Skeletal muscle adaptation to endurance training in patients with chronic obstructive pulmonary disease
Skeletal muscle adaptation to endurance training in patients with chronic obstructive pulmonary disease
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DOI：
10.1164/ajrccm.154.2.8756820
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发表时间：
1996-08-01
影响因子：
24.7
通讯作者：
Belleau, R
中科院分区：
文献类型：
--
作者：
Maltais, F;LeBlanc, P;Belleau, R
本研究的目的是通过观察骨骼肌酶活性的变化来评估中度至重度气流阻塞患者对耐力训练的生理反应。11名患者（年龄= 65 ± 7岁，平均值± SD，FEV（1）= 36 ± 11%的预测值，范围= 24 - 54%）在耐力训练计划前后进行了评估。每次评估均包括股外侧肌经皮活检和逐步运动试验，运动试验以达到他/她的最大能力。在运动试验中测定VE、VO 2、VCO 2和连续动脉血乳酸浓度。两种氧化酶，柠檬酸合成酶（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。训练包括30分钟的运动课程上校准的ergocycle，每周3次，12周。有氧能力在基线时严重降低（VO（2）max = 54 +/- 12%的预测值），训练后增加了14%（p < 0.05）。对于相同的运动负荷，训练后VE（34.5 +/- 10.0 vs 31.9 +/- 9.0 L/min，p < 0.05）和动脉乳酸浓度（3.4 +/- 1.3 vs 2.8 +/- 0.9 mmol/L，p < 0.01）显著降低。乳酸阈也在训练后增加（p < 0.01），而三种糖酵解酶的活性在两次评估时相似。相比之下，CS和HADH的活性在训练后显著增加（CS为22.3 +/- 3.5对25.8 +/- 3.8 μ mol/min/g肌肉，p < 0.05，HADH为5.5 +/- 2.9对7.7 +/- 2.5 μ mol/min/g肌肉，p < 0.01）。CS和HADH活性的百分比变化与运动期间动脉乳酸的百分比变化之间存在显著的负相关关系（p = 0.01）。我们的结论是，耐力训练可以减少运动诱导的乳酸酸中毒，提高骨骼肌氧化能力的中度至重度慢性阻塞性肺疾病（COPD）患者。
The purpose of this study was to evaluate the physiologic responses to endurance training in patients with moderate to severe airflow obstruction by specifically looking at changes in skeletal muscle enzymatic activities. Eleven patients (age = 65 +/- 7 yr, mean +/- SD, FEV(1) = 36 +/- 11% of predicted value, range = 24 to 54%) were evaluated before and after an endurance training program. Each evaluation included a percutaneous biopsy of the vastus lateralis and a stepwise exercise test on an ergocycle up to his/her maximal capacity. VE, VO2, VCO2, and serial arterial lactic acid concentration were measured during the exercise test. 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 was determined. The training consisted of 30-min exercise sessions on a calibrated ergocycle, 3 times a week for 12 wk. The aerobic capacity was severely reduced at baseline (VO(2)max = 54 +/- 12% of predicted) and increased by 14% after training (p < 0.05). For an identical exercise workload, there was a significant reduction in VE (34.5 +/- 10.0 versus 31.9 +/- 9.0 L/min, p < 0.05) and in arterial lactic acid concentration (3.4 +/- 1.3 versus 2.8 +/- 0.9 mmol/L, p < 0.01) after training. The lactate threshold also increased after training (p < 0.01) while the activity of the three glycolytic enzymes was similar at the two evaluations. In contrast, the activity of CS and HADH increased significantly after training (22.3 +/- 3.5 versus 25.8 +/- 3.8 mu mol/min/g muscle for CS, p < 0.05, and 5.5 +/- 2.9 versus 7.7 +/- 2.5 mu mol/min/g for HADH, p < 0.01). A significant inverse relationship was found between the percent changes in the activity of CS and HADH, and the percent changes in arterial lactic acid during exercise (p = 0.01). We conclude that endurance training can reduce exercise-induced lactic acidosis and improve skeletal muscle oxidative capacity in patients with moderate to severe chronic obstructive pulmonary disease (COPD).