Mitochondrial dynamic remodeling in strenuous exercise-induced muscle and @entity2383 : regulatory effects of XXXX .

@entity10740 @entity3978 @entity8 @entity7504 @entity2508 @entity18468 @entity6229 @entity1295 @entity36719 @entity18467 @entity35 @entity2383
Physical exercise is considered to exert a positive effect on health, whereas strenuous or excessive exercise (Exe) causes @entity1295 and damage to muscle and immune functions. The underlying molecular mechanisms are still unclear. We designed a protocol to mimic Exe and explore the ensuing cellular damage and involvement of mitochondrial dynamics. We found that Exe was prone to decrease endurance capacity and induce @entity8 and the immune system. Muscle atrophy markers @entity18467 and @entity18468 mRNA were increased by Exe, accompanied by increased autophagy and mitochondrial fission in skeletal muscle. Exe caused a decrease in @entity6229 and complex I expression; it also activated JNK and @entity2508 pathways and consequently induced @entity10740 , @entity7504 , and MnSOD expression in skeletal muscle. The involvement of oxidant-induced autophagy and @entity2383 was confirmed in C2C12 myoblasts. @entity36719 (HT), a natural olive @entity3978 , efficiently enhanced endurance capacity and prevented Exe-induced @entity8 . Also, HT treatment inhibited both the Exe-induced increase in autophagy and mitochondrial fission and the decrease in @entity6229 expression. In addition, HT enhanced mitochondrial fusion and mitochondrial complex I and II activities in muscle of Exe @entity35 . These results demonstrate that Exe-induced @entity1295 and damage to muscle and immune functions may be mediated via the regulation of mitochondrial dynamic remodeling, including the downregulation of mitochondrial biogenesis and upregulation of autophagy. HT supplementation may regulate mitochondrial dynamic remodeling and enhance antioxidant defenses and thus improve exercise capacity under Exe conditions.
