Studies were made on the mechanism of high frequency fatigue with
in vivo Phosphorus-31 Magnetic Resonance Spectroscopy (
31P-MRS) and compound muscle action potential. The sciatic nerve of Wistar-Kyoto rats (WKY) was stimulated electrically at 67Hz and 4V to induce high frequency fatigue of the gastrocnemius and soleus muscles. Energy metabolism in the skeletal muscles was evaluated by
31P-MRS, and the compound muscle action potential (M wave) was measured to assess neuromuscular transmission. The energy level of the muscles was evaluated by the phosphocreatine (PCr)/{inorganic phosphate (Pi)+phosphomonoester (PME)} ratio, PCr/(Pi+PME), and the intracellular pH was calculated by chemical shift of Pi.
The initial tension of the muscles was 383.8±35.8 dynes. During the remainder of the periods of stimulation, the tension decreased gradually. The PCr/(Pi+PME) and the intracellular pH in the first 2min of stimulation rapidly decreased to 0.6±0.1 and 6.62±0.04, respectively. Later, both the PCr/(Pi+PME) and the intracellular pH returned with time. The percentage M wave amplitude of the control value of gastrocnemius muscle rapidly dropped to 33.7±10.2% in the first 2min of stimulation, which indicated neuromuscular transmission failure during stimulation, and later maintained lower levels of M wave amplitude during stimulation.
These results suggest that high frequency fatigue is ascribable not to a decreased energy level and intracellular pH of the muscles, but to neuromuscular transmission failure resulting from a raised threshold intensity of excitation-contraction coupling during stimulation.
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