Does muscle-tendon adaptation differentiate outcomes of SLAP lesion surgical repair? - PROJECT SUMMARY. While neuromuscular plasticity is the basis of the field of physical medicine and rehabilitation, how the most functionally meaningful muscle architecture parameters adapt has not been rigorously studied in humans. Commonly, orthopaedic surgery implements significant geometric re-designs to the musculoskeletal system. Frequently, these re-designs are substantial enough that, theoretically, they should induce long-term adaptation in optimal fascicle length. Thus, studying muscle response to orthopaedic intervention provides novel opportunities to advance our understanding of these adaptations and their resultant functional effects. We have chosen to study orthopaedic surgical repair of the Type II SLAP lesion of the long head of the biceps tendon because, due to the current standard of care, it presents a unique model system to evaluate skeletal muscle structural adaptation in vivo. Type II lesions are typically repaired in one of three manners: SLAP repair, biceps tenotomy, or biceps tenodesis. Importantly, because each surgical approach addresses reattachment of the tendon uniquely, different muscle-tendon structures are imposed. In SLAP repair, the superior labrum and biceps tendon are reattached to the glenoid, attempting to restore the muscle-tendon unit to approximately pre-tear length and, presumably, tension. In tenotomy, the tendon is detached completely (sparing its full length) and allowed to retract into the bicipital groove where it frequently adheres. In tenodesis, the tendon is resected and reattached to the proximal humerus. The overall objective for this pilot study is to identify if the different origin-to-insertion distances imposed by three surgical approaches to Type II SLAP lesion repair lead to chronic differences in fascicle length substantial enough to yield measurable effects on isometric and isokinetic elbow supination strength. In Aim 1a, we will utilize extended field-of-view ultrasound to measure fascicle length. This retrospective study will quantify muscle architecture of the biceps brachii, in vivo, in both arms of individuals who have undergone unilateral Type II lesion repair from each of the three primary surgical groups and in a control, nonsurgical group. In Aim 1b, we will characterize biceps tendon geometry following repair and a non-surgical population, providing foundational knowledge which will be useful to surgeons in determining feasible repair strategies. For completeness, we will also quantify muscle volume. In Aim 2, we will determine if these changes in muscle-tendon structure map to measurable effects in muscle strength. We will quantify active muscle function in both arms of the same participants using isometric and isokinetic dynamometry. Upon successful completion of the proposed research, we expect to provide novel in vivo data in humans, characterizing fiber adaptation among three orthopaedic surgical techniques, including corresponding measures of active muscle function. This contribution is expected to be immediately significant for orthopaedic surgeons who treat Type II SLAP lesions. More broadly, these data will improve our understanding of adaptation in the neuromuscular system, which is critical to the design of effective clinical interventions.
