Sarcopenia, the age-related progressive decline in skeletal muscle mass, strength, and function, is closely linked to impaired mitochondrial quality control in post-mitotic muscle fibers. A hallmark of mitochondrial aging is disruption of the fusion-fission equilibrium, marked by downregulation of fusion proteins OPA1 and MFN1 and dysregulated expression of fission mediators FIS1 and DRP1, leading to network fragmentation, reduced bioenergetic capacity, and myofiber atrophy. We hypothesized that combining aerobic exercise training (AET) and epigallocatechin gallate (EGCG) would produce synergistic restorative effects on mitochondrial dynamics. This study examined the individual and combined effects of six weeks of AET and EGCG supplementation on mitochondrial fusion-fission gene expression and muscle fiber morphology in aged rat soleus muscle. Twenty-five male Wistar rats were assigned to Young, Elderly, Elderly+EGCG, Elderly+AET, and Elderly+EGCG+AET groups (n=5/group). Aged rats underwent progressive swimming training, and EGCG (100 mg/kg) was administered daily by gavage. OPA1, MFN1, FIS1, and DRP1 mRNA levels were quantified by real-time PCR, and muscle fiber cross-sectional area (CSA) was assessed by H&E staining. One-way ANOVA revealed significant intergroup differences (all p<0.0001). AET alone increased OPA1 and reduced FIS1 and DRP1. The combined EGCG+AET intervention produced the most pronounced pro-fusion shift, with robust OPA1/MFN1 upregulation and FIS1/DRP1 suppression (all p<0.0001 vs. Elderly), while EGCG alone showed limited effects. CSA differed significantly (p<0.0001), with combined treatment yielding the greatest structural preservation. These findings demonstrate that combined AET and EGCG synergistically restore mitochondrial fusion-fission balance and provide superior protection against sarcopenic muscle atrophy.