Original researchMuscle atrophy contributes to quadriceps weakness after anterior cruciate ligament reconstruction
Introduction
Quadriceps weakness is nearly ubiquitous following anterior cruciate ligament (ACL) injury and reconstruction (ACLr).1 Strength deficits upwards of 30% in the reconstructed compared to the contralateral limb have been reported six months post-operatively,2 a time when patients often return to full activity. The presence of quadriceps weakness may be hazardous to the patient. The quadriceps is important to lower limb control during dynamic activity and quadriceps weakness could alter movement strategies potentiating re-injury.3 To optimally prepare patients to return to full activity, complete quadriceps function must be restored. However, before quadriceps strength deficits can be effectively countered, a deeper understanding of why quadriceps weakness persists throughout rehabilitation is needed.
Quadriceps disuse atrophy occurs following knee joint immobilization and may contribute to quadriceps weakness after ACL injury and reconstruction.4 Konishi and colleagues5 previously reported an approximately 7% deficit in total quadriceps volume in the reconstructed versus contralateral limb in patients 6–12 months following ACL reconstruction. Deficits of 3% in volume6 and cross sectional area7 (CSA) remained 12–18 months post-operatively. Similar magnitudes of quadriceps atrophy were reported by Lorentzon et al.8 in people with ACL deficiency, though no relation between atrophy and strength was identified. The authors concluded that muscle atrophy alone did not cause quadriceps weakness suggesting, instead, that incomplete volitional muscle activation may contribute.8
Quadriceps activation failure (QAF) is a common consequence of ACL injury and reconstruction. QAF is often associated with joint damage, effusion, and pain.4 These factors alter the afferent signal sent to the central nervous system, which leads to an inhibitory signal transmitted to the quadriceps α-motoneuron pool and a decrease in voluntary muscle activity.4 Previous reports of QAF following ACLr suggest deficits upwards of 15% present two years post-operatively.1 In patients undergoing total knee arthroplasty, a population with similar magnitude quadriceps dysfunction to those following ACL injury,9 QAF accounted for nearly twice the quadriceps strength deficit as muscle atrophy in the acute post-operative period.9 Elucidating how quadriceps muscle atrophy and QAF contribute to lingering weakness when patients return to full activity seems imperative. Thus, the purpose of this study was to determine if quadriceps atrophy and QAF contribute to persistent knee extension strength deficits in patients when they were cleared to return to full activity after ACL reconstruction. We hypothesized that persistent quadriceps weakness would result from a combination of QAF (measured by central activation ratio [CAR]) and muscle atrophy (measured through cross sectional area [CSA]) and that QAF would more strongly predict quadriceps weakness than would muscle atrophy. We further hypothesized that greater quadriceps weakness, QAF, and CSA would be present in the injured compared with the uninjured limb.
Section snippets
Methods
Twenty-two patients were recruited for participation; one was excluded after secondary screening revealed she did not fulfill all of the inclusion criteria. Another individual reported for magnetic resonance imaging (MRI) testing but failed to report for CAR assessment. He could not be reached for follow-up and was excluded from analysis, leaving 20 patients (7 males, 13 females; age: 20.65 ± 5.17 years; height: 1.72 ± 0.08 m; mass: 74.47 ± 14.49 kg) who underwent patellar tendon autograft ACL
Results
The IKDC scores were 75.99 ± 15.86. Tegner scores were 5.90 ± 2.10. Peak quadriceps strength differed between limbs, with the injured (148.39 ± 37.91 N m) being significantly weaker than the uninjured limb (212.98 ± 62.57 N m; p < 0.001; LSI 0.70). Similarly, the injured limb (68.81 ± 17.80 cm2) had a smaller CSA than the uninjured limb (81.10 ± 21.58 cm2; p < 0.001; LSI 0.85; Fig. 3). Quadriceps CAR did not differ between the injured (0.87 ± 0.12) and uninjured limbs (0.85 ± 0.14; p = 0.571; LSI 1.02). Joint effusion was
Discussion
Quadriceps weakness presents frequently after ACL injury and reconstruction. While the precise cause of quadriceps weakness is unknown, peripheral and central mechanisms have been implicated. The present study sought to determine the contributions of muscle CSA and CAR to lingering quadriceps strength deficits following ACL reconstruction. When examined together, quadriceps CAR and CSA were associated with knee extension MVIC following ACLr. Previous studies9, 11 demonstrated quadriceps muscle
Conclusion
CSA is related to muscle strength at return to full activity following ACLr. Substantial side-to-side deficits were demonstrated for strength and CSA, while bilateral deficits in QAF were present. The presence of these deficits suggests that current post-operative rehabilitation efforts may insufficiently restore muscle size, activation, and strength. Continued emphasis needs to be placed on establishing the optimal methods by which to remove atrophy and QAF during post-operative rehabilitation.
Practical implications
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Patients demonstrate side-to-side strength deficits and bilateral QAF when they return to full activity following ACLr and post-operative rehabilitation.
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Rehabilitation following ACLr should emphasize improving quadriceps voluntary activation bilaterally.
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Continued emphasis on improving quadriceps strength after surgery is necessary.
Acknowledgements
The authors would like to thank Mark Villwock, MS and Lindsey Lepley, PhD, ATC for their assistance with patient recruitment and data collection. The project described was supported by Grant Number 1 K08 AR05315201A2 from NIAMS/NIH and a doctoral dissertation grant from the National Athletic Trainers’ Association Research and Education Foundation.
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2023, Annals of Physical and Rehabilitation MedicineCitation Excerpt :Overall, these findings suggest that muscle strength may play an important role in KOA, especially for women at earlier disease stages, and therefore potentially merit particular targeting strategies. Muscle size is an important aspect of neuromuscular function, and previous studies of people with a knee injury history showed that muscle size may explain strength deficits [60]. Therefore, changes in muscle size in people with KOA can be expected because they also present muscle strength impairments around their knee joint.