The inverse association between skeletal muscle mass to visceral fat ratio (SVR) and sleep disturbance: the mediating role of inflammation and aging acceleration

BACKGROUND: A growing body of evidence has linked body composition to poor sleep quality. The skeletal muscle mass-to-visceral fat ratio (SVR) is a valid indicator of body composition that integrates appendicular skeletal muscle mass and visceral fat, reflecting the severity of sarcopenic obesity (SO). However, the association between SVR and sleep disturbance has not been well established. This study aimed to investigate the relationship between SVR and sleep disturbance among U.S. adults, along with the mediating roles of inflammation and biological aging. METHODS: A total of 1,564 participants from the National Health and Nutrition Examination Survey (NHANES) with complete data on SVR, sleep parameters, and other essential covariates were included. Weighted multivariable logistic regression models, subgroup and interaction analyses, and restricted cubic spline (RCS) analyses were used to explore the association between SVR and sleep disturbance. Furthermore, mediation analysis was used to explore the mediating role of aggregate index of systemic inflammation (AISI), C-reactive Protein-Albumin-Lymphocyte index (CALLY), and Phenotypic age acceleration (PhenoAgeAccel) in this association. RESULTS: 15.22% of participants reported sleep disturbance. After full covariate adjustment, SVR was inversely associated with sleep disturbance: each unit increase in SVR was linked to a 91.1% lower risk (OR = 0.089, 95% CI: 0.024-0.334), and the highest versus lowest SVR quartile showed a 57.4% reduced risk (OR = 0.426, 95% CI: 0.241-0.752; P-trend = 0.006). RCS analyses confirmed a significant linear dose-response relationship between SVR and sleep disturbance (P-nonlinearity = 0.907). Subgroup analyses and interaction tests showed a more pronounced association in females (OR = 0.42 vs. males: OR = 0.01) and individuals with depression (OR = 0.16 vs. non-depressed individuals: OR < 0.01). Additionally, after adjusting for alternative mediators in sensitivity analyses, AISI, CALLY, and PhenoAgeAccel statistically mediated 10.64%, 36.43%, and 15.99% of the association, respectively (all P < 0.05). CONCLUSIONS: SVR was inversely associated with sleep disturbance, with inflammation and biological aging statistically explaining a significant portion of this association. Further studies with longitudinal or interventional designs are warranted to clarify the causal links of body composition with inflammation, biological aging and sleep disturbance given the cross-sectional design. CLINICAL TRIAL NUMBER: Not applicable.