0483 Skeletal Muscle Mass Predicts Physiologic but Not Subjective Sleep Disruption Across Sleep Phenotypes

Introduction Skeletal muscle mass reflects metabolic and physiologic resilience and may influence sleep through effects on ventilatory stability, inflammatory tone, and arousal susceptibility. Yet its relationship with subjective insomnia severity and PSG-defined sleep fragmentation remains poorly characterized across different sleep disorder phenotypes. This study aimed to determine whether skeletal muscle mass is associated with subjective insomnia symptoms, and to evaluate its relationship with objective arousal metrics on PSG across OSA (Obstructive Sleep Apnea), COMISA (Comorbid Insomnia and Sleep Apnea), and PI (Primary Insomnia) groups. Methods We retrospectively examined 231 adults (OSA n=109, COMISA n=53, PI n=69) who underwent overnight PSG and body composition assessment using direct segmental multi-frequency bioelectrical impedance. Patients were categorized as follows: OSA (AHI ≥5, ISI < 15), COMISA (AHI ≥15, ISI ≥15), and PI (AHI < 5, ISI ≥15). Skeletal muscle mass was designated as the primary muscle index. ISI1a (sleep onset), ISI1b (maintenance), ISI1c (early awakening), and ISI total were compared across OSA, COMISA, and PI groups. Pearson correlations assessed associations between muscle mass, ISI components, and PSG parameters. Results Mean ages across groups ranged from the early to late 50s, with a male predominance in OSA (81%), COMISA (55%), and PI (33%). Insomnia severity (ISI) was comparable across groups. When examining skeletal muscle mass, lower values were modestly but significantly associated with increased spontaneous (r=–0.20) and movement related arousals (r=–0.26), suggesting a link between reduced muscle status and physiologic sleep fragmentation. In contrast, skeletal muscle mass showed no significant correlation with insomnia severity indices (ISI subscales or total scores) either in the overall sample or within diagnostic subgroups (all p>0.10). Conclusion Skeletal muscle mass showed a modest, subclinical association with increased non-respiratory arousal events on PSG, suggesting a potential contribution to physiologic sleep fragmentation. In contrast, muscle mass was not related to patient-reported insomnia severity. These findings indicate that PSG-based evaluation may be particularly informative in individuals with reduced muscle mass, in whom subjective assessments alone may underestimate the extent of sleep disruption. Support (if any)