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Bioengineering Laboratory, Department of Orthopaedic Surgery, Louisiana State University Medical Center, New Orleans, Louisiana
Bioengineering Laboratory, Department of Orthopaedic Surgery, Louisiana State University Medical Center, New Orleans, Louisiana
Bioengineering Laboratory, Department of Orthopaedic Surgery, Louisiana State University Medical Center, New Orleans, Louisiana
Bioengineering Laboratory, Department of Orthopaedic Surgery, Louisiana State University Medical Center, New Orleans, Louisiana
Bioengineering Laboratory, Department of Orthopaedic Surgery, Louisiana State University Medical Center, New Orleans, Louisiana
Bioengineering Laboratory, Department of Orthopaedic Surgery, Louisiana State University Medical Center, New Orleans, Louisiana
The objective of this study was to quantify the coacti vation patterns of the knee flexor and extensor muscles as part of continued efforts to identify the role of the antagonist muscles in maintaining joint stability.
The simultaneous EMG from the flexor and extensor muscles of the knee were recorded during maximal effort, slow isokinetic contractions (15 deg/sec) on the plane parallel to the ground to eliminate the effect of gravity. The processed EMG from the antagonist mus cle was normalized with respect to its EMG as agonist at maximal effort for each joint angle. The plots of normalized antagonist EMG versus joint angle for each muscle group were shown to relate inversely to their moment arm variations over the joint range of motion. Additional calculations demonstrated that the antago nist exerts nearly constant opposing torque throughout joint range of motion. Comparison of data recorded from normal healthy subjects with that of high perform ance athletes with hypertrophied quadriceps demon strated strong inhibitory effects on the hamstrings coac tivations. Athletes who routinely exercise their ham strings, however, had a coactivation response similar to that of normal subjects.
We concluded that coactivation of the antagonist is necessary to aid the ligaments in maintaining joint stability, equalizing the articular surface pressure dis tribution, and regulating the joint's mechanical imped ance. The reduced coactivation pattern of the unexer cised antagonist to a hypertrophied muscle increases the risk of ligamentous damage, as well as demon strates the adaptive properties of the antagonist muscle in response to exercise. It was also concluded that reduced risk of knee injuries in high performance ath letes with muscular imbalance could result from com plementary resistive exercise of the antagonist muscle.
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