Chronic heart failure: The role of exercise in the associated myopathy and angiogenesis of skeletal muscle

The pathophysiology of chronic heart failure (CHF) involves peripheral myopathy (PM), and skeletal muscle atrophy plays an important role in the muscle dysfunction and limited exercise capacity of patients with CHF. PM appears to be the determining factor of a variety of their symptoms, including dyspnea, severe muscle fatigue and decreased aerobic capacity. PM is associated with multiple functional, histological and molecular alterations in skeletal muscle, and decreased capillary density and activation of inflammation-related factors are observed in the skeletal muscle of patients with CHF. It is widely accepted that exercise induces angiogenesis and can promote the expression of both pro-and anti-inflammatory cytokines in skeletal muscle. Inflammation has been shown to have beneficial effects on skeletal muscle remodeling, by activating angiogenic and hypertrophic pathways in muscle tissue. This is a review of the potential role of exercise in CHF-induced peripheral myopathy. The pathogenetic mechanisms in PM are described, and the molecular interactions are delineated between the various factors and signaling pathways involved in the angiogenesis process and induced by exercise in the skeletal muscle of patients with CHF.