However, this study utilized a task consisting of brief phasic dorsiflexions, where visual feedback of EMG traces was provided, but where contraction strength was not controlled, which may contribute to explaining the seemingly divergent results.
The leg was positioned with ~90[degrees] flexion at the hip joint, ~115[degrees] flexion at the knee joint, and ~120[degrees] dorsiflexion at the ankle joint.
First, subjects performed three maximal isometric dorsiflexion contractions (MVC), separated by 30 s rest, as a measure of maximal voluntary dorsiflexion strength.
Subsequently, subjects performed a static contraction, where they were asked to maintain a force level of 10% MVC during isometric dorsiflexion for two minutes.
For data obtained during static dorsiflexion, coherence was calculated between EEG and [TA.sub.prox]; EEG and [TA.sub.dist]; and between [TA.sub.prox] and [TA.sub.dist].
EEG, EMG, autospectra, and coherence results from a single young subject during static dorsiflexion are shown in Figure 3.
Each subject performed 3 dorsiflexions with maximal effort.
To assess modulation of spinal reciprocal inhibition, we measured the suppression of the soleus H-reflex at the onset of dorsiflexion, and to assess the central drive to the agonist motor pool (dorsiflexors), we measured the size of coupled oscillations in tibialis anterior motor units.
Functional reciprocal inhibition was evaluated by comparing the size of soleus H-reflexes at rest with H-reflexes elicited at the onset of explosive dorsiflexion contractions.
To produce comparable afferent input to the soleus motoneuron pool at rest and at the onset of dorsiflexion contraction, the tibial nerve stimulation intensity was adjusted, if necessary, to elicit an M-response of approximately 10% of [M.sub.max] in all trials.
At least 45 trials, 15 tibial nerve stimulation and 30 no stimulation trials randomly interspersed, were obtained during dorsiflexion contraction.
Also, two participants with CP could not produce a voluntary dorsiflexion contraction.