Possible mechanism of quadriceps femoris weakness in patients with ruptured anterior cruciate ligament

Purpose: The purpose of this study was to test the hypothesis that loss of afferent feedback due to rupture of anterior cruciate ligament (ACL) is the cause of quadriceps femoris (QF) weakness through gamma loop. Two experiments were designed to prove our hypothesis. Methods: In experiment 1, the maximal voluntary contraction (MVC) of knee extension and integrated electromyogram (I-EMG) of vastus medialis (VM), vastus lateralis (VL), and rectus femoris (RF) were measured in 13 patients with ruptured ACL and 7 healthy volunteers before and after injection of anesthetic agent into the knee. In experiment 2, MVC of knee extension and I-EMG of the VM, VL, and RF were measured in 13 patients with ruptured ACL, 7 knee-anesthetized healthy subjects, and 12 normal subjects, before and after 20-min vibration stimulation applied to the infrapatellar tendon. Results: The results of experiment 1 revealed that injection of anesthetic agent into the knee capsule resulted in significant decrease of MVC and I-EMGs. In experiment 2, the mean percentage change of MVC in the control group was significantly lower than that in the other two groups. There was no significant difference between knee-anesthetized group and patients with ruptured ACL. The mean percentage change of I-EMG showed a pattern similar to that of MVC. Conclusion: Our results suggest that loss of feedback from mechanoreceptors in ACL is the underlying mechanism of weakness of QF in patients with ACL lesion. This conclusion is based on chronic suppression of recruitment of high-threshold motor units during voluntary contraction because ACL lesion leads to chronic reduction in Ia-feedback to muscles around the knee due to a lack of feedback from ACL to gamma motor neurons.