title: Implications of chronic heart failure on peripheral vasculature and skeletal muscle before and after exercise training.
abstract: The pathophysiology of chronic heart failure (CHF) is typically conceptualized in terms of cardiac dysfunction. However, alterations in peripheral blood flow and intrinsic skeletal muscle properties are also now recognized as mechanisms for exercise intolerance that can be modified by therapeutic exercise. This overview focuses on blood delivery, oxygen extraction and utilization that result from heart failure. Related features of inflammation, changes in skeletal muscle signaling pathways, and vulnerability to skeletal muscle atrophy are discussed. Specific focus is given to the ways in which perfusion and skeletal muscle properties affect exercise intolerance and how peripheral improvements following exercise training increase aerobic capacity. We also identify gaps in the literature that may constitute priorities for further investigation.
authors.affiliation: Duke University Medical Center, Box 3022, Durham, NC 27710, USA. Dusch001@mc.duke.edu
authors.forename: Brian D
authors.initials: BD
authors.lastname: Duscha
authors.forename: P Christian
authors.initials: PC
authors.lastname: Schulze
authors.forename: Jennifer L
authors.initials: JL
authors.lastname: Robbins
authors.forename: Daniel E
authors.initials: DE
authors.lastname: Forman
mesh_terms: D000818:Animals; D017209:Apoptosis; D002908:Chronic Disease; D015444:Exercise / Q000502:physiology*; D005081:Exercise Therapy; D017079:Exercise Tolerance; D006333:Heart Failure / Q000503:physiopathology* / Q000534:rehabilitation*; D006439:Hemodynamics; D006801:Humans; D007249:Inflammation; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D007866:Leg / Q000098:blood supply* / Q000502:physiology; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000502:physiology; D010101:Oxygen Consumption; D012039:Regional Blood Flow / Q000502:physiology; D015398:Signal Transduction
chemical_list: D007334:Insulin-Like Growth Factor I