Central fatigue was investigated under an isolated active condition whereby
the possible effects of supraspinal fatigue were minimized. Therefore, ten
subjects were fatigued by simultaneously and repeatedly mechanically stret
ching and electrically stimulating their calf muscles for 1 h. This was per
formed using an ankle ergometer. The active fatigue task included a total o
f 2400 muscle stretches with an intensity of 10% of the maximal voluntary c
ontraction (MVC). This protocol clearly impaired neuromuscular function, as
revealed by a significant reduction in MVC (P < 0.01) and the neural input
to the muscle (average EMG) (P<0.01-0.001). The interpolated nerve stimula
tion compensated for this force loss by 4.28% (P < 0.05). Stretch-reflex re
cordings revealed a notable post-fatigue reduction in the peak-to-peak ampl
itude (59.1%, P < 0.01) and stretch-resisting force of the muscle (14.1%, P
< 0.01). The maximal H-reflex declined by 50.5% (P < 0.001) and did not re
cover while the leg was kept ischemic. It is suggested that the existing pr
otocol with minor metabolic loading can,induce central fatigue, which seems
to be of reflex origin from the fatigued muscle. Although the role of pres
ynaptic inhibition of la terminals is possibly reinforced, disfacilitation
via reduced spindle sensitivity cannot be excluded.