Cytochrome c Oxidase Deficiency in Human Posterior Cricoarytenoid Muscle

Abstract

Mitochondrial alterations occur in skeletal muscle fibers throughout the normal aging process, resulting from increased accumulation of reactive oxide species (ROS). These result in respiratory chain abnormalities, which decrease the oxidative capacity of muscle fibers, leading to decreased contractile force, sarcopenia, or fiber necrosis. Intrinsic laryngeal muscles are a cranial muscle group that possesses some distinctive genotypic, phenotypic, and physiologic properties. Their susceptibility to mitochondrial alterations resulting from biological processes that increase levels of oxidative stress may be one of these distinctive characteristics. The incidence of cytochrome c oxidase (COX) deficiency (COX(-)) was determined in human posterior cricoarytenoid (PCA) muscle when compared with the human thyrohyoid (TH) muscle, an extrinsic laryngeal muscle that served as "control" muscle. Ten PCA and 10 TH muscles were harvested postlaryngectomy from 10 subjects ranging in age from 55 to 86 years. Differences in COX(-) were compared within and between muscle types using tissue section staining and standard morphometric analysis. COX(-) fibers were identified in both the PCA and TH muscles. The PCA muscle had 10 times as may affected fibers as the TH muscle, with significant differences in COX(-) found between muscle type and fiber type (P=0.003). Almost all of this effect was the result of elevated levels of COX(-) in type I fibers from the PCA muscle (P=0.002) that showed a strong positive correlation with increased age. These results suggest that increased mitochondrial alterations may occur in the PCA muscle during normal aging.