Six-week combined exercise modulates mitochondrial dynamics (MFN1/DRP1) and oxidative stress (MDA/SOD) in fast- and slow-twitch muscles of aged rats

Aging is associated with mitochondrial dysfunction, which leads to decreased cellular function and the development of age-related diseases. Exercise training is considered one of the most effective strategies for improving muscle cell function. The aim of the present study was to investigate the effect of six-week combined exercise on mitochondrial dynamics and biogenesis markers (MFN1, DRP1) as well as oxidative stress markers (MDA and SOD) in fast- and slow-twitch muscles of aged rats. In this study, 16 male Wistar rats (463.2 ± 9.3 g) were randomly divided into two groups (n=8 per group): control and resistance-endurance training. The training group underwent combined resistance-endurance training, 6 days a week for 6 weeks (3 resistance days, 3 endurance days). Forty-eight hours after the last training session, animals were sacrificed and fast-twitch (gastrocnemius) and slow-twitch (soleus) muscle tissues were collected. Gene expression levels of mitofusin 1 (MFN1), dynamin-related protein 1 (DRP1) were measured by real-time PCR (RT-PCR). In slow-twitch muscle, exercise training significantly increased mRNA expression levels of SOD genes, and significantly decreased mRNA expression of DRP1 and the concentration of MDA compared to the control group (p<0.05). Similarly, in fast-twitch muscle, six weeks of combined training significantly increased SOD gene expressions and decreased DRP1 mRNA and MDA levels compared to controls (p<0.05). Combined exercise training positively modulates mitochondrial biogenesis and dynamics markers (decreased DRP1 mRNA) and enhances antioxidant capacity (increased SOD gene expression and enzyme activity, decreased MDA levels) in both fast- and slow-twitch muscles of aged rats, highlighting its significant role in mitigating age-associated mitochondrial dysfunction. These findings reflect improvements in markers of mitochondrial quality control and oxidative stress rather than direct measurements of mitochondrial function.