The control exerted by individual motor cortical cells on their fatigu
ed target muscles was assessed by analyzing the discharge patterns and
electromyographic (EMG) postspike effects of cortical cells in monkey
s making repeated forceful, but submaximal, isometric flexions of the
elbow to produce fatigue. Two monkeys were trained to perform self-pac
ed isometric contractions (for longer than 2 s) at forces greater than
35% maximal contraction, with three sets of 20 consecutive contractio
ns; 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 as
sessed 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 d
ifferent experimental sessions. Before fatigue, cortical cells were cl
assified as phasic-tonic (18), phasic-ramp (three), or tonic (five). T
wenty cells briskly fired to passive elbow extension, and 9 also respo
nded 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 ha
d mixed effects: 5 of them inhibited at least one flexor, and 1 cell o
nly facilitated the extensor. Most cells (24/26) still produced EMG po
stspike effects in their target muscles during fatigue, and the number
of facilitated muscles increased: 21 cells facilitated the flexors, a
nd 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. Increas
es involved 10 cells excited by passive elbow extension. Fourteen cell
s 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 cort
ical cells, which in turn establish functional linkages with their tar
get muscles before and during fatigue, the changes in cell firing freq
uencies during fatigue demonstrate the active participation of the mot
or cortex in the control of compensation for the peripheral adjustment
s concomitant with muscle fatigue.