Excitation frequency and muscle fatigue: Mechanical responses during voluntary and stimulated contractions

During continuous high-frequency stimulation, much of the fatigue is due to failure of electrical propagation, probably largely at the muscle fiber membrane; and in voluntary contractions where no similar failure was observed, muscle fatigue is minimized by a progressive reduction in motor unit activation.

Abstract

The loss of force that occurs during maximal isometric voluntary contraction (MVC) of human muscle was compared with that due to 60 s of maximal nerve stimulation at different frequencies. For the unfatigued adductor pollicis, maximal nerve stimulation at 80 Hz was required to match the force of an MVC. Prolonged stimulation at 80 Hz resulted in a faster rate of force loss than in a sustained MVC. The rate of force loss during 80 Hz tetani was also greater than during those at 20 Hz. After 20 s more force was generated by stimulating at the lower frequency. Changing from high- to low-frequency stimulation in a fatigued muscle resulted in an increase in force. When isolated curarized mouse muscle was stimulated directly in the same manner, the force changes were similar to those seen in human muscle stimulated via the nerve. In the isolated muscle a reduction of the extracellular [Na+] increased the rate of force loss in a similar way to increasing the stimulus frequency. We suggest that the loss of force during high-frequency fatigue may not be entirely due to neuromuscular block, but also, in part, to a reduced excitability of the muscle fiber membrane. The time course of an MVC could be imitated by a tetanus in which the stimulus frequency was initially high but then progressively reduced. We conclude that in sustained MVCs force fatigue in response to high-frequency stimulation is reduced by a progressive decline in motor neuron firing frequency.