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- W2899768129 abstract "Abstract Skeletal muscle dysfunction in chronic heart failure (CHF) contributes to exercise intolerance and activation of the sympathetic nervous system. Exercise training has been advocated for patients with CHF and has been shown to improve quality of life and longevity. While enhanced protein degradation and oxidative stress contributes to this dysfunction exercise training of patients with CHF can reverse many of these abnormalities. The so-called “Exercise Pressor Reflex” (EPR) contributes to enhanced sympatho-excitation in CHF. This chapter discusses the mechanisms that contribute to increased sensitivity of the EPR and its reduction following exercise training. In this chapter, we provide the experimental evidence that group III skeletal muscle afferent neurons are primarily responsible for this sensitization. This sensitization may be due to enhanced purinergic signaling and increased oxidative stress. Importantly, exercise training reduces the EPR sensitivity, in part, by upregulation of the Transient Receptor Potential Vanilloid 1 receptor (TRPV1) and downregulation of P2X3 receptors in skeletal muscle of animals with CHF." @default.
- W2899768129 created "2018-11-16" @default.
- W2899768129 creator A5030477066 @default.
- W2899768129 creator A5085052851 @default.
- W2899768129 creator A5089415637 @default.
- W2899768129 date "2019-01-01" @default.
- W2899768129 modified "2023-09-26" @default.
- W2899768129 title "Sympatho-Excitation in Heart Failure" @default.
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