Muscle reflex in heart failure: the role of exercise training
- Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE, USA
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.
Keywords: physical training, myocardial infarction, muscle afferents, exercise, sympathetic nerve activity
Citation: Wang H-J, Zucker IH and Wang W (2012) Muscle reflex in heart failure: the role of exercise training. Front. Physio. 3:398. doi: 10.3389/fphys.2012.00398
Received: 07 June 2012; Paper pending published: 23 July 2012;
Accepted: 20 September 2012; Published online: 05 October 2012.
Edited by:Paul J. Fadel, University of Missouri, USA
Reviewed by:Robert A. Augustyniak, Oakland University William Beaumont School of Medicine, USA
Scott A. Smith, University of Texas Southwestern Medical Center at Dallas, USA
Copyright © 2012 Wang, Zucker and Wang. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and subject to any copyright notices concerning any third-party graphics etc.
*Correspondence: Wei Wang, Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE 68198-5850, USA. e-mail: email@example.com