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

Abstract

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.