Abstract

Alterations in knee joint loading and hind limb kinematics following anterior cruciate ligament transection (ACLT) have been associated with the onset of osteoarthritis (OA) through a reduction in joint loads. Knee joint loads have been directly measured nine days following ACLT, and subsequent changes in joint kinematics have been documented over the span of one year. However, the magnitude and duration of muscle activation adaptations in the hindlimb remain unknown following ACLT. PURPOSE: To quantify long-term changes in cat hindlimb muscle activation patterns following ACLT. METHODS: In this pilot study, indwelling bipolar electromyographic (EMG) electrodes were surgically implanted in four synergist muscle pairs on the cat hindlimb: rectus femoris (RF) and vastus lateralis (VL); semitendonosis (ST) and semimembranosus (SM); extensor digitorum longus (EDL) and tibialis anterior (TA); and medial gastrocnemius (MG) and soleus (SOL). EMG and high speed video data were recorded during level treadmill walking before ACLT and at 1, 2, 3, 4, and 6 weeks, and at 2, 6, 8, and 9 months following ACLT. RESULTS: Following ACLT, there was a reduction in mean EMG activation of the VL during stance, with an immediate increase in mean EMG amplitude in the RF during swing phase only. Both the SM and ST increased activity during stance phase for nine months after ACLT. Following ACLT, the EDL exhibited an extra burst of activity just prior to, or at paw strike in addition to the increased activity at paw off. Activity in the MG also increased during stance up to nine months, and the onset of muscle activation occurred earlier following ACLT for the SOL and MG. CONCLUSION: Following ACLT the knee flexor and extensor muscles demonstrate compensatory activation patterns that may stiffen the hindlimb, and predispose the knee joint to increased loads. The two-joint EDL muscle is recruited at paw strike following ACLT, suggesting that this muscle may function to assist in stabilizing the ACL deficient joint as a knee extensor in co-contraction with the hamstring muscles. Furthermore, long term increases in activation of the dorsiflexor and plantarflexor muscles during stance may further contribute to increasing joint loads leading to OA.

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