, 5). Along these lines, nitric oxide synthase (NOS) inhibition blunts the magnitude of restoration of forearm blood flow (FBF) and vascular conductance (FVC) during exercise with acute hypoperfusion by 10 -20% (4). The fact that a substantial flow restoration still occurs despite NOS inhibition suggests that additional vasodilator signals are likely involved in this response.In general, prostaglandins (PGs) do not appear to contribute significantly to the exercise hyperemic response to dynamic contractions (9,16,20,29,31). These findings are based on little to no change in muscle blood flow following PG synthesis inhibition. However, PGs have been reported to be involved in the regulation of skeletal muscle ...

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Section: Restoration Of Flow Via Local Vasodilator Mechanismscontrasting

confidence: 57%

Section: Data Analysis and Statisticsmentioning

confidence: 99%

Prostaglandins do not contribute to the nitric oxide-mediated compensatory vasodilation in hypoperfused exercising muscle

Casey

Joyner

2011

American Journal of Physiology-Heart and Circulatory Physiology

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“…These sensory neurons project to the central nervous system, eliciting a reflex pressor response consisting of increases in efferent sympathetic nerve activity (SNA), mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), plasma levels of vasoactive hormones, and peripheral vasoconstriction termed the muscle metaboreflex (MMR) (1, 2, 8, 12, 14, 19, 21, 25-28, 30, 32, 33, 35-38, 42, 44). These mechanisms act in concert to partially restore blood flow and arterial oxygen delivery to the hypoperfused muscles (27,31). Previous studies have shown that in normal dogs exercising at mild and moderate workloads, the increases in MAP elicited by this MMR activation are mainly due to increases in CO.…”

mentioning

confidence: 99%

Muscle metaboreflex control of ventricular contractility during dynamic exercise

Sala‐Mercado¹,

Hammond²,

Kim³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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When oxygen delivery to active skeletal muscle is insufficient for the metabolic demands, afferent nerves within muscles are activated, which elicit reflex increases in heart rate (HR), cardiac output (CO), and arterial pressure (AP), termed the muscle metaboreflex (MMR). To what extent the increases in CO are the result of increased ventricular contractility is unclear. A widely accepted index of contractility is maximal left ventricular elastance (Emax), the slope of the end-systolic pressure-volume relationship, such as during rapidly imposed reductions in preload. The objective of the present study was to determine whether MMR activation elicits increases in Emax. Experiments were performed using conscious dogs chronically instrumented to measure left ventricular pressure and volume at rest and during mild or moderate treadmill exercise with and without partial hindlimb ischemia to elicit MMR responses. At both workloads, MMR activation significantly increased CO, HR, AP, and maximum rate of change of left ventricular pressure. During both mild and moderate exercise, MMR activation increased Emax to 159.6 Ϯ 8.83 and 155.8 Ϯ 6.32% of the exercise value under free-flow conditions, respectively. We conclude that the increase of ventricular elastance associated with MMR activation indicates that a substantial increase in ventricular contractility contributes to the rise in CO during dynamic exercise. elastance; pressor response; cardiac function DURING DYNAMIC EXERCISE, when oxygen delivery to active skeletal muscle is insufficient to meet the metabolic demands, metabolites (e.g., lactic acid, adenosine, potassium, diprotonated phosphate, H ϩ , arachidonic acid products, and others) accumulate within the active muscle and stimulate group III and IV afferent neurons. These sensory neurons project to the central nervous system, eliciting a reflex pressor response consisting of increases in efferent sympathetic nerve activity (SNA), mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), plasma levels of vasoactive hormones, and peripheral vasoconstriction termed the muscle metaboreflex (MMR) (1, 2, 8, 12, 14, 19, 21, 25-28, 30, 32, 33, 35-38, 42, 44). These mechanisms act in concert to partially restore blood flow and arterial oxygen delivery to the hypoperfused muscles (27,31). Previous studies have shown that in normal dogs exercising at mild and moderate workloads, the increases in MAP elicited by this MMR activation are mainly due to increases in CO. The rise in CO likely results from increases in ventricular performance, HR, and central blood volume mobilization (26, 35). In this way the MMR-induced increases in ventricular performance act to sustain or slightly increase stroke volume (SV) despite decreases in ventricular filling time due to the reflex tachycardia (2, 26, 44). Furthermore, O'Leary an Augustyniak (26) showed that in normal dogs in which HR was fixed at 225 beats/min during mild exercise, MMR activation caused such a rise in SV that the increases in CO were approximately equal to t...

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“…This reflex response consists of increases in efferent sympathetic nerve activity (SNA) and mean arterial pressure (MAP) (1, 3, 11, 17, 18, 24, 31-35, 39, 40, 43, 46, 47, 52, 53). In addition, MMR activation causes increases in cardiac output (CO), heart rate (HR), and plasma levels of vasoactive hormones and produces vasoconstriction in the renal and the nonischemic active skeletal muscle vasculature to partially restore arterial O 2 delivery and blood flow to the hypoperfused muscles (25,33,36). The rise in CO likely results from increases in ventricular performance, HR, and central blood volume mobilization (32,42,43).…”

mentioning

confidence: 99%

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

Sala‐Mercado¹,

Hammond²,

Kim³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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DS. Heart failure attenuates muscle metaboreflex control of ventricular contractility during dynamic exercise. Am J Physiol Heart Circ Physiol 292: H2159 -H2166, 2007. First published December 22, 2006; doi:10.1152/ajpheart.01240.2006.-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 (E max) 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, E max, 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, E max and PRSW did not change. In addition, MMR activation caused no significant change in CO, E max, 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. pressor response; elastance; preload recruitable stroke work WHEN EXERCISING SKELETAL MUSCLE does not receive sufficient blood flow to meet the ongoing metabolic demands, by-products of metabolism such as lactic acid, H ϩ , adenosine, potassium, diprotonated phosphate, and arachidonic acid products, among others, accumulate within the muscle and stimulate group III and IV afferent neurons, which evokes a reflex response known as the muscle metaboreflex (MMR). This reflex response consists of increases in efferent sympathetic nerve activity (SNA) and mean arterial pressure (MAP) (1, 3, 11, 17, 18, 24, 31-35, 39, 40, 43, 46, 47, 52, 53). In addition, MMR activation causes increases in cardiac output (CO), heart rate (HR), and plasma levels of vasoactive hormones and produces vasoconstriction in the renal and the nonischemic active skeletal muscle vasculature to partially restore arterial O 2 delivery and blood flow to the hypoperfused muscles (25,33,36). The rise in CO likely results from increases in ventricular performance, HR, and central blood volume mobilization (32,42,43). By this means the MMR-induced increases in ventricular performance act to slightly increase or sustain stroke volume (SV) despite decreas...

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Is the muscle metaboreflex important in control of blood flow to ischemic active skeletal muscle in dogs?

Cited by 76 publications

References 0 publications

Prostaglandins do not contribute to the nitric oxide-mediated compensatory vasodilation in hypoperfused exercising muscle

Prostaglandins do not contribute to the nitric oxide-mediated compensatory vasodilation in hypoperfused exercising muscle

Muscle metaboreflex control of ventricular contractility during dynamic exercise

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

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