Institute for Experimental Medical Research, Oslo University Hospital, Ullevaal, Oslo, Norway.
Heart Fail Rev. 2012 May;17(3):421-36. doi: 10.1007/s10741-011-9289-4.
Chronic heart failure (CHF) patients frequently experience impaired exercise tolerance due to skeletal muscle fatigue. Studies suggest that this in part is due to intrinsic alterations in skeletal muscle of CHF patients, often interpreted as a disease-specific myopathy. Knowledge about the mechanisms underlying these skeletal muscle alterations is of importance for the pathophysiological understanding of CHF, therapeutic approach and rehabilitation strategies. We here critically review the evidence for skeletal muscle alterations in CHF, the underlying mechanisms of such alterations and how skeletal muscle responds to training in this patient group. Skeletal muscle characteristics in CHF patients are very similar to what is reported in response to chronic obstructive pulmonary disease (COPD), detraining and deconditioning. Furthermore, skeletal muscle alterations observed in CHF patients are reversible by training, and skeletal muscle of CHF patients seems to be at least as trainable as that of matched controls. We argue that deconditioning is a major contributor to the skeletal muscle dysfunction in CHF patients and that further research is needed to determine whether, and to what extent, the intrinsic skeletal muscle alterations in CHF represent an integral part of the pathophysiology in this disease.
慢性心力衰竭（CHF）患者常常由于骨骼肌疲劳而导致运动耐力受损。研究表明，这在一定程度上是由于 CHF 患者骨骼肌的内在改变，通常被解释为一种特定于疾病的肌病。了解这些骨骼肌改变的机制对于 CHF 的病理生理理解、治疗方法和康复策略非常重要。我们在这里批判性地回顾了 CHF 患者骨骼肌改变的证据，这些改变的潜在机制以及骨骼肌在该患者群体中对训练的反应。CHF 患者的骨骼肌特征与慢性阻塞性肺疾病（COPD）、脱训和失健的报道非常相似。此外，CHF 患者的骨骼肌改变可以通过训练来逆转，而且 CHF 患者的骨骼肌似乎至少和匹配的对照组一样可训练。我们认为，失健是 CHF 患者骨骼肌功能障碍的主要原因，需要进一步研究确定 CHF 中的内在骨骼肌改变是否以及在何种程度上代表该疾病病理生理的一个组成部分。
