Gerwyn Morris, Maes Michael
Tir Na Nog, Bryn Road seaside 87, Llanelli, SA15 2LW, Wales, UK.
IMPACT Strategic Research Centre, Deakin University, School of Medicine and Barwon Health, Geelong, VIC, Australia.
Curr Rheumatol Rep. 2017 Jan;19(1):1. doi: 10.1007/s11926-017-0628-x.
Here, we review potential causes of muscle dysfunction seen in many patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) such as the effects of oxidative and nitrosative stress (O&NS) and mitochondrial impairments together with reduced heat shock protein production and a range of metabolic abnormalities.
Several studies published in the last few years have highlighted the existence of chronic O&NS, inflammation, impaired mitochondrial function and reduced heat shock protein production in many patients with ME/CFS. These studies have also highlighted the detrimental effects of chronically elevated O&NS on muscle functions such as reducing the time to muscle fatigue during exercise and impairing muscle contractility. Mechanisms have also been revealed by which chronic O&NS and or impaired heat shock production may impair muscle repair following exercise and indeed the adaptive responses in the striated muscle to acute and chronic increases in physical activity. The presence of chronic O&NS, low-grade inflammation and impaired heat shock protein production may well explain the objective findings of increased muscle fatigue, impaired contractility and multiple dimensions of exercise intolerance in many patients with ME/CFS.
在此,我们回顾许多肌痛性脑脊髓炎/慢性疲劳综合征(ME/CFS)患者出现肌肉功能障碍的潜在原因,如氧化应激和亚硝化应激(O&NS)的影响、线粒体损伤、热休克蛋白生成减少以及一系列代谢异常。
过去几年发表的多项研究强调了许多ME/CFS患者存在慢性O&NS、炎症、线粒体功能受损以及热休克蛋白生成减少的情况。这些研究还强调了慢性升高的O&NS对肌肉功能的有害影响,例如缩短运动期间肌肉疲劳的时间以及损害肌肉收缩力。慢性O&NS和/或热休克蛋白生成受损损害运动后肌肉修复以及横纹肌对急性和慢性体力活动增加的适应性反应的机制也已被揭示。慢性O&NS、低度炎症和热休克蛋白生成受损的存在很可能解释了许多ME/CFS患者肌肉疲劳增加、收缩力受损以及运动不耐受多方面的客观表现。