Abdominal Muscle Density Is Inversely Related to Adiposity Inflammatory Mediators

Skeletal muscle is the largest regulator of glucose metabolism, but few population-based studies have examined the associations between muscle and inflammation. We studied the relationships between abdominal muscle area and density with selected adiposity-associated inflammatory mediators.

Nearly 2000 subjects underwent computed tomography of the abdomen and had venous fasting blood drawn concomitantly. The computed tomography scans were interrogated for visceral and subcutaneous fat, as well as abdominal lean muscle areas and densities. We then categorized the muscle into locomotion (psoas) and stabilization (rectus, obliques, and paraspinal) groups. Blood samples were assayed for interleukin-6 (IL-6), resistin, C-reactive protein, and TNF-α.

The mean age was 64.7 yr, and 49% were female. Forty percent were white, 26% Hispanic/Latino American, 21% African American, and 13% Chinese American. The mean body mass index was 28.0 kg·m, and 30% were obese (body mass index, >30 kg·m). Using multivariable linear regression models that included adjustment for abdominal muscle area, a 1-SD increment in the mean densities for total, stabilization, and locomotive abdominal muscle were each significantly associated with lower levels of IL-6 (β = -15%, -15%, and -9%, P < 0.01 for all) and resistin (β = -0.11, -0.11, and -0.07 ng·mL, P < 0.02 for all), but not C-reactive protein or TNF-α. Conversely, muscle area was not independently associated with any of the inflammatory mediators studied.

Higher densities of several muscle groups in the abdomen are significantly associated with lower IL-6 and resistin levels, independent of the muscle area in these groups. Techniques that enhance muscle density may reduce levels of adiposity-associated inflammatory mediators.