Vorgerd M, Zange J
Department of Neurology, Neuromuscular Centre Ruhrgebiet, Ruhr-University Bochum, Germany.
Acta Myol. 2007 Jul;26(1):61-3.
McArdle's disease is caused by genetic defects of the muscle-specific isozyme of glycogen phosphorylase, which block ATP formation from glycogen in skeletal muscle. Creatine supplementation and ketogenic diet have been tested as potential supplements for muscle energy metabolism which may improve muscle symptomatic. Outcome measures were clinical scores describing muscle symptomatic and parameters derived from 31P-MRS examinations on working muscle. In two placebo controlled cross-over studies low dose creatine showed beneficial effects on muscle symptoms and performance whereas high dose creatine distinctly worsened muscle symptomatic in patients. In both studies, however, the absence of an elevation in phosphocreatine indicated the absence of a creatine uptake by the muscle fibre. The effects of creatine on muscle symptomatic may be independent from energy metabolism in muscle. In a case study, ketogenic diet improved muscle symptomatic and performance. However, these effects again did not result in 31P-MRS visible changes in muscle energy metabolism.
麦克尔迪氏病由糖原磷酸化酶的肌肉特异性同工酶的基因缺陷引起,该缺陷阻碍了骨骼肌中糖原形成三磷酸腺苷(ATP)。已对补充肌酸和生酮饮食作为肌肉能量代谢的潜在补充剂进行了测试,这可能会改善肌肉症状。结果指标是描述肌肉症状的临床评分以及从工作肌肉的31P-磁共振波谱(31P-MRS)检查得出的参数。在两项安慰剂对照的交叉研究中,低剂量肌酸对肌肉症状和表现显示出有益效果,而高剂量肌酸则明显使患者的肌肉症状恶化。然而,在两项研究中,磷酸肌酸均未升高,表明肌肉纤维未摄取肌酸。肌酸对肌肉症状的影响可能与肌肉中的能量代谢无关。在一项病例研究中,生酮饮食改善了肌肉症状和表现。然而,这些效果同样未导致31P-MRS可见的肌肉能量代谢变化。