Mitochondrial bioenergetics rearrangement in type 2 diabetes: a comparative analysis of the effects of continuous and intermittent aerobic training on the mitochondrial biogenesis axis (PGC-1α/TFAM) and mitochondrial fusion-fission homeostasis (MFN1/DRP1) in skeletal muscle

Abstract

Mitochondrial dysfunction in type 2 diabetes is one of the hidden but decisive links in the decline in skeletal muscle metabolic capacity. The aim of the present study was to compare the effects of continuous and intermittent aerobic training on the mitochondrial biogenesis axis including PGC-1α and TFAM and mitochondrial fusion-fission homeostasis including MFN1 and DRP1 in skeletal muscle of mice with type 2 diabetes. This study was conducted experimentally and with an interventional design. After inducing type 2 diabetes through high-fat diet and streptozotocin injection, male Wistar rats were divided into six groups: healthy control, healthy + continuous training, healthy + intermittent training, diabetic control, diabetic + continuous training, and diabetic + intermittent training. The training protocols were performed for eight weeks and five sessions per week. After the end of the intervention, the gastrocnemius muscle was extracted and the expression of PGC-1α, TFAM, MFN1, and DRP1 genes was evaluated by RT-qPCR. The data were analyzed using two-way analysis of variance and Tukey's post hoc test. The results showed that type 2 diabetes caused a significant decrease in the expression of PGC-1α, TFAM, and MFN1 and an increase in DRP1, indicating an impairment of biogenesis and a disruption in the balance of mitochondrial fusion-fission. Both types of aerobic training improved mitochondrial indices; However, interval training had a more pronounced effect on increasing PGC-1α and TFAM, while continuous training showed a more pronounced response in modifying MFN1 and DRP1. Overall, the findings suggest that the type and intensity of training play a decisive role in the rearrangement of mitochondrial bioenergetics in diabetic skeletal muscle.