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During the stance phase of a normal gait, the triceps surae muscle controls the advancement of the tibia, which contributes to knee extension. Plantar flexor weakness results in excessive dorsiflexion, and consequently, the knee loses this contribution. However, increasing knee flexion is also seen in patients with cerebral palsy who do not have plantar flexor weakness. We aimed to understand this mechanism through the use of a musculoskeletal dynamic model. The model consists of solid segments connected with rotatory joints and springs to represent individual muscles. It was positioned at different degrees of ankle plantarflexion, knee flexion, and hip flexion. The soleus muscle was activated concentrically to produce plantarflexion and push the foot against the ground. The resulting knee extension was analyzed. The principal determinant of knee flexion or extension associated with ankle plantarflexion was the position of the knee joint center. When this was anterior to the line of action of the ground reaction force (GRF), the soleus contraction resulted in increased knee flexion. The knee extension was obtained when the knee was flexed less than approximately 25°. The relation between joint angles, anthropometric parameters, and the position of the GRF was expressed in a mathematical formulation. The clinical relevance of this model is that it explains the failure of plantar flexor control on knee extension in patients with cerebral palsy, when increased knee flexion can occur even if there is a normal or plantarflexed foot position. Full article