Muscle reflex in heart failure: the role of exercise training

Han-Jun Wang,Irving H Zucker,Wei Wang

doi:10.3389/fphys.2012.00398

Abstract

Exercise evokes sympathetic activation and increases blood pressure and heart rate (HR). Two neural mechanisms that cause the exercise-induced increase in sympathetic discharge are central command and the exercise pressor reflex (EPR). The former suggests that a volitional signal emanating from central motor areas leads to increased sympathetic activation during exercise. The latter is a reflex originating in skeletal muscle which contributes significantly to the regulation of the cardiovascular and respiratory systems during exercise. The afferent arm of this reflex is composed of metabolically sensitive (predominantly group IV, C-fibers) and mechanically sensitive (predominately group III, A-delta fibers) afferent fibers. Activation of these receptors and their associated afferent fibers reflexively adjusts sympathetic and parasympathetic nerve activity during exercise. In heart failure, the sympathetic activation during exercise is exaggerated, which potentially increases cardiovascular risk and contributes to exercise intolerance during physical activity in chronic heart failure (CHF) patients. A therapeutic strategy for preventing or slowing the progression of the exaggerated EPR may be of benefit in CHF patients. Long-term exercise training (ExT), as a non-pharmacological treatment for CHF increases exercise capacity, reduces sympatho-excitation and improves cardiovascular function in CHF animals and patients. In this review, we will discuss the effects of ExT and the mechanisms that contribute to the exaggerated EPR in the CHF state.

Highlights

A hallmark of patients suffering from chronic heart failure (CHF) is exercise intolerance characterized by fatigue and shortness of breath during exercise (Francis, 1985; Cohn, 1990; Sullivan et al, 1990; Wilson, 1995)
In addition to vasoconstriction in skeletal muscle, hyperventilation is another consequence of the exaggerated exercise pressor reflex (EPR) during exercise, both of which accentuates the symptoms of exercise intolerance
In animal studies, using a decerebrate rat model, Smith et al (2003, 2005a,b) conducted a series of convincing experiments designed to examine EPR function in CHF and to determine the contribution of the muscle mechanoreflex and metaboreflex to the EPR in this disease. Their findings suggest (1) that the overactive cardiovascular response to exercise in CHF is mediated, in part, by an exaggerated EPR; (2) that the muscle metaboreflex is blunted and that the muscle mechanoreflex is enhanced in CHF; (3) that the mechanoreflex mediates the exaggerated EPR activity observed in CHF; (4) that the decreased sensitivity of group IV afferent neurons is important to the development of EPR hyperactivity

Summary

Introduction

A hallmark of patients suffering from chronic heart failure (CHF) is exercise intolerance characterized by fatigue and shortness of breath during exercise (Francis, 1985; Cohn, 1990; Sullivan et al, 1990; Wilson, 1995). Their findings suggest (1) that the overactive cardiovascular response to exercise in CHF is mediated, in part, by an exaggerated EPR; (2) that the muscle metaboreflex is blunted and that the muscle mechanoreflex is enhanced in CHF; (3) that the mechanoreflex mediates the exaggerated EPR activity observed in CHF; (4) that the decreased sensitivity of group IV afferent neurons is important to the development of EPR hyperactivity.

Results

Conclusion