The Effect of ACL Reconstruction on Involved and Contralateral Limb Vastus Lateralis Morphology and Histology: A Pilot Study

Abstract

Quadriceps muscle weakness is a commonly reported issue post anterior cruciate ligament reconstruction (ACLR), with minimal information related to skeletal muscle morphology following surgery. The purpose is to examine the morphological and functional differences in the vastus lateralis muscle from patient's ACLR and contralateral leg. Three physically active ACLR participants were recruited and secured to a dynamometer to perform maximal voluntary isometric knee extension contractions (MVIC) of the ACLR and contralateral limb. Muscle biopsies of the ACLR and contralateral vastus lateralis were performed, then sectioned, and stained for myosin isoforms to determine fiber type. Confocal images were acquired, and ImageJ software was used to determine the fiber type and cross-sectional area (CSA). There was a significant reduction in CSA of the type IIa and type IIx muscle fiber cells between healthy (IIa: 7,718 ± 1,295 µm2; IIx; 5,800 ± 601 µm2) and ACLR legs (IIa: 4,139 ± 709 µm2; IIx: 3,708 ± 618 µm2) (p < 0.05), while there was no significant difference in knee extension MVIC torque between legs (healthy limb: 2.42 ± 0.52 Nm/kg; ACLR limb: 2.05 ± 0.24 Nm/kg, p = 0.11). The reduction in the cross-sectional area of the ACLR type II fibers could impair function and increase secondary injury risk.

Arthrogenic Muscle Inhibition Following Anterior Cruciate Ligament Injury

“…62,84 These data suggest that evaluation of intramuscular fat content by means of ultrasound imaging may serve as a useful clinical measure. Previous studies have also reported acute 92 and persistent 93 atrophy among type IIa and IIx muscle fibers in the vastus lateralis following ACLR. In addition to a smaller fiber diameter, a metabolic shift has also been observed within the vastus medialis, such that the muscle becomes more endurant.…”

Differenzierte Analyse des neuronalen Antriebs nach Kniebandverletzungen

“…Die beschriebene volumetrisch-numerische Typ-II-Faseratrophie des VM [32][33][34] oder VL [7] nach Verletzungen oder Erkrankungen des Kniegelenks konnten die Ergebnisse unserer Untersuchungen an insgesamt 20 Fußballspielern nach wiederholter ipsilateraler VKB-Ruptur nicht bestätigen [13]. Vermutlich sind Einflüsse wie Dauer der Immobilisation und Reduktion des Aktivitätslevels verantwortlich für die beschriebene Faseratrophie des VM.…”

“…Einzelne Beobachtungen an Leistungssportlern weisen jedoch, abhängig vom Ausmaß der Seitenpräferenz, auch Kraftwerte auf der betroffenen Seite auf, die über denen der nicht betroffenen Seite liegen [6]. Ein niedrigerer Frequenzinhalt des EMG-Leistungsspektrums des M. vastus medialis [3] belegt indirekt eine mögliche Veränderung des Faserspektrums der betroffenen Muskulatur [7]. Jedoch können sich Kompensationen infolge von Verletzungen auf unterschiedlichen Ebenen des neuromuskulären Systems manifestieren.…”

Mechanisms of Arthrogenic Muscle Inhibition

“…What is currently known in the context of AMI is that muscle processes that are tightly regulated by neural signaling experience adaptations after injury. For instance, in patients with ACLR, investigators have reported that muscle undergoes adaptations in fiber-type expression [85][86][87] and becomes more fatty and fibrotic. 88 The accumulation of inhibited fibers 87 may disrupt the intracellular calcium signaling cascades, leading to adaptations in tissue quality and phenotypic expression in those with AMI.…”