High intensity interval training ameliorates mitochondrial dysfunction in the left ventricle of mice with type 2 diabetes

摘要: Both human and animal studies have shown mitochondrial contractile dysfunction in hearts of type 2 diabetes mellitus (T2DM). Exercise training has positive effects on cardiac function, but its effect the mitochondria been insufficiently explored. The aim this study was to assess exercise function T2DM hearts. We divided mice (db/db) into a sedentary an interval group at 8 weeks age used heterozygote db/+ as controls. After training, we evaluated structure well levels mRNA proteins involved key metabolic processes from left ventricle. db/db animals showed decreased oxidative phosphorylation capacity fragmented mitochondria. Mitochondrial respiration blunted response Ca2+ along with reduced protein calcium uniporter. ameliorated complex (C) I + II, CII CIV, not CI or response. fragmentation partially restored. isocitrate, succinate oxoglutarate dehydrogenase were increased normalized by training. induced upregulation two transcripts peroxisome proliferator activated receptor gamma coactivator 1 alpha (PGC1α1 PGC1α4) previously linked endurance adaptations strength adaptations, respectively. heart multiple some, all dysfunctions.