The broad objective of this study is a more precise definition of potential muscle fatigue mechanisms beyond the traditional claim of neuromuscular junction failure, or depletion of energy supplies. A tentative hypothesis has been made that during continuous high frequency stimulation, sodium depletion and potassium accumulation in the intracellular spaces (including the t-tubules) appear to interfere with action potential propagation within the muscle cell. Such an occurrence is apparently avoided during maximal voluntary efforts by a natural reduction in the firing frequency of the motor neurons. This has been quantified by measurement of action potential counts/units time from small areas of muscle sampled by intramuscular electrodes. No failure of neuromuscular transmission was detected, nor any substantial change in either conduction velocity or single fiber action potential wave form. The physicological events underlying the shift in the EMG power spectrum with fatigue were also investigated. When the small changes in conduction velocity observed in normal fatigue, were generated instead by muscle cooling in the absence of fatigue much smaller shifts in the EMG power spectrum occurred. Thus, some factor other than conduction velocity changes must, therefore, be involved. One such factor often observed during fatigue might be the transition from assynchronous to synchronous discharging of the alpha motoneurones. Experiment have therefore been designed to assess the amount of synchronization present in unfatigued isometric contraction and how this may change as fatigue progresses. Other experiments are directed towards more precise measurement of changing motor neuron firing rates; correlating these with specific motor unit types; and investigating the mechanisms by which they are controlled.