A prevalent feature of neuromuscular fatigue is a decline in the extracellularly recorded myoelectric signal. One factor that could underlie this change is a decrease in the amplitude of the sarcolemmal action potential. Based on observed reductions in action potential amplitude without effect on force, it has been argued that changes in the action potential during sustained activity would be unlikely to contribute to fatigue. However, those observations were primarily from experiments in which 1) high frequency stimulation may have caused signal cancellation due to action potential overlap; or 2) sustained membrane depolarization may have directly activated excitation-contraction coupling. The relatively low and narrow range of membrane depolarization required for full activation of amphibian and slow-twitch mammalian fibers makes them resistant to incomplete activation if action potentials are depressed during fatigue. Mammalian fast- twitch fibers, on the other hand, require greater depolarization for full activation and also exhibit a greater decrease in action potential amplitude with fatigue. Therefore, it seems probable that fatigue-related decline in action potential amplitude in these fibers leads to incomplete activation and loss of force.
|Original language||English (US)|
|Number of pages||5|
|Journal||Advances in experimental medicine and biology|
|State||Published - Jan 1 1995|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)