Muscle redox status regulates diverse aspects of skeletal muscle function, including mitochondrial energetics and contractile performance. In aging skeletal muscle mitochondrial dysfunction contributes to altered redox homeostasis creating a feedforward cycle. Despite this, the role of redox status and its dynamic nature has not been adequately explored as it relates to the decline in skeletal muscle performance with age. To identify mechanisms linking redox status to aged skeletal muscle function we used two long-term treatment strategies to reduce oxidative stress and restore redox homeostasis in aged mice. The first treatment strategy used a short mitochondrial-targeted peptide, elamipretide (SS-31), that our lab has previously shown to acutely improve mitochondrial bioenergetics and muscle fatiguability while also enhancing glutathione redox potential in aged mice. Treating with SS-31 (3 mg/kg) for 8 weeks recapitulates all of the acute improvements while also increasing resting ATP levels and improving treadmill performance compared to both pre-treatment baseline performance and age matched controls. Increased performance was associated with improved redox status as indicated by lower 4-hydroxynonenal-protein adducts and reversal of age-related changes in protein S-glutathionylation. Our second treatment strategy used the powerful antioxidant astaxanthin delivered through the chow of mice at a target dose of 300 mg/kg/day. Astaxanthin treatment paired with exercise training for 8 weeks in aged animals showed a significant improvement in skeletal muscle specific force compared to untreated controls and a trend toward improved treadmill performance. Taken together these results suggest that altering skeletal muscle oxidative stress to restore redox homeostasis is a viable strategy for improving muscle function with age.