Patients with chronic myosteatosis have a reduction in muscle fiber force production and disrupted myofibril architecture (1163.18)

Abstract

A persistent atrophy of muscle fibers and an accumulation of fat, collectively referred to as myosteatosis, commonly occurs in patients with chronic muscle tears. The rotator cuff muscle group develops substantial myosteatosis after chronic tears, and patients with these injuries often have marked reductions in upper extremity function and quality of life. As the etiology of myosteatosis has not been well characterized in humans, our objective was to determine changes in muscle fiber structure and function in patients with chronic rotator cuff tears. We hypothesized that muscles from patients with chronic rotator cuff tears have reduced muscle fiber force production, disordered myofibrils and an accumulation of inflammatory macrophages.Compared with control muscles, there was no difference in muscle fiber cross‐sectional area, but torn supraspinatus muscles had a 30% reduction in maximum isometric force production and a 29% reduction in normalized force. Using electron microscopy and histology, disordered sarcomeres were noted, along with an accumulation of lipid‐laden macrophages in the extracellular matrix surrounding muscle fibers. The size of the tear correlated well (R2=0.49, P<0.01) with reductions in force production. The results of the study indicate that patients with myosteatosis have marked reductions in muscle fiber force production, disrupted myofibril architecture and an accumulation of inflammatory macrophages in the muscle extracellular matrix. This work will help to establish future therapies to restore muscle function for patients with myosteatosis.