PDF(Pubmed)
Abstract：
Molecular mechanisms associated to improvement of metabolic syndrome (MetS) during exercise are not fully elucidated. MetS was induced in 250 g male Wistar rats by 30% sucrose in drinking water. Control rats receiving tap water were controls, both groups received solid standard diet. After 14 weeks, an endurance exercised group, and a sedentary were formed for 8 weeks. The soleus and extensor digitorum longus (EDL) muscles were dissected to determine contractile performance, expression of myosin heavy chain isoforms, PGC1α, AMPKα2, NFATC1, MEF2a, SIX1, EYA1, FOXO1, key metabolic enzymes activities. Exercise mildly improved MetS features. MetS didn\'t alter the contractile performance of the muscles. Exercise didn\'t altered expression of PGC1α, NFATC1, SIX1 and EYA1 on MetS EDL whereas NFATC1 increased in soleus. Only citrate synthase was affected by MetS on the EDL and this was partially reverted by exercise. Soleus α-ketoglutarate dehydrogenase activity was increased by exercise but MetS rendered the muscle resistant to this effect. MetS affects mostly the EDL muscle, and endurance exercise only partially reverts this. Soleus muscle seems more resilient to MetS. We highlight the importance of studying both muscles during MetS, and their metabolic remodeling on the development and treatment of MetS by exercise.
摘要：
与运动过程中代谢综合征（MetS）改善相关的分子机制尚未完全阐明。通过饮用水中的30％蔗糖在250g雄性Wistar大鼠中诱导MetS。接受自来水的对照大鼠为对照，两组均接受固体标准饮食.14周后,一个耐力锻炼的团体，并形成了8周的久坐。解剖比目鱼肌和指长伸肌（EDL）以确定收缩性能，肌球蛋白重链亚型的表达，PGC1α,AMPKα2,NFATC1,MEF2a,SIX1，EYA1，FOXO1，关键代谢酶活性。锻炼轻度改善的MetS功能。MetS没有改变肌肉的收缩性能。运动没有改变PGC1α的表达，MetSEDL上的NFATC1，SIX1和EYA1，而比目鱼中的NFATC1增加。只有柠檬酸合酶受到EDL上MetS的影响，并且通过运动部分恢复。运动可增加比目鱼α-酮戊二酸脱氢酶的活性，但MetS使肌肉对这种作用具有抵抗力。MetS主要影响EDL肌肉，耐力运动只能部分恢复这一点。比目鱼肌似乎对MetS更有弹性。我们强调在MetS期间研究肌肉的重要性，以及它们的代谢重塑对运动代谢综合征的发展和治疗。
