In reply to Lupine Lacuna:
I may be somewhat inferior in the degree willy waving contest, with only an almost completed BSc in human anatomy, but I thought I would take a stab at answering the question.
The following is relatively quickly researched and even more hastily written; a full list of references can be provided if anyone would like to read further into the subject. I have potentially barked up the wrong tree entirely but my suggestion is:
Motoneurons are capable of continuing to fire repetitively after stimulation by a brief, excitatory synaptic input (self-sustained firing). This self sustained firing (SSF) is the result of the activation of persistent inward calcium and sodium currents (PICs), which are themselves influenced by both serotonin and norepinephrine(adrenaline). Adrenaline and serotonin are monoamines which arise mainly from the brain stem; their levels are significantly elevated during periods of excitement or stress. Activation of 5HT2 and ¦Á-1 receptors, serotonin and adrenaline receptors respectively, on the motorneuron facilitate these low-voltage activated PICs producing sustained depolarisations, also referred to as plateau potentials.
These plateau potentials allow motor units, recruited through even slight stimulation, to continue to fire in a self-sustained manner following the removal of the excitatory stimulus; the stimulus usually needs to be present for ¡Ý2s however repeated activation or further increases in adrenaline, or serotonin, reduce this requirement.
Plateau potentials are primarily seen in type I motor neurons, whose units are recruited first in a muscular contraction and are relatively resistant to fatigue, though larger units can demonstrate the same effect.
The high serotonin concentrations demonstrated during 'central fatigue' may trigger an increase in plateau potentials and hence SSF, as might extracellular accumulation of K+, synonymous with fatiguing contractions. Increased extracellular [k+] decreases the concentration gradient and so reduces K+ transport out of the cell. High intracellular [K+] leads to further activation of plateau potentials and gradually increases motor unit depolarisation generating a stronger and stronger contraction.
The above would suggest that both adrenaline and serotonin levels may be responsible for disco leg while muscular fatigue is also an entirely plausable contributing factor. Experiments on this phenomenon have made use of caffeine and amphetamines to stimulate greater adrenaline release.