Evangelismos Hospital, National and Kapodistrian University of Athens, Dept of Critical Care Medicine and Pulmonary Services, Pulmonary Rehabilitation Centre, Athens, Greece.
Eur Respir J. 2010 Aug;36(2):301-10. doi: 10.1183/09031936.00112909. Epub 2010 Jan 28.
It is known that non-cachectic patients with chronic obstructive pulmonary disease (COPD) respond well to pulmonary rehabilitation, but whether cachectic COPD patients are capable of adaptive responses is both important and unknown. 10 cachectic and 19 non-cachectic COPD patients undertook high-intensity cycling training, at the same relative intensity, for 45 min x day(-1), 3 days x week(-1) for 10 weeks. Before and after rehabilitation vastus lateralis muscle biopsies were analysed morphologically and for the expression of muscle remodelling factors (insulin-like growth factor (IGF)-I, myogenic differentiation factor D (MyoD), tumour necrosis factor (TNF)-alpha, nuclear factor (NF)-kappaB and myostatin) and key components of ubiquitin-mediated proteolytic systems (muscle ring finger protein (MURF)-1 and Atrogin-1). Rehabilitation improved peak work-rate and the 6-min walk distance similarly in non-cachectic (18+/-3% and 42+/-13 m, respectively) and cachectic (16+/-2% and 53+/-16 m, respectively) patients, but quality of life only improved in non-cachectic COPD. Mean muscle fibre cross-sectional area increased in both groups, but significantly less in cachectic (7+/-2%) than in non-cachectic (11+/-2%) patients. Both groups equally decreased the proportion of type IIb fibres and increased muscle capillary/fibre ratio. IGF-I mRNA expression increased in both groups, but IGF-I protein levels increased more in non-cachectic COPD. MyoD was upregulated, whereas myostatin was downregulated at the mRNA and protein level only in non-cachectic patients. Whilst rehabilitation had no effect on TNF-alpha expression, it decreased the activation of the transcription factor NF-kappaB in both groups by the same amount. Atrogin-1 and MURF-1 expression were increased in cachectic COPD, but it was decreased in non-cachectic patients. Cachectic COPD patients partially retain the capacity for peripheral muscle remodelling in response to rehabilitation and are able to increase exercise capacity as much as those without cachexia, even if they exhibit both quantitative and qualitative differences in the type of muscle fibre remodelling in response to exercise training.
已知非恶病质慢性阻塞性肺疾病（COPD）患者对肺康复反应良好，但恶病质 COPD 患者是否能够适应这种反应既重要又未知。10 名恶病质和 19 名非恶病质 COPD 患者接受了高强度的循环训练，在相同的相对强度下，每天进行 45 分钟 x 1 次，每周进行 3 天 x 1 次，共进行 10 周。在康复前后，对股外侧肌进行了组织学分析，并检测了肌肉重塑因子（胰岛素样生长因子（IGF）-I、成肌分化因子 D（MyoD）、肿瘤坏死因子（TNF）-α、核因子（NF）-κB 和肌肉生长抑制素）和泛素介导的蛋白水解系统的关键成分（肌肉环指蛋白（MURF）-1 和 Atrogin-1）的表达。康复同样改善了非恶病质（分别增加 18+/-3%和 42+/-13 米）和恶病质（分别增加 16+/-2%和 53+/-16 米）患者的峰值工作率和 6 分钟步行距离，但只有非恶病质 COPD 患者的生活质量得到改善。两组患者的平均肌纤维横截面积均增加，但恶病质患者的增加幅度明显小于非恶病质患者（分别为 7+/-2%和 11+/-2%）。两组患者均减少了 IIb 型纤维的比例，增加了肌肉毛细血管/纤维比。两组 IGF-I mRNA 表达均增加，但非恶病质 COPD 患者的 IGF-I 蛋白水平增加更多。MyoD 在两组中的表达均上调，而肌肉生长抑制素在非恶病质患者中的 mRNA 和蛋白水平下调。虽然康复对 TNF-α的表达没有影响，但它使两组 NF-κB 的转录因子的激活量减少相同。Atrogin-1 和 MURF-1 在恶病质 COPD 中表达增加，但在非恶病质患者中表达减少。恶病质 COPD 患者对康复有一定的外周肌肉重塑能力，能够像没有恶病质的患者一样，增加运动能力，尽管他们在对运动训练的肌肉纤维重塑类型上表现出数量和质量上的差异。
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