Effect of Intracellular and Extracellular Ion Changes on E–C Coupling and Skeletal Muscle Fatigue

摘要: The causative factors in muscle fatigue are multiple, and vary depending on the intensity duration of exercise, fibre type composition muscle, individual's degree fitness. Regardless aetiology, is characterized by inability to maintain required power output decline can be attributed a reduced force velocity. Following high-intensity peak has been shown recover biphasically with an initial rapid (2 min) recovery followed slower (50 return pre-fatigued condition. resting membrane potential depolarizes 10-15 mV, while action overshoot declines similar magnitude. high-frequency stimulation frog semitendinous we observed intracellular potassium [K+]1 decrease from 142 +/- 5 97 8 mM, sodium [Na+]i rose 16 1 49 6 mM. [K+]i loss was that fatigued mouse human skeletal which suggests there may limit before associated depolarization begins frequency. Fibre to- 60 mV (a value some cells) caused significant reduction t-tubular charge movement, extent inversely related concentration extracellular Ca2+. A pH (pHi) 6.0 observed, it suggested low disrupt E-C coupling directly inhibiting SR Ca2+ release channel. However, Lamb at al. (1992) had no effect release, found pHi have movement (Q) or Q vs. Vm relationship. released plays three important roles regulation coupling. As rises, binds inner surface sensor increase (Q gamma) thus opens channels not voltage-regulated, as [Ca2+]i increases further feeds back close same channels. late stages part release. exact cause unknown, but mechanism appears involve direct inhibition