Purpose: The present study was designed to investigate whether central neural mechanisms limit the duration of a sustained low-force isometric contraction and the maximal force-generating capacity of the knee extensors.
Methods: Fourteen healthy males (28 ± 7 yr) were asked to sustain, until voluntary exhaustion, an isometric contraction with their right knee extensor muscles at a target force equal to 20% of their maximal voluntary contraction (MVC) force. At task failure, the muscle was immediately electrically stimulated for 1 min aiming the same target force (20% MVC force). Subsequently, subjects were asked to resume the voluntary contraction for as long as possible. Knee extensor neuromuscular function was assessed before and after the entire protocol for comparison.
Results: When electrically stimulated at the point of task failure, all subjects developed the 20% MVC force target, indicating that lack of force-generating capacity from peripheral impairment had not limited the duration of the first task. We observed a reduction in MVC force after the entire protocol (−57% ± 12%), which correlated with a decrease in potentiated peak doublet force (−48% ± 17%, P < 0.001). The level of voluntary activation, as quantified with the interpolated twitch technique, was slightly depressed after the entire protocol (from 93% ± 7% to 87% ± 10%, P < 0.01).
Conclusions: It follows that task failure from a sustained isometric contraction is mainly affected by central/motivational factors, whereas MVC force loss is largely explained by the extent of contractile failure of the muscle.
1Institute of Movement Sciences and Sports Medicine, University of Geneva, Geneva, SWITZERLAND; and 2Neuromuscular Research Laboratory, Schulthess Clinic, Zurich, SWITZERLAND
Address for correspondence: Nicolas Place, Ph.D., Institute of Movement Sciences and Sports Medicine, Faculty of Medicine, University of Geneva, Rue du Conseil Général 10, 1205 Geneva, Switzerland; E-mail: firstname.lastname@example.org.
Submitted for publication July 2011.
Accepted for publication December 2011.