Determine the Role of Mitochondrial Dysfunction in Age-Associated Sarcopenia

Document Type

Poster

Date of Original Version

3-27-2026

Abstract

As global life expectancy increases, the prevalence of age-related diseases such as sarcopenia continues to rise. Mitochondrial dysfunction is a key hallmark of aging, characterized by cellular and tissue damage, elevated reactive oxygen species, and impaired glucose metabolism. Age-associated glycogen accumulation has been observed in various cell types, including neurons, astrocytes, and muscle cells. In this study, we investigated glycogen accumulation in association with mitochondrial impairment using the mtDNA mutator (PolgAD257A/D257A) mouse, a model of accelerated aging caused by systemic mitochondrial dysfunction due to increased mtDNA mutations. Histological analyses with Periodic Acid–Schiff (PAS) and diastase–PAS (dPAS) staining and colorimetric glycogen quantification analyses revealed that mitochondrial dysfunction promotes glycogen deposition in both cardiac and skeletal muscle. These findings suggest that mitochondrial impairment disrupts glycogen metabolism, leading to abnormal glycogen processing and free glycogen accumulation in metabolically active tissues. We propose that this glycogen buildup may impair contractile and metabolic functions, thereby contributing to sarcopenia, the age-related loss of muscle mass and strength. Future studies with a muscle specific mitochondrial dysfunction mouse model we will further investigate the relationship between glycogen accumulation and age-associated sarcopenia, as well as determine whether interventions such as exercise can mitigate these effects by enhancing oxidative metabolism and promoting efficient glycogen utilization. Together, these findings identify disrupted glycogen metabolism as a potential biochemical hallmark linking mitochondrial dysfunction to systemic aging and muscle decline.

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