Abstract
Heart failure with reduced ejection fraction is associated with increased exercise intolerance, morbidity, and mortality. Importantly, exercise intolerance in heart failure with reduced ejection fraction is a key factor limiting patient quality of life and survival. Exercise intolerance in heart failure with reduced ejection fraction stems from a multi-organ failure to maintain homeostasis at rest and during exercise, including the heart, skeletal muscle, and autonomic nervous system, lending itself to a system constantly trying to "catch-up". Hemodynamic control during exercise is regulated primarily by the autonomic nervous system, whose operation, in turn, is partly regulated via reflexive information from exercise-stimulated receptors throughout the body (e.g., arterial baroreflex, central and peripheral chemoreceptors, and the muscle metabo- and mechanoreflexes). Persons with heart failure with reduced ejection fraction exhibit malfunctioning autonomic reflexes, which lead to exaggerated sympathoexcitation and attenuated parasympathetic tone. Chronic elevation of sympathetic activity is associated with increased morbidity and mortality. In this review, we provide an overview of how each main exercise-related autonomic reflex is changed in heart failure with reduced ejection fraction, and the role of exercise training in attenuating or reversing the counterproductive changes.
Highlights
Chronic heart failure (HF) is a complex clinical syndrome [1] that 26 million people live with worldwide [2]
HF is characterized by severe exercise intolerance (i.e., low peak oxygen uptake (VO2)) [1,3,4,5,6,7,8,9], which limits daily activities, reduce quality of life [6], and increase the risk of adverse events in persons living with HF with reduced ejection fraction (HFrEF; EF ≤40%) [7,8]
Patients with HFrEF exhibit blunted muscle vasodilation during both central and peripheral chemoreflex activation compared to controls, likely attributable to the greater increase in muscle sympathetic nerve activity (MSNA) observed in the patients [12]
Summary
Chronic heart failure (HF) is a complex clinical syndrome [1] that 26 million people live with worldwide [2]. Patients with HFrEF classically have impaired cardiac output control and increased sympathetic outflow to muscle, vasculature, and the renal system at rest [10,11,12,13,14,15] and in response to exercise [16,17,18,19]. The HFrEF syndrome entails both myocardial and autonomic dysfunction [20], with the latter factor being the focus of this review. We will discuss the pathways and mechanisms by which the autonomic nervous system controls our hemodynamic responses to exercise, including the exercise pressor reflex (muscle metaboreflex and muscle mechanoreflex), the arterial baroreflex, and the chemoreflexes (central and peripheral) in the situation of HFrEF, i.e., autonomic dysfunction
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