Traumatic peripheral injury, like ACL rupture, may alter neurobiological structure and function, with regional reductions in sensorimotor circuit excitability and altered activity patterns in the prefrontal cortex. PURPOSE: To examine the long-term neurobiological consequences of ACL rupture on cortical silent periods (CSPs) in the motor cortical (M1) representations of the vastus lateralis (VL). METHODS: Nine women with a history of unilateral ACL rupture, repair and rehabilitation (3.3 ± 1.2 years prior) participated in the study. Maximal voluntary isometric contraction force (MVIC) was obtained for each leg during a bilateral, closed kinetic chain movement. Active stimulus response curves were produced at 15% MVIC. Biphasic single pulse transcranial magnetic stimulation (TMS) was delivered to the left or right VL hotspot at 40, 50, 60, 70, 80, and 90% stimulator output (SO). Five pulses were delivered during each 25s contraction, with 30s rest between contractions. SO order and leg were randomized. Contralateral CSPs were measured from TMS stimulus onset to the visual resumption of muscle contractile activity. Responses to each leg-specific SO were averaged for each subject and analyzed via two-way repeated measures ANOVA with Fisher’s LSD pairwise comparisons. RESULTS: Because CSPs were consistently produced above 70% SO, quantitative analysis was limited to 70, 80, and 90% SO. Significant main effects were observed for SO (p=0.001) and Leg (p=0.026). CSP duration increased in parallel with SO intensity (80% vs. 70% Δ=32.1ms, p=0.002; 90% vs. 70% Δ=54.5ms, p=0.002; 90% vs. 80% Δ=22.4ms, p=0.015). CSPs were generally longer in the injured leg (Δ=21.6ms, p=0.026). At 70 and 80% SO, CSPs were longer in the injured leg (70% SO: 25.8ms Δ, p=0.017; 80% SO: 18.3ms Δ, p=0.026; 90% SO: 20.6ms Δ, p=0.099). A trend of increased CSP duration at 90% SO may reflect ceiling effects in the silent period of the injured leg. CONCLUSIONS: Injured-leg M1 representation stimulation increased CSP durations compared to the uninjured leg. These deficits persisted years after rehabilitation, and were reproducibly detected during bilateral closed kinetic chain movements at 15% MVIC and SOs above 70%. Our observations indicate long-term reductions in the strength of the sensorimotor circuits governing the injured leg.