Muscle fatigue is an exercise-induced reduction in maximal voluntary muscle
force. It may arise not only because of peripheral changes at the level of
the muscle, but also because the central nervous system fails to drive the
motoneurons adequately. Evidence for "central" fatigue and the neural mech
anisms underlying it are reviewed, together with its terminology and the me
thods used to reveal it. Much data suggest that voluntary activation of hum
an motoneurons and muscle fibers is suboptimal and thus maximal voluntary f
orce is commonly less than true maximal force. Hence, maximal voluntary str
ength can often be below true maximal muscle force. The technique of twitch
interpolation has helped to reveal the changes in drive to motoneurons dur
ing fatigue. Voluntary activation usually diminishes during maximal volunta
ry isometric tasks, that is central fatigue develops, and motor unit firing
rates decline. Transcranial magnetic stimulation over the motor cortex dur
ing fatiguing exercise has revealed focal changes in cortical excitability
and inhibitability based on electromyographic (EMG) recordings, and a decli
ne in supraspinal "drive" based on force recordings. Some of the changes in
motor cortical behavior can be dissociated from the development of this "s
upraspinal" fatigue. Central changes also occur at a spinal level due to th
e altered input from muscle spindle, tendon organ, and group Ill and IV mus
cle afferents innervating the fatiguing muscle. Some intrinsic adaptive pro
perties of the motoneurons help to minimize fatigue. A number of other cent
ral changes occur during fatigue and affect, for example, proprioception, t
remor, and postural control. Human muscle fatigue does not simply reside in
the muscle.