Engelen Mariëlle P K J, Schols Annemie M W J
Department of Pulmonology, University Hospital Maastricht, PO Box 5800, 6202 AZ Maastricht, The Netherlands.
Curr Opin Clin Nutr Metab Care. 2003 Jan;6(1):73-8. doi: 10.1097/00075197-200301000-00011.
Wasting of muscle mass, commonly present in patients with chronic obstructive pulmonary disease, is a complex process involving changes in the control of intermediary metabolism as well as in muscle cell status. Although research exploring intermediary metabolism in chronic obstructive pulmonary disease is still in its infancy, there is an increased interest in a potential role for amino acids in modulating muscle anabolism. This review aims at summarizing and critically evaluating the available clinical studies examining alterations in amino acid profile in plasma and skeletal muscle of patients with chronic obstructive pulmonary disease.
All studies show pronounced alterations in plasma and muscle amino acid status in patients with chronic obstructive pulmonary disease but no consistent "disease specific" pattern for most amino acids. Variability is likely influenced by the heterogeneity of the disease with respect to lung function and nutritional state. Nevertheless, general consistency exists in chronic obstructive pulmonary disease with respect to (1) a reduced plasma branched-chain amino acid level, and (2) a decreased muscle glutamate concentration. Alterations in branched-chain amino acid metabolism appear to be influenced by the degree of muscle wasting, while the reduction in muscle glutamate is related to the diffusing capacity as a hallmark of emphysema. The reduction in glutamate status is associated with reduced muscle glutathione levels and appears to be linked to enhanced glycolysis as evidenced from an accelerated increase in plasma lactate during exercise.
Underlying mechanisms of the observed alterations in amino acid profile in chronic obstructive pulmonary disease, and the influences of disease associated mediators such as chronic low-grade inflammation and (chronic and intermittent) hypoxia are speculative and need to be explored in experimental study designs.
肌肉质量消耗常见于慢性阻塞性肺疾病患者中，这是一个复杂的过程，涉及中间代谢控制以及肌肉细胞状态的变化。尽管探索慢性阻塞性肺疾病中间代谢的研究仍处于起步阶段，但人们对氨基酸在调节肌肉合成代谢中的潜在作用兴趣日益增加。本综述旨在总结和批判性评估现有的临床研究，这些研究考察了慢性阻塞性肺疾病患者血浆和骨骼肌中氨基酸谱的变化。
所有研究均显示慢性阻塞性肺疾病患者血浆和肌肉氨基酸状态有显著改变，但大多数氨基酸没有一致的“疾病特异性”模式。这种变异性可能受疾病在肺功能和营养状态方面的异质性影响。然而，慢性阻塞性肺疾病在以下方面存在总体一致性：（1）血浆支链氨基酸水平降低；（2）肌肉谷氨酸浓度降低。支链氨基酸代谢的改变似乎受肌肉消耗程度的影响，而肌肉谷氨酸的减少与作为肺气肿标志的弥散能力有关。谷氨酸状态的降低与肌肉谷胱甘肽水平降低有关，并且似乎与糖酵解增强有关，运动期间血浆乳酸加速增加证明了这一点。
慢性阻塞性肺疾病中观察到的氨基酸谱改变的潜在机制，以及疾病相关介质如慢性低度炎症和（慢性和间歇性）缺氧的影响尚属推测，需要在实验研究设计中进行探索。
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