Laboratorio de Fisiología y Biofisíca del Músculo, IBE, UCV, Caracas, Venezuela.
J Muscle Res Cell Motil. 2010 Jul;31(1):13-33. doi: 10.1007/s10974-009-9195-8. Epub 2010 Jan 5.
Repetitive activation of skeletal muscle fibers leads to a reduced transmembrane K(+) gradient. The resulting membrane depolarization has been proposed to play a major role in the onset of muscle fatigue. Nevertheless, raising the extracellular K(+) K(+)(O) concentration (K(+)) to 10 mM potentiates twitch force of rested amphibian and mammalian fibers. We used a double Vaseline gap method to simultaneously record action potentials (AP) and Ca(2+) transients from rested frog fibers activated by single and tetanic stimulation (10 pulses, 100 Hz) at various K(+) and membrane potentials. Depolarization resulting from current injection or raised K(+ produced an increase in the resting [Ca(2+)]. Ca(2+) transients elicited by single stimulation were potentiated by depolarization from -80 to -60 mV but markedly depressed by further depolarization. Potentiation was inversely correlated with a reduction in the amplitude, overshoot and duration of APs. Similar effects were found for the Ca(2+) transients elicited by the first pulse of 100 Hz trains. Depression or block of Ca(2+) transient in response to the 2nd to 10th pulses of 100 Hz trains was observed at smaller depolarizations as compared to that seen when using single stimulation. Changes in Ca(2+) transients along the trains were associated with impaired or abortive APs. Raising K(+) to 10 mM potentiated Ca(2+) transients elicited by single and tetanic stimulation, while raising K(+) to 15 mM markedly depressed both responses. The effects of 10 mM K(+)(O) on Ca(2+) transients, but not those of 15 mM K(+)(O), could be fully reversed by hyperpolarization. The results suggests that the force potentiating effects of 10 mM K(+)(O) might be mediated by depolarization dependent changes in resting [Ca(2+)] and Ca(2+) release, and that additional mechanisms might be involved in the effects of 15 mM K(+)(O) on force generation.
重复激活骨骼肌纤维会导致跨膜 K(+)梯度降低。由此产生的膜去极化被认为在肌肉疲劳的发生中起主要作用。然而，将细胞外 K(+) K(+)(O)浓度升高至 10 mM 会增强休息状态下的两栖类和哺乳类纤维的单次收缩力。我们使用双 Vaseline 间隙方法，同时记录休息状态下的青蛙纤维的动作电位 (AP) 和 Ca(2+) 瞬变，这些纤维通过单次和强直刺激 (10 个脉冲，100 Hz) 在不同的 K(+) 和膜电位下被激活。电流注入或升高 K(+ 引起的去极化导致静息 [Ca(2+)]增加。从 -80 到 -60 mV 的去极化增强了由单次刺激引起的 Ca(2+) 瞬变，但进一步的去极化则显著抑制了 Ca(2+) 瞬变。增强作用与 AP 幅度、超射和持续时间的减少呈反比关系。对于 100 Hz 串的第一个脉冲引起的 Ca(2+) 瞬变，也发现了类似的效果。与使用单次刺激时相比，在较小的去极化时，观察到对 100 Hz 串的第 2 到第 10 个脉冲的 Ca(2+) 瞬变的抑制或阻断。随着 100 Hz 串的进行，Ca(2+) 瞬变的变化与 AP 受损或中止有关。将 K(+) 升高至 10 mM 增强了由单次和强直刺激引起的 Ca(2+) 瞬变，而将 K(+) 升高至 15 mM 则显著抑制了这两种反应。10 mM K(+)(O) 对 Ca(2+) 瞬变的影响，但不是 15 mM K(+)(O) 的影响，可以通过超极化完全逆转。结果表明，10 mM K(+)(O) 的增强力作用可能是通过去极化依赖性的静息 [Ca(2+)]和 Ca(2+) 释放变化介导的，而 15 mM K(+)(O) 对力产生的影响可能涉及其他机制。
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