Some myopathies are accompanied by abnormal calcium homeostasis. Electromyography (EMG) in such patients shows signs of normal or myopathic EMG when detected by a single-fiber electrode and abnormally increased values in macro EMG. As calcium accumulation might be accompanied by changes in intracellular action potential (IAP) and muscle-fiber propagation velocity, we simulated the effects of such changes on motor unit potentials (MUPs) recorded by different kinds of electrodes. We found that: (1) the requirements for what potential can be accepted as a single-fiber action potential (SFAP) are too rigorous; (2) macro MUP amplitude can increase while SFAP amplitude can decrease when there is an increase in the spatial length of IAP spike; and (3) changes in the second phase of a belly-tendon-detected MUP or M wave could be used for noninvasive detection of increased IAP depolarizing (negative) after-potential.

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A unique mechanism is proposed according to which processes within the internodal axolemma are responsible for repetitive activation of myelinated axon with deficit of internodal potassium conductance. A numerical simulation of activity in axon with 21 nodes was performed. The axon was represented by cables for axoplasmic and periaxonal spaces. Accumulation and diffusion of ions were taken into account. Fine segmentation of each internode (338 segments) allowed simulation of internodal activation in response to a normal saltatorial action potential initiated by a short stimulus. The internodal membrane without potassium conductance experienced considerable depolarization. This resulted in formation of a transition zone and significant currents that caused repetitive activation of the internode and neighbor node. Decline of periaxonal sodium concentration during the spike production or lowering of sodium channel density decreased the sodium currents. As a result, the interspike intervals increased up to cessation of the burst. The cessation was reversible.

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