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Context: Distinct from the muscle atrophy that develops from inactivity or disuse, atrophy that occurs after traumatic joint injury continues despite the patient being actively engaged in exercise. Recognizing the multitude of factors and cascade of events that are present and negatively influence the regulation of muscle mass after traumatic joint injury will likely enable clinicians to design more effective treatment strategies. To provide sports medicine practitioners with the best strategies to optimize muscle mass, the purpose of this clinical review is to discuss the predominant mechanisms that control muscle atrophy for disuse and posttraumatic scenarios, and to highlight how they differ. Evidence Acquisition: Articles that reported on disuse atrophy and muscle atrophy after traumatic joint injury were collected from peer-reviewed sources available on PubMed (2000 through December 2019). Search terms included the following: disuse muscle atrophy OR disuse muscle mass OR anterior cruciate ligament OR ACL AND mechanism OR muscle loss OR atrophy OR neurological disruption OR rehabilitation OR exercise. Study Design: Clinical review. Level of Evidence: Level 5. Results: We highlight that (1) muscle atrophy after traumatic joint injury is due to a broad range of atrophy-inducing factors that are resistant to standard resistance exercises and need to be effectively targeted with treatments and (2) neurological disruptions after traumatic joint injury uncouple the nervous system from muscle tissue, contributing to a more complex manifestation of muscle loss as well as degraded tissue quality. Conclusion: Atrophy occurring after traumatic joint injury is distinctly different from the muscle atrophy that develops from disuse and is likely due to the broad range of atrophy-inducing factors that are present after injury. Clinicians must challenge the standard prescriptive approach to combating muscle atrophy from simply prescribing physical activity to targeting the neurophysiological origins of muscle atrophy after traumatic joint injury.

Context After knee-joint injury, pain, effusion, and mechanoreceptor damage alter afferent signaling, which can result in quadriceps inhibition and subsequent weakness. The individual contributions of each factor to inhibition remain unclear due to confounding knee-joint injuries and indirect experimental models. Objective To characterize the influence of naturally occurring knee damage and pain on quadriceps neuromuscular function in individuals with patellar tendinopathy. Design Cross-sectional study. Setting Research laboratory. Patients or Other Participants Twenty participants who self-reported patellar tendinopathy (PT) and 10 healthy control individuals underwent ultrasonic tendon assessment. Injured participants were dichotomized by an orthopaedic surgeon into groups with (1) pain and structural tendon abnormality and (2) regional pain alone. Main Outcome Measure(s) Quadriceps inhibition was assessed with the Hoffman reflex and the central activation ratio via the superimposed-burst technique. Normally distributed measures were analyzed using a 1-way analysis of variance and post hoc independent t tests. Kruskal-Wallis tests with post hoc Mann-Whitney U tests were used to analyze nonnormally distributed data. An a priori α level of P ≤ .05 was set. Results Control participants presented with more spinal-reflex excitability (0.37 ± 0.23) than the PT (0.10 ± 0.06; P = .03) and regional-pain (0.18 ± 0.05; P = .02) groups. Knee-extension strength was greater in the control (3.37 ± 0.59 Nm/kg) than in the PT (2.41 ± 0.67 Nm/kg; P = .01) group but not the regional-pain group (3.05 ± 0.66 Nm/kg; P = .24). Control individuals presented with more quadriceps activation (97.93% ± 3.12) than the PT (84.44% ± 16.98; P < .01) and regional-pain (91.17% ± 10.56; P = .01) groups. No differences were present for any measures between the PT and regional-pain groups (P values > .05). Conclusions Deficits in spinal-reflex excitability, quadriceps activation, and strength were present in both the PT and regional-pain groups. A combination of pain and structural damage appeared to have the greatest negative effect on quadriceps function, as only the PT group presented with neuromuscular outcomes that failed to meet clinical thresholds.

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Many patients with anterior cruciate ligament (ACL) injuries have persistent quadriceps muscle atrophy, even after considerable time in rehabilitation. Understanding the factors that regulate muscle mass, and the time course of atrophic events, is important for identifying therapeutic interventions. Using a non-invasive animal model of ACL injury, a longitudinal study was performed to elucidate key parameters underlying quadriceps muscle atrophy. Male Long-Evans rats were euthanized at 6, 12, 24, 48-hrs and 1, 2, 4-wks after ACL injury that was induced via tibial compression overload; controls were not injured. Vastus Lateralis muscle size was determined by wet weight and fiber CSA. Evidence of disrupted neuromuscular communication was assessed via the expression of NCAM and genes associated with denervation and neuromuscular junction instability. Abundance of MuRF-1, MAFbx, and 45s pre-rRNA along with 20S proteasome activity were determined to investigate mechanisms related to muscle atrophy. Lastly, muscle damage-related parameters were assessed by measuring IgG permeability, centronucleation, CD68 mRNA and satellite cell abundance. Compared to controls, we observed a greater percentage of NCAM positive fibers at 6-hrs post-injury, followed by higher MAFbx abundance 48-hrs post-injury, and higher 20S proteasome activity at 1-wk post-injury. A loss of muscle wet weight, smaller fiber CSA and the elevated expression of Runx1 were also observed at the 1-wk post-injury time point relative to controls. There also were no differences observed in any damage markers. These results indicate that alterations in neuromuscular communication precede the upregulation of atrophic factors that regulate quadriceps muscle mass early after non-invasive ACL injury.