Goldstein S A, Thomashow B, Askanazi J
Clin Chest Med. 1986 Mar;7(1):141-51.
In conclusion, the weight loss in COPD is associated with hypermetabolism. Under these circumstances, caloric intake may be insufficient to meet increased metabolic demands, thereby contributing to progressive weight loss. This is in contrast to depleted surgical patients who have energy expenditures 5% below predicted. There is an increased VE in patients receiving a high-carbohydrate diet, secondary to an increased VCO2 that is similar to that seen in patients with neither COPD nor weight loss. Neither diet composition, whether high-carbohydrate or high-fat, nor refeeding have any effect on PaCO2. However, ventilatory drive does appear to be influenced by nutritional repletion. There was an increased sensitivity to PaCO2, independent of diet composition, during a high caloric intake. Respiratory and skeletal muscle function increased, particularly strength, endurance, and work efficiency, indicating that the increased metabolic demand can be well tolerated. It should be noted, however, that refeeding the COPD patient must be done as a preventive measure at the start of weight loss. Patients with long-term weight loss and end-stage COPD appear unable to tolerate any increase in metabolic demand; consequently, they cannot improve respiratory and skeletal muscle function through refeeding.
总之，慢性阻塞性肺疾病（COPD）患者体重减轻与高代谢有关。在这种情况下，热量摄入可能不足以满足增加的代谢需求，从而导致体重逐渐减轻。这与能量消耗比预测值低5%的外科术后营养缺乏患者形成对比。接受高碳水化合物饮食的患者通气量增加，这是由于二氧化碳排出量（VCO2）增加所致，这与既无COPD也未体重减轻的患者情况相似。饮食组成，无论是高碳水化合物还是高脂肪，以及再喂养对动脉血二氧化碳分压（PaCO2）均无影响。然而，通气驱动似乎受营养补充的影响。高热量摄入期间，对PaCO2的敏感性增加，且与饮食组成无关。呼吸和骨骼肌功能增强，尤其是力量、耐力和工作效率，这表明增加的代谢需求能够得到良好耐受。然而，应该注意的是，必须在COPD患者体重减轻开始时就采取再喂养措施作为预防手段。长期体重减轻且处于COPD终末期的患者似乎无法耐受任何代谢需求的增加；因此，他们无法通过再喂养改善呼吸和骨骼肌功能。
