Amelioration of Endurance Training on Cardiac Mitochondrial Quality Control System in the Post-infarction Rats



Aerobic interval training (AIT) has been reported to exert beneficial effects on various cardiovascular diseases. However, effects of AIT on the post-myocardial infarction (MI)–associated mitochondrial dysfunction was still unclear. In this study, we investigated the favorable protection of AIT on myocardial mitochondria in the post-MI rats by focusing on mitochondrial dynamics and biogenesis. Mitochondrial ultrastructure and respiratory functions (respiratory control ratio [RCR], value of P/O), complex activities, dynamic proteins (mitofusin [mfn] 1/2, type 1 optic atrophy [OPA1] and dynamin-related protein1 [Drp1]), biogenesis, oxidative signaling of extracellular signal-regulated kinase [ERK] 1/2, (c-Jun NH2-terminal protein kinase [JNK] and P53 were determined. Post-MI rats exhibited adverse mitochondrial ultrastructure changes and dysfunctions. Also, reduced fusion and increased fission accidents were observed, which were revealed to associate with activated ERK1/2-JNK-P53 signaling. Furthermore, mitochondrial biogenesis was decreased. After AIT, not only did mitochondria appeared more normal in structure, but also improved MI-associated mitochondrial dysfunction (elevated RCR and P/O, enhanced activities of complex I, III and IV), which were accompanied by increased fusion (mfn2 and OPA1) and biogenesis, decreased fission (Drp1) and inactivated ERK1/2-JNK-P53 signal pathway. These data showed that AIT may restore mitochondrial functions by protecting structural integrity, inhibiting dynamics pathological remodelling and increasing biogenesis.


Myocardial Infarction, Mitochondrial Dysfunction, Fusion, Fission, Mitochondrial Biosynthesis, Endurance Training


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