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The Journal of Sports Medicine and Physical Fitness 2002 March;42(1):19-25

language: English

Muscle activation and torque development during maximal unilateral and bilateral isokinetic knee extensions

Berthoin S., Pelayo P., Baquet G., Marais G., Allender H., Robin H.

From the Department of Neuroscience Karolinska Institute and Stockholm University College of Physical Education and Sports Stockholm, Sweden


Background. The aim of this study was to investigate whether or not a bilateral strength deficit occurs during bilateral (BL) velocity controlled dynamic knee extensions and if the neural control of the knee extensors and flexors is altered during homologous muscle BL efforts.
Methods. Twenty-eight healthy and habitually active subjects, 13 female and 15 male, performed maximal unilateral (UL) and BL isokinetic leg extensions at a velocity of 60º.s-1 through a 90º range of motion of the knee joint (90 to 180º). Knee extension torque and electromyographic activity (EMG) of the quadriceps and hamstrings muscles were recorded.
Results. The mean knee extensor torque produced in the BL condition (168±52 Nm) was 17% less than the sum of the two UL conditions (Σ=202±56 Nm). During BL conditions, quadriceps EMG activity was less in both legs (left, 8.2±7.4% less and right, 13.9±9.1% less, respectively). There were no significant differences between BL and UL efforts for either left or right hamstrings activity. Eighteen subjects, who when asked to perform a maximal knee extension simultaneously activated their contralateral hamstrings, had significantly higher bilateral deficits (21%) compared to those who exhibited little or no contralateral hamstrings EMG activity (14%).
Conclusions. The main findings of the study were that a bilateral strength deficit occurred when simultaneously maximally activating the homologous knee extensor muscles. This deficit was in all likelihood due to a less than maximal efferent drive to the quadriceps muscles. Hamstrings EMG activity was not greater during the BL knee extensions, which supports the notion that antagonistic muscle activity was not primarily responsible for the observed bilateral deficit.

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