Paraspinal myosteatosis is associated with COPD: a cross-sectional MRI analysis from the population-based KORA cohort.

backgroundMuscle dysfunction in chronic obstructive pulmonary disease (COPD) represents a significant extrapulmonary manifestation. Yet, the role of muscle fat infiltration (myosteatosis) in paraspinal muscles remains incompletely characterized. This study investigated whether paraspinal myosteatosis and its distribution patterns are associated with COPD and pulmonary function.

methodsWithin the population-based KORA cohort, 214 participants underwent whole-body magnetic resonance imaging and pulmonary function testing. Paraspinal myosteatosis was quantified by chemical shift-encoded MRI at lumbar vertebra 3 (L3), from which proton density fat fraction (PDFF, in %) maps were derived. Intramyocellular (IMCL) and extramyocellular lipids (EMCL) were determined through voxel-based analysis using validated PDFF thresholds. COPD was defined spirometrically as FEV1/FVC below the lower limit of normal. Associations were examined using multivariable regression models adjusted for age, sex, smoking status, physical activity, and body mass index.

resultsAmong participants (mean age 58.5 ± 5.8 years, 56.1% male), 24 (11.2%) had spirometrically defined COPD. Participants with COPD showed higher paraspinal PDFF (19.9 ± 7.0% vs. 18.3 ± 7.6%) and lower IMCL/EMCL ratios (1.0 ± 0.4 vs. 1.2 ± 0.6) compared to those without COPD. After adjustment, higher PDFF was independently associated with increased odds of COPD (OR 1.69, 95% CI: 1.01-2.84, p = 0.046), while a higher IMCL to EMCL ratio showed protective associations (OR 0.49, 95% CI: 0.24-1.00, p = 0.050). Both total paraspinal PDFF and EMCL were negatively associated with pulmonary gas exchange capacity (TLCO/VA: β=-0.19, 95% CI: -0.35-0.04, p = 0.016 and β=-0.18, 95% CI: -0.33-0.03, p = 0.022, respectively). Conversely, higher IMCL/EMCL ratios were associated with better gas exchange (TLCO/VA: β = 0.15, 95% CI: 0.01-0.29, p = 0.031).

conclusionsThis population-based study demonstrates that while increased total paraspinal muscle fat content is associated with higher COPD risk, its compartmental distribution reveals distinct patterns: A higher proportion of IMCL relative to EMCL shows protective associations, potentially reflecting preserved type I oxidative muscle fiber characteristics. These findings suggest that muscle fat distribution patterns may serve as imaging markers of metabolic adaptation in COPD, offering new perspectives for disease monitoring and therapeutic approaches.