Review Article
Aerobic Exercise and Pharmacological Therapies for Skeletal Myopathy in Heart Failure: Similarities and Differences
Figure 1
Effects of β-adrenergic receptor activation in skeletal muscle. In skeletal muscle, sympathetic activity is mediated mainly by -adrenergic receptors (-ARs) and leads to beneficial acute and chronic effects on muscle metabolism, function, and mass. In this sense, keeping -ARs signaling in early stage HF might be reasonable since it can delay skeletal myopathy. In contrast, long-term and sustained sympathetic hyperactivity (figure inset) in severe heart failure exerts toxic effects on skeletal muscles leading to -AR desensitization/downregulation and loss of function, which will further aggravate skeletal myopathy. In this case, the use of selective (acting on -AR) versus nonselective (acting on both -AR and -AR) β-blockers to counteract skeletal myopathy needs further investigation. Akt: protein kinase B, Atrogin-1/MAFbx: muscle atrophy F-box protein, MuRF-1: muscle RING-finger protein-1, FoxO: forkhead family of transcription factors, and mTOR: mammalian target of rapamycin.