Functional deficits may be explained by plantarflexor remodeling following Achilles tendon rupture repair: Preliminary findings

Abstract

Achilles tendon ruptures are common injuries that often lead to long-term functional deficits. Despite the prevalence of these injuries, the mechanism responsible for limited function has not yet been established. Therefore, the purpose of this study was to present preliminary findings that support a hypothesis that skeletal muscle remodeling is the driving factor of poor outcomes in some patients. Biomechanical and ultrasonography assessments were performed on a patient that presented with poor functional outcomes 2.5 years after a surgically-repaired acute Achilles tendon rupture. Single-leg heel raise height was decreased by 75% in the affected limb (3.0 cm compared to 11.9 cm) while walking mechanics showed no deficits. Ultrasonography revealed that the affected medial gastrocnemius muscle was less thick and had shorter, more pennate fascicles compared to the unaffected limb. A simple computational model of a maximal-effort plantarflexion contraction was employed to test the implications of changes in muscle architecture on single-leg heel raise function. Subject-specific measurements of fascicle length and pennation were input into the model, which supported these architectural parameters as being drivers of heel raise function. These preliminary findings support the hypothesis that an Achilles tendon rupture elicits changes in skeletal muscle architecture, which reduces the amount of work and power the joint can generate. This multidisciplinary framework of biomechanical, imaging, and computational modeling provides a unique platform for studying the complex interactions between structure and function in patients recovering from Achilles tendon injuries.