Deficit in knee extension strength following anterior cruciate ligament reconstruction is explained by a reduced neural drive to the vasti muscles.

The persistence of quadriceps weakness represents a major concern following anterior cruciate ligament reconstruction (ACLR). The underlying adaptations occurring in the activity of spinal motoneurons are still unexplored. This study examined the discharge patterns of large populations of motor units (MUs) in the vastus lateralis (VL) and vastus medialis (VM) muscles following ACLR. Nine ACLR individuals and ten controls performed unilateral trapezoidal contractions of the knee extensor muscles at 35%, 50% and 70% of the maximal voluntary isometric force (MVIF). High-density surface electromyography (HDsEMG) was used to record the myoelectrical activity of the vasti muscles in both limbs. HDsEMG signals were decomposed with a convolutive blind source separation method and MU properties were extracted and compared between sides and groups. The ACLR group showed a lower MVIF on the reconstructed side compared to the contralateral side (28.1%; P<0.001). This force deficit was accompanied by reduced MU discharge rates (~21%; P<0.05), lower absolute MU recruitment and derecruitment thresholds (~22% and ~22.5%, respectively; P<0.05) and lower input-output gain of motoneurons (27.3%; P=0.009). Deficits in MU discharge rates of the VL and in absolute recruitment and derecruitment thresholds of both vasti MUs were associated with deficits in MVIF (P<0.05). A strong between-side correlation was found for MU discharge rates of the VL of ACLR individuals (P<0.01). There were no significant between-group differences (P>0.05). These results indicate that mid-to-long term strength deficits following ACLR may be attributable to a reduced neural drive to vasti muscles, with potential changes in excitatory and inhibitory synaptic inputs.