Renaud J M, Light P
University of Ottawa, Department of Physiology, Ont., Canada.
Can J Physiol Pharmacol. 1992 Sep;70(9):1236-46. doi: 10.1139/y92-172.
The effects of increasing the extracellular K+ concentration on the capacity to generate action potentials and to contract were tested on unfatigued muscle fibers isolated from frog sartorius muscle. The goal of this study was to investigate further the role of K+ in muscle fatigue by testing whether an increased extracellular K+ concentration in unfatigued muscle fibers causes a decrease in force similar to the decrease observed during fatigue. Resting and action potentials were measured with conventional microelectrodes. Twitch and tetanic force was elicited by field stimulation. At pHo (extracellular pH) 7.8 and 3 mmol K+.L-1 (control), the mean resting potential was -86.6 +/- 1.7 mV (mean +/- SEM) and the mean overshoot of the action potential was 5.6 +/- 2.5 mV. An increased K+ concentration from 3 to 8.0 mmol.L-1 depolarized the sarcolemma to -72.2 +/- 1.4 mV, abolished the overshoot as the peak potential during an action potential was -12.0 +/- 3.9 mV, potentiated the twitch force by 48.0 +/- 5.7%, but did not affect the tetanic force (maximum force) and the ability to maintain a constant force during the plateau phase of a tetanus. An increase to 10 mmol K+.L-1 depolarized the sarcolemma to -70.1 +/- 1.7 mV and caused large decreases in twitch (31.6 +/- 26.1%) and tetanic (74.6 +/- 12.1%) force. Between 3 and 9 mmol K+.L-1, the effects of K+ at pHo 7.2 (a pHo mimicking the change in interstitial pH during fatigue) and 6.4 (a pHo known to inhibit force recovery following fatigue) on resting and action potentials as well as on the twitch and tetanic force were similar to those at pHo 7.8. Above 9 mmol K+.L-1 significant differences were found in the effect of K+ between pHo 7.8 and 7.2 or 6.4. In general, the decrease in peak action potential and twitch and tetanic force occurred at higher K+ concentrations as the pHo was more acidic. The results obtained in this study do not support the hypothesis that an accumulation of K+ at the surface of the sarcolemma is sufficiently large to suppress force development during fatigue. The possibility that the K+ concentration in the T tubules reaches the critical K+ concentration necessary to cause a failure of the excitation-contraction coupling mechanism is discussed.
在从青蛙缝匠肌分离出的未疲劳肌纤维上，测试了增加细胞外钾离子浓度对产生动作电位和收缩能力的影响。本研究的目的是通过测试未疲劳肌纤维中细胞外钾离子浓度升高是否会导致力量下降，类似于疲劳期间观察到的下降，来进一步研究钾离子在肌肉疲劳中的作用。使用传统微电极测量静息电位和动作电位。通过场刺激引发单收缩和强直收缩力。在细胞外pH值（pHo）7.8和3 mmol K⁺·L⁻¹（对照）时，平均静息电位为-86.6±1.7 mV（平均值±标准误），动作电位的平均超射为5.6±2.5 mV。钾离子浓度从3 mmol·L⁻¹增加到8.0 mmol·L⁻¹使肌膜去极化至-72.2±1.4 mV，消除了超射，因为动作电位期间的峰值电位为-12.0±3.9 mV，单收缩力增强了48.0±5.7%，但不影响强直收缩力（最大力）以及在强直收缩平台期维持恒定力的能力。增加到10 mmol K⁺·L⁻¹使肌膜去极化至-70.1±1.7 mV，并导致单收缩力（31.6±26.1%）和强直收缩力（74.6±12.1%）大幅下降。在3至9 mmol K⁺·L⁻¹之间，pHo 7.2（模拟疲劳期间间质pH变化的pHo）和6.4（已知抑制疲劳后力量恢复的pHo）下钾离子对静息电位和动作电位以及单收缩和强直收缩力的影响与pHo 7.8时相似。高于9 mmol K⁺·L⁻¹时，发现pHo 7.8与7.2或6.4时钾离子的作用存在显著差异。一般来说，随着pHo更酸性，动作电位峰值以及单收缩和强直收缩力的下降发生在更高的钾离子浓度下。本研究获得的结果不支持肌膜表面钾离子积累足够大以抑制疲劳期间力量发展的假设。讨论了横管中的钾离子浓度达到导致兴奋-收缩偶联机制失效所需的临界钾离子浓度的可能性。
