Hambrecht R, Niebauer J, Fiehn E, Kälberer B, Offner B, Hauer K, Riede U, Schlierf G, Kübler W, Schuler G
St. Vincentius-Krankenhäuser Karlsruhe, Abteilung III-Kardiologie, Germany.
J Am Coll Cardiol. 1995 May;25(6):1239-49. doi: 10.1016/0735-1097(94)00568-B.
The present study was designed to evaluate the effect of an ambulatory training program on ultrastructural morphology and the oxidative capacity of skeletal muscle and its relation to central and peripheral hemodynamic variables in patients with chronic heart failure.
Clinical evidence supports the hypothesis that exercise intolerance in patients with chronic heart failure is not only a consequence of low cardiac output, but is also a result of alterations in oxidative metabolism of skeletal muscle.
Twenty-two patients were prospectively randomized either to a training group (mean [+/-SD] ejection fraction 26 +/- 9%, n = 12) participating in an ambulatory training program or to a physically inactive control group (ejection fraction 27 +/- 10%, n = 10). At baseline and after 6 months, patients underwent symptom-limited bicycle exercise testing, and central and peripheral hemodynamic variables were measured. Percutaneous needle biopsy samples of the vastus lateralis muscle were obtained at baseline and after 6 months. The ultrastructure of skeletal muscle was analyzed by ultrastructural morphometry.
After 6 months, patients in the training group achieved an increase in oxygen uptake at the ventilatory threshold of 23% (from 0.86 +/- 0.2 to 1.07 +/- 0.2 liters/min, p < 0.01 vs. control group) and at peak exercise of 31% (from 1.49 +/- 0.4 to 1.95 +/- 0.4 liters/min, p < 0.01 vs. control group). There was no significant change in oxygen uptake at the ventilatory threshold and at peak exercise in the control group. The total volume density of mitochondria and volume density of cytochrome c oxidase-positive mitochondria increased significantly by 19% (from 4.7 +/- 1.5 to 5.6 +/- 1.5 vol%, p < 0.05 vs. control group) and by 41% (from 2.2 +/- 1.0 to 3.1 +/- 1.0 vol%, p < 0.05 vs. control group) after 6 months of regular physical exercise. Cardiac output at rest and at submaximal exercise remained unchanged but increased during maximal symptom-limited exercise from 11.9 +/- 4.0 to 14.1 +/- 3.3 liters/min in the training group (p < 0.05 vs. baseline; p = NS vs. control group). Peak leg oxygen consumption increased significantly by 45% (from 510 +/- 172 to 740 +/- 254 ml/min, p < 0.01 vs. control group). Changes in cytochrome c oxidase-positive mitochondria were significantly related to changes in oxygen uptake at the ventilatory threshold (r = 0.82, p < 0.0001) and at peak exercise (r = 0.87, p < 0.0001).
Regular physical training increases maximal exercise tolerance and delays anaerobic metabolism during submaximal exercise in patients with stable chronic heart failure. Improved functional capacity is closely linked to an exercise-induced increase in the oxidative capacity of skeletal muscle.
本研究旨在评估门诊训练计划对慢性心力衰竭患者骨骼肌超微结构形态、氧化能力的影响，及其与中心和外周血流动力学变量的关系。
临床证据支持这样的假设，即慢性心力衰竭患者运动不耐受不仅是心输出量降低的结果，也是骨骼肌氧化代谢改变的结果。
22例患者被前瞻性随机分为训练组（平均[±标准差]射血分数26±9%，n = 12），参加门诊训练计划，或不运动的对照组（射血分数27±10%，n = 10）。在基线和6个月后，患者进行症状限制的自行车运动试验，并测量中心和外周血流动力学变量。在基线和6个月后获取股外侧肌的经皮针刺活检样本。通过超微结构形态计量学分析骨骼肌的超微结构。
6个月后，训练组患者在通气阈值时的摄氧量增加了23%（从0.86±0.2升至1.07±0.2升/分钟，与对照组相比p < 0.01），在峰值运动时增加了31%（从1.49±0.4升至1.95±0.4升/分钟，与对照组相比p < 0.01）。对照组在通气阈值和峰值运动时的摄氧量无显著变化。定期体育锻炼6个月后，线粒体的总体积密度和细胞色素c氧化酶阳性线粒体的体积密度分别显著增加了19%（从4.7±1.5升至5.6±1.5体积%，与对照组相比p < 0.05）和41%（从2.2±1.0升至3.1±1.0体积%，与对照组相比p < 0.05）。训练组静息和次最大运动时的心输出量保持不变，但在最大症状限制运动时从11.9±4.0升至14.1±3.3升/分钟（与基线相比p < 0.05；与对照组相比p = 无显著性差异）。腿部峰值耗氧量显著增加了45%（从510±172升至740±254毫升/分钟，与对照组相比p < 0.01）。细胞色素c氧化酶阳性线粒体的变化与通气阈值时（r = 0.82，p < 0.0001）和峰值运动时（r = 0.87，p < 0.0001）的摄氧量变化显著相关。
规律的体育训练可提高稳定型慢性心力衰竭患者的最大运动耐力，并延迟次最大运动时的无氧代谢。功能能力的改善与运动诱导的骨骼肌氧化能力增加密切相关。
