The E3 ligase Parkin has been implicated in the regulation of mitophagy, a quality control process whereby defective mitochondria are sequestered in autophagosomes and delivered to lysosomes for degradation. Parkin has been mainly studied for its implication in neuronal degeneration in Parkinson but its role in other tissues remains unknown. In this study, we used a murine model of Parkin deficiency to test the hypothesis that Parkin is important for mitochondrial quality control in the mitochondria‐rich skeletal muscle, a tissue in which autophagy/mitophagy play an important regulatory role. Our results indicate that Parkin is abundant in normal skeletal muscle, and that Parkin deficiency leads to mitochondria‐related abnormalities including 1) lower respiratory rates and acceptor control ratio, 2) reduced activities of respiratory chain complexes containing mtDNA encoded subunits, 3) increased susceptibility to opening of the permeability transition pore, and 4) increased expression of Bnip3 and Bax, which respectively regulate mitophagy and apoptosis. Parkin deficiency is also associated with an increased expression of ER‐stress markers (CHOP, GRP78), and a greater proportion of enlarged muscle fibers, which suggest broader phenotypic changes within skeletal muscle. Overall, these results establish the role of Parkin in the maintenance of normal mitochondrial function in skeletal muscle.