Abstract

Deficits in plantarflexor kinetics are associated with poor outcomes in patients following Achilles tendon rupture. In this longitudinal study, we analyzed the fascicle length and pennation angle of the medial gastrocnemius muscle and the length of the Achilles tendon using ultrasound imaging. To determine the relationship between muscle remodeling and deficits in plantarflexor kinetics measured at 14 wk after injury, we correlated the reduction in fascicle length and increase in pennation angle with peak torque measured during isometric and isokinetic plantarflexor contractions. We found that the medial gastrocnemius underwent an immediate change in structure, characterized by decreased length and increased pennation of the muscle fascicles. This decrease in fascicle length was coupled with an increase in tendon length. These changes in muscle-tendon structure persisted throughout the first 14 wk following rupture. Deficits in peak plantarflexor torque were moderately correlated with decreased fascicle length at 120 degrees per second (R2 = 0.424, P = 0.057) and strongly correlated with decreased fascicle length at 210 degrees per second (R2 = 0.737, P = 0.003). However, increases in pennation angle did not explain functional deficits. These findings suggest that muscle-tendon structure is detrimentally affected following Achilles tendon rupture. Plantarflexor power deficits are positively correlated with the magnitude of reductions in fascicle length. Preserving muscle structure following Achilles tendon rupture should be a clinical priority to maintain plantarflexor kinetics.NEW & NOTEWORTHY In our study, we found that when the Achilles tendon ruptures due to excessive biomechanical loading, the neighboring skeletal muscle undergoes rapid changes in its configuration. The magnitude of this muscle remodeling explains the amount of ankle power loss demonstrated by these patients once their Achilles tendons are fully healed. These findings highlight the interconnected relationship between muscle and tendon. Isolated injuries to the tendon stimulate detrimental changes to the muscle, thereby limiting joint-level function.

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