Adaptation of the precentral cortical command to elbow muscle fatigue.

The control exerted by individual motor cortical cells on their fatigued target muscles was assessed by analyzing the discharge patterns and electromyographic (EMG) postspike effects of cortical cells in monkeys making repeated forceful, but submaximal, isometric flexions of the elbow to produce fatigue. Two monkeys were trained to perform self-paced isometric contractions (for longer than 2 s) at forces greater than 35% maximal contraction, with three sets of 20 consecutive contractions; the first and last sets were at the same force level. Pairs of EMG electrodes were implanted in the biceps brachii, brachioradialis, and triceps brachii. The cortical cell discharges were modulated with the active and passive movements of the elbow and produced consistent EMG postspike effects during isometric contraction. Muscle fatigue was assessed as a statistically significant (P < 0.05) drop in the mean power frequency of the EMG power spectrum in one or both flexors in the last set of contractions. Clear signs of muscular fatigue occurred in 20 different experimental sessions. Before fatigue, cortical cells were classified as phasic-tonic (18), phasi-cramp (three), or tonic (five). Twenty cells briskly fired to passive elbow extension, and 9 also responded to passive flexion. Only 6 cells showed a decreased discharge to passive extension. A 22-30% increase in the contraction force produced a higher discharge frequency in 13 cells, and a lower frequency in 5 cells. All cells exerted EMG postspike effects in their target muscles: 20 cells facilitated the flexors, and some of these also inhibited (3 cells) or cofacilitated (5 cells) the extensor; the other 6 cells had mixed effects: 5 of them inhibited at least one flexor, and 1 cell only facilitated the extensor. Most cells (24/26) still produced EMG postspike effects in their target muscles during fatigue, and the number of facilitated muscles increased: 21 cells facilitated the flexors, and 12 of them cofacilitated the extensor. Only 3 cells still inhibited the flexors and were tonic cells. The cortical cell firing frequency increased during fatigue in 13 cells and decreased in 8 cells. Increases involved 10 cells excited by passive elbow extension. Fourteen cells showed parallel changes in firing frequency with fatigue and force, and 9 of these cells facilitated both extensors and flexors in fatigue. Increases were found in 8 cells, decreases in 5 cells and no change in 1 cell. As muscle afferents provide substantial information to cortical cells, which in turn establish functional linkages with their target muscles before and during fatigue, the changes in cell firing frequencies during fatigue demonstrate the active participation of the motor cortex in the control of compensation for the peripheral adjustments concomitant with muscle fatigue.