Non-Work-Matched HIIT and MIIT Partially Restore Exerkine-Related and Mitochondrial Gene Expression in Diabetic Rat Skeletal Muscle

Skeletal muscle mitochondrial dysfunction and altered myokine signaling contribute to insulin resistance in type 2 diabetes. This study compared the effects of non-work-matched high-intensity interval training (HIIT) and moderate-intensity interval training (MIIT) on skeletal muscle exerkine/myokine- and mitochondrial biogenesis-related gene expression and systemic metabolic indices in streptozotocin-nicotinamide-induced diabetic rats. Twenty-four male Wistar rats were initially allocated to healthy control, diabetic control, MIIT, or HIIT groups; after predefined treadmill-familiarization exclusions, five animals per group were analyzed. Training was performed for 6 weeks, three sessions per week, with MIIT prescribed at 70% maximal aerobic speed and HIIT at 90% maximal aerobic speed. Gastrocnemius expression of FNDC5, OSTN, PGC-1α, TFAM, CCO, and UCP3 was quantified by RT-qPCR, and fasting glucose, insulin, lipid variables, HOMA-IR, HOMA-β, QUICKI, and TyG index were assessed. Diabetes reduced all targeted transcripts and impaired insulin-related metabolic indices. Both MIIT and HIIT partially restored myokine- and mitochondrial-related transcripts compared with diabetic controls, with no significant differences between training protocols for most molecular outcomes. HIIT produced lower fasting insulin and HOMA-IR than MIIT but imposed a greater estimated cumulative workload. These findings indicate that interval training partly attenuates diabetes-associated transcriptional and insulin-related metabolic disturbances, while intensity-specific conclusions require work-matched designs.