Neuromuscular Research Unit, Department of Neurology, and the Copenhagen Muscle Research Centre, Copenhagen, Denmark.
Eur J Neurol. 2009 Dec;16(12):1336-9. doi: 10.1111/j.1468-1331.2009.02660.x. Epub 2009 May 27.
It is unknown whether prolonged training is a safe treatment to alleviate exercise intolerance in patients with mitochondrial DNA (mtDNA) mutations.
The effect of 3 and 12 months training and 3-12 months deconditioning was studied in four patients carrying different mtDNA mutations.
Three-month moderate-intensity training increased oxidative capacity by 23%, which was sustained after 6-12 months of low-intensity training. Training and deconditioning did not induce adverse effects on clinical symptoms, muscle morphology and mtDNA mutation load in muscle.
Long-term training effectively improves exercise capacity in patients with mitochondrial myopathy, and appears to be safe.
目前尚不清楚延长训练是否是一种安全的治疗方法,可以缓解线粒体 DNA(mtDNA)突变患者的运动不耐受。
本研究观察了 4 名携带不同 mtDNA 突变的患者接受 3 个月和 12 个月训练以及 3-12 个月停训的效果。
3 个月的中等强度训练使氧化能力增加了 23%,6-12 个月的低强度训练后仍能维持。训练和停训均未引起临床症状、肌肉形态和肌肉中 mtDNA 突变负荷的不良影响。
长期训练可有效改善线粒体肌病患者的运动能力,且似乎安全。