Oxidative capacity of the skeletal muscle and lactic acid kinetics during exercise in normal subjects and in patients with COPD
Oxidative capacity of the skeletal muscle and lactic acid kinetics during exercise in normal subjects and in patients with COPD
复制标题
DOI：
10.1164/ajrccm.153.1.8542131
复制
发表时间：
1996-01-01
影响因子：
24.7
通讯作者：
Janvier, R
中科院分区：
文献类型：
--
作者：
Maltais, F;Simard, AA;Janvier, R
在慢性阻塞性肺疾病（COPD）中已报告了运动期间的早期乳酸酸中毒和骨骼肌功能异常，但尚未评估这两种异常之间的可能关系。本研究的目的是比较9名COPD患者（年龄= 62 ± 5岁，平均值± SD，FEV（1）为预测值的40 ± 9%）和9名年龄相似的正常受试者（54 ± 3岁）在运动过程中动脉乳酸（La）的增加与骨骼肌的氧化能力之间的相关性。股外侧肌经皮活检后，每个受试者进行逐步运动试验的ergocycle他或她的最大能力，在此期间，5呼吸平均耗氧量（VO 2），并获得一系列的La浓度测量。从肌肉活检标本，两种氧化酶，柠檬酸合酶（CS）和3-羟酰辅酶A脱氢酶（HADH），和三个糖酵解酶，乳酸脱氢酶，己糖激酶，磷酸果糖激酶的活性进行了测定。运动期间的La/VO 2关系由La = a + B（VO 2）形式的指数函数拟合，其中B表示关系的形状。COPD患者的氧化酶活性明显低于对照组（CS为22.8 +/- 3.3对36.8 +/- 8.6 μ mol/min/g肌肉，HADH为3.1 +/- 1.1对5.5 +/- 1.4 μ mol/min/g，p < 0.0005），COPD患者乳酸的增加更陡（B = 4.3 +/- 2.0，而正常受试者为2.1 +/- 0.2，p = 0.0005）。CS、HADH和B之间呈显著负相关。两组糖酵解酶无差异。我们的结论是，在慢性阻塞性肺疾病的增加，在运动过程中动脉La是过度的，骨骼肌的氧化能力降低，这两个结果是相互关联的。
Early lactic acidosis during exercise and abnormal skeletal muscle function have been reported in chronic obstructive pulmonary disease (COPD) but a possible relationship between these two abnormalities has not been evaluated. The purpose of this study was to compare and correlate the increase in arterial lactic acid (La) during exercise and the oxidative capacity of the skeletal muscle in nine COPD patients (age = 62 +/- 5 yr, mean +/- SD, FEV(1) 40 +/- 9% of predicted) and in nine normal subjects of similar age (54 +/- 3 yr). Following a transcutaneous biopsy of the vastus lateralis, each subject performed a stepwise exercise test on an ergocycle up to his or her maximal capacity during which 5-breath averages of oxygen consumption (VO2), and serial La concentration measurements were obtained. From the muscle biopsy specimen, the activity of two oxidative enzymes, citrate synthase (CS) and 3-hydroxyacyl CoA dehydrogenase (HADH), and of three glycolytic enzymes, lactate dehydrogenase, hexokinase, and phosphofructokinase were determined. The La/VO2 relationship during exercise was fitted by an exponential function in the form La = a + b(VO2), where b represents the shape of the relationship. The activity of the oxidative enzymes was significantly lower in COPD than in control subjects (22.8 +/- 3.3 versus 36.8 +/- 8.6 mu mol/min/g muscle for CS, and 3.1 +/- 1.1 versus 5.5 +/- 1.4 mu mol/min/g for HADH, p < 0.0005) and the increase in lactic acid was steeper in COPD (b = 4.3 +/- 2.0 versus 2.1 +/- 0.2 for normal subjects, p = 0.0005). A significant inverse relationship was found between CS, HADH, and b. No difference was found between the two groups for the glycolytic enzymes. We conclude that in COPD the increase in arterial La during exercise is excessive, the oxidative capacity of the skeletal muscle is reduced, and that these two results are interrelated.