Purpose Accumulation of mitochondrial DNA (mtDNA) deletions and the resultant impaired oxidative phosphorylation may play a pathogenic role in the mediation of age-related sarcopenia. Methods Twenty four participants of the New Mexico Aging Process Study were classified as normal lean (n=15) or sarcopenic (n=9) based on body composition determined by Dual Energy X-ray Absorptiometry. Complex I and IV activities were measured in the skeletal muscle samples obtained from gastrocnemius muscle. A two-stage nested PCR strategy was used to identify the mtDNA deletions in the entire mitochondrial genome in the skeletal muscle samples. Results While complex I activity was not significantly different (5.5 ± 0.9 vs. 4.6 ± 0.7 mU/mg protein, p>0.05), complex IV activity was higher in sarcopenic subjects (1.4 ± 0.3 vs. 1.0 ± 0.1 mU/mg protein, p<0.05). mtDNA deletions were mostly located in the region of complex I and spanned from NADH dehydrogenase (ND)1 to ND6. Deletions in the 8577–10407 bp and 10233–11249 bp regions were associated with a significant decrease in complex I activity (p<0.05 and p=0.02 respectively). Total cumulative deletion, defined as the sum of individual length of deletions in a subject, was comparable in subjects with and without sarcopenia (1760 ± 726 vs. 1782 ± 888 bp, p>0.05). The magnitude of mtDNA deletion, however, correlated positively with lean body mass (r=0.43, p<0.05). Conclusion Thus, mtDNA deletions are common in elderly subjects and are negatively related to complex I activity. The positive association between mtDNA deletions and lean body mass needs to be confirmed by studies in a larger study population.
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