Abstract
An increased fatigability associated with anterior cruciate ligament (ACL) injury may persist several months after surgery. The purpose of this study was to investigate the behavior of muscle fiber conduction velocity (CV) as a descriptor of myoelectric fatigue, at different stages after rehabilitation, post-ACL reconstruction. Nineteen subjects acted as control group (CG), 10 patients had undergone surgery within 12 months (R12), and 23 patients were more than 24 months post-surgery (R24+). Surface electromyography (EMG) signals were detected from the quadriceps femoris using bidimensional arrays during isometric contractions at 20% and 60% maximal voluntary contraction (MVC). We observed a lower fatigability in the R24+ group during the 60% MVC contraction, with respect to the other groups. Lower fatigability of quadriceps muscle after ACL reconstruction in the long term may be linked to a recovery from a transitory altered motor unit recruitment strategy due to surgery, observed in the R12 group. Therefore, the findings of this study do not suggest an impaired fatigability of the quadriceps muscle during sustained isometric contractions in active patients in the long term.
Highlights
Anterior cruciate ligament reconstruction (ACLr) is known to induce neuromuscular alterations of the quadriceps leading to substantial muscle weakness [1], deficits in muscle voluntary activation [2], and atrophy [3]
Group CG: 19 subjects with no previous history of knee injury or painful conditions of the lower limb acted as the control group; Group R12: 10 patients, up to 12 months after ACLr (10 ̆ 4 months); Group R24+: patients, more than months after ACLr (59 ̆ 38 months)
This study investigated for the first time the behavior of muscle fiber conduction velocity (CV) as a descriptor of peripheral fatigue in distinct groups of patients after ACLr
Summary
Anterior cruciate ligament reconstruction (ACLr) is known to induce neuromuscular alterations of the quadriceps leading to substantial muscle weakness [1], deficits in muscle voluntary activation [2], and atrophy [3]. In addition to a history of ACLr, fatigue can induce changes in the neuromuscular control of the quadriceps. Fatigue associated with ACL injury, may reduce the ability of the muscle to generate strength and may induce changes in lower extremity biomechanics and deficits in postural control, increasing the risk of repeated ACL injury [4,5,6,7]. Patients who have undergone ACLr, even after rehabilitation, tend to exhibit a deficit in strength and neuromuscular control [8,9,10,11]. Combined central and peripheral processes contribute to neuromuscular fatigue. Central fatigue can originate from any structure above the neuromuscular junction from the central nervous system to
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