Adamopoulos S, Coats A J, Brunotte F, Arnolda L, Meyer T, Thompson C H, Dunn J F, Stratton J, Kemp G J, Radda G K
Cardiac Department, John Radcliffe Hospital, Oxford, London, England.
J Am Coll Cardiol. 1993 Apr;21(5):1101-6. doi: 10.1016/0735-1097(93)90231-o.
This study investigated the effects of physical training on skeletal muscle metabolism in patients with chronic heart failure.
Skeletal muscle metabolic abnormalities in patients with chronic heart failure have been associated with exercise intolerance. Muscle deconditioning is a possible mechanism for the intrinsic skeletal muscle metabolic changes seen in chronic heart failure.
We used phosphorus-31 nuclear magnetic resonance spectroscopy to study muscle metabolism during exercise in 12 patients with stable ischemic chronic heart failure undergoing 8 weeks of home-based bicycle exercise training in a randomized crossover controlled trial. Changes in muscle pH and concentrations of phosphocreatine and adenosine diphosphate (ADP) were measured in phosphorus-31 spectra of calf muscle obtained at rest, throughout incremental work load plantar flexion until exhaustion and during recovery from exercise. Results were compared with those in 15 age-matched control subjects who performed a single study only.
Before training, phosphocreatine depletion, muscle acidification and the increase in ADP during the 1st 4 min of plantar flexion exercise were all increased (p < 0.04) compared with values in control subjects. Training produced an increase (p < 0.002) in incremental plantar flexion exercise tolerance. After training, phosphocreatine depletion and the increase in ADP during exercise were reduced significantly (p < 0.003) at all matched submaximal work loads and at peak exercise, although there was no significant change in the response of muscle pH to exercise. After training, changes in ADP were not significantly different from those in control subjects, although phosphocreatine depletion was still greater (p < 0.05) in trained patients than in control subjects. The phosphocreatine recovery half-time was significantly (p < 0.05) shorter after training, although there was no significant change in the half-time of adenosine diphosphate recovery. In untrained subjects, the initial rate of phosphocreatine resynthesis after exercise (a measure of the rate of oxidative adenosine triphosphate [ATP] synthesis) and the inferred maximal rate of mitochondrial ATP synthesis were reduced compared with rates in control subjects (p < 0.003) and both were significantly increased (p < 0.05) by training, so that they were not significantly different from values in control subjects.
The reduction in phosphocreatine depletion and in the increase in ADP during exercise, and the enhanced rate of phosphocreatine resynthesis in recovery (which is independent of muscle mass) indicate that a substantial correction of the impaired oxidative capacity of skeletal muscle in chronic heart failure can be achieved by exercise training.
本研究调查了体育锻炼对慢性心力衰竭患者骨骼肌代谢的影响。
慢性心力衰竭患者的骨骼肌代谢异常与运动不耐受有关。肌肉失健是慢性心力衰竭中所见的骨骼肌内在代谢变化的一种可能机制。
在一项随机交叉对照试验中，我们使用磷-31核磁共振波谱法研究了12例稳定型缺血性慢性心力衰竭患者在进行为期8周的家庭自行车运动训练期间运动时的肌肉代谢。在静息状态、整个递增负荷足底屈曲直至力竭以及运动恢复期间，测量小腿肌肉磷-31波谱中的肌肉pH值、磷酸肌酸和二磷酸腺苷（ADP）浓度的变化。将结果与15名仅进行单次研究的年龄匹配对照受试者的结果进行比较。
训练前，与对照受试者相比，足底屈曲运动前4分钟内的磷酸肌酸消耗、肌肉酸化和ADP增加均有所增加（p<0.04）。训练使递增性足底屈曲运动耐力增加（p<0.002）。训练后，在所有匹配的次最大负荷和峰值运动时，运动期间的磷酸肌酸消耗和ADP增加均显著降低（p<0.003），尽管肌肉pH值对运动的反应没有显著变化。训练后，ADP的变化与对照受试者无显著差异，尽管训练患者的磷酸肌酸消耗仍高于对照受试者（p<0.05）。训练后磷酸肌酸恢复半衰期显著缩短（p<0.05），尽管二磷酸腺苷恢复半衰期没有显著变化。在未训练的受试者中，运动后磷酸肌酸再合成的初始速率（氧化三磷酸腺苷[ATP]合成速率的一种度量）和推断的线粒体ATP合成最大速率与对照受试者相比降低（p<0.003），并且两者均因训练而显著增加（p<0.05），因此与对照受试者的值无显著差异。
运动期间磷酸肌酸消耗的减少和ADP增加的减少，以及恢复过程中磷酸肌酸再合成速率的提高（与肌肉质量无关）表明，通过运动训练可以显著纠正慢性心力衰竭患者骨骼肌受损的氧化能力。
