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.