Context: Arthrogenic muscle inhibition (AMI) impedes the recovery of muscle function following joint injury, and in a broader sense, acts as a limiting factor in rehabilitation if left untreated. Despite a call to treat the underlying pathophysiology of muscle dysfunction more than three decades ago, the continued widespread observations of post-traumatic muscular impairments are concerning, and suggest that interventions for AMI are not being successfully integrated into clinical practice. Objectives: To highlight the clinical relevance of AMI, provide updated evidence for the use of clinically accessible therapeutic adjuncts to treat AMI, and discuss the known or theoretical mechanisms for these interventions. Evidence Acquisition: PubMed and Web of Science electronic databases were searched for articles that investigated the effectiveness or efficacy of interventions to treat outcomes relevant to AMI. Evidence Synthesis: 122 articles that investigated an intervention used to treat AMI among individuals with pathology or simulated pathology were retrieved from 1986 to 2021. Additional articles among uninjured individuals were considered when discussing mechanisms of effect. Conclusion: AMI contributes to the characteristic muscular impairments observed in patients recovering from joint injuries. If left unresolved, AMI impedes short-term recovery and threatens patients’ long-term joint health and well-being. Growing evidence supports the use of neuromodulatory strategies to facilitate muscle recovery over the course of rehabilitation. Interventions should be individualized to meet the needs of the patient through shared clinician–patient decision-making. At a minimum, we propose to keep the treatment approach simple by attempting to resolve inflammation, pain, and effusion early following injury.

Context: : Central and peripheral neural adaptations have been identified after anterior cruciate ligament (ACL) injury and reconstruction (ACLR) and are hypothesized to contribute to posttraumatic muscle dysfunction. Limited evidence exists about the temporal nature of neuromuscular adaptations during early and late-term phases of recovery after ACLR, and no researchers have studied patients with posttraumatic osteoarthritis. Objective: : To compare quadriceps neuromuscular function less than 2 years (early) and more than 2 years (late) after ACLR, including in patients who experienced posttraumatic knee osteoarthritis. Design: : Cross-sectional study. Setting: : Laboratory. Patients or Other Participants: : A total of 72 patients after ACLR, consisting of 34 early (9.0 ± 4.3 months postsurgery), 30 late (70.5 ± 41.6 months postsurgery), and 8 with osteoarthritis (115.9 ± 110.0 months postsurgery), and 30 healthy control volunteers. Main Outcome Measure(s): : Quadriceps function was measured bilaterally during a single visit to determine normalized Hoffmann reflex (H : M ratio), knee-extension maximal voluntary isometric contraction torque (Nm/kg), central activation ratio (%), fatigue index (% decline), and active motor threshold (%). Comparisons were made using 2-way analyses of variance to identify the effect of limb and group on each outcome measure. We calculated Cohen d effect sizes to assess the magnitude of difference between ACLR and matched control limbs for each group. Results: : Compared with healthy control limbs, involved-limb maximal voluntary isometric contraction was lower among all patients after ACLR (P < .001, Cohen d values = −1.00 to −1.75). The central activation ratio (P < .001, Cohen d = −1.74) and fatigue index (P = .003, Cohen d = −0.95) were lower among patients only early after ACLR. The active motor threshold was higher among all patients after ACLR (P < .001, Cohen d values = −0.42 to −1.56). Conclusions: : Neuromuscular impairments were present in patients early and late after ACLR, regardless of osteoarthritis status. Quadriceps strength and corticospinal excitability were impaired at each time point compared with values in healthy control individuals, suggesting the need to address cortical function early after ACLR.