Geometric modeling predicts architectural adaptations are not responsible for the force deficit following tenotomy in the rotator cuff.

Tenotomy, or the severing of then tendinous connection between muscle and bone, is an experimental model frequently used to assess muscular changes in response to unloading with retraction. It is most translationally relevant to rotator cuff (RC) tendon tears as these frequently progress to chronic muscle retraction and thus most recent tenotomy animal models have used RC muscles. Tenotomy induces chronic changes to muscle architecture including reduced muscle mass, muscle length, fiber length and pennation angle. However, most RC studies evaluating the physiological consequences of tenotomy do not account for changes in architecture, in part because these are difficult to measure in RC muscles. This is a critical omission as architectural changes can dramatically impact muscle force generating capacity. In this work, we develop a geometric model to predict changes in fiber length and pennation angle of the mouse supraspinatus and infraspinatus muscles given a measured muscle length. We then validate this model with detailed architectural measurements in tenotomized muscles and show a close match between predicted and experimental values. Finally, using this model, we find that predicted changes in architecture cannot explain the force deficit in tenotomized muscle. The contributions of this work are 1) a simple geometric model that predicts changes in architecture with retraction, validated in the mouse RC but with potential application across muscles and species and 2) data indicating that architectural adaptation is not solely responsible for the force deficit with tenotomy which suggests future research should focus on intrinsic changes to the myofiber.