A dynamic network involving M1-S1, SII-insular, medial insular, and cingulate cortices controls muscular activity during an isometric contraction reaction time task.

Magnetoencephalographic, electromyographic (EMG), work, and reaction time (RT) were recorded from nine subjects during visually triggered intermittent isometric contractions of the middle finger under two conditions: unloaded and loaded (30% of maximal voluntary contraction). The effect of muscle fatigue was studied over three consecutive periods under both conditions. In the loaded condition, the motor evoked field triggered by the EMG onset decreased with fatigue, whereas movement-evoked fields (MEFs) increased (P < 0.01). Fatigue was demonstrated in the loaded condition, since (i) RT increased due to an increase in the electromechanical delay (P < 0.002); (ii) work decreased from Periods 1 to 3 (P < 0.005), while (iii) the myoelectric RMS amplitude of both flexor digitorum superficialis and extensor muscles increased (P < 0.003) and (iv) during Period 3, the spectral deflection of the EMG median frequency of the FDS muscle decreased (P < 0.001). In the unloaded condition and at the beginning of the loaded condition, a parallel network including M1-S1, posterior SII-insular, and posterior cingulate cortices accounted for the MEF activities. However, under the effect of fatigue, medial insular and posterior cingulate cortices drove this network. Moreover, changes in the location of insular and M1-S1 activations were significantly correlated with muscle fatigue (increase of RMS-EMG; P < 0.03 and P < 0.01, respectively). These results demonstrate that a plastic network controls the strength of the motor command as fatigue occurs: sensory information, pain, and exhaustion act through activation of the medial insular and posterior cingulate cortices to decrease the motor command in order to preserve muscle efficiency and integrity.