Duscha Brian D, Schulze P Christian, Robbins Jennifer L, Forman Daniel E
Duke University Medical Center, Box 3022, Durham, NC 27710, USA.
Heart Fail Rev. 2008 Feb;13(1):21-37. doi: 10.1007/s10741-007-9056-8.
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.
慢性心力衰竭(CHF)的病理生理学通常根据心脏功能障碍来进行概念化理解。然而,外周血流和骨骼肌内在特性的改变现在也被认为是运动不耐受的机制,而治疗性运动可以对其进行改善。本综述聚焦于心力衰竭导致的血液输送、氧提取和利用。还讨论了炎症的相关特征、骨骼肌信号通路的变化以及骨骼肌萎缩的易感性。特别关注灌注和骨骼肌特性影响运动不耐受的方式,以及运动训练后外周改善如何提高有氧运动能力。我们还指出了文献中的空白,这些空白可能构成进一步研究的重点。