BACKGROUND: This study aimed to elucidate the possible activity of the mitochondrial-mediated apoptotic pathway (MMAP) in obstructive sleep apnea-hypopnea syndrome (OSAHS).

MATERIAL AND METHODS: A control group, a mild OSAHS group, a moderate OSAHS group, and a severe OSAHS group were included. Masson staining, hematoxylin and eosin staining, and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay were performed to assess collagen fiber hyperplasia, pathological morphology, and cell apoptosis, respectively, in muscle samples.

RESULTS: In the OSAHS groups, the palatopharyngeal muscle fibers were larger, with apparent hypertrophy and increased elastic fiber content. The proportions of type I fibers were markedly higher in the control group than in the moderate and severe OSAHS groups (P<0.05). Moreover, apoptosis was significantly enhanced in the muscle cells of the OSAHS groups. The Bax expression levels gradually increased across the 4 groups (lowest in the control group and highest in the severe OSAHS group) (P<0.05); conversely, the p38 and p62 expression levels did not significantly differ among groups (P>0.05).

CONCLUSIONS: A decrease in the proportion of the different fiber types can result in collapse of the upper airway. The pathogenesis of OSAHS appears to involve muscle cell apoptosis via MMAP.

Keywords: Muscle Fibers, Skeletal, Pharyngeal Muscles, Sleep apnea, obstructive, Cardiac Myosins, Mitochondria, Myosin Heavy Chains, Polysomnography, Prospective Studies, bcl-2-Associated X Protein