Renaud J M, Comtois A
University of Ottawa, Department of Physiology, Ontario, Canada.
J Muscle Res Cell Motil. 1994 Aug;15(4):420-31. doi: 10.1007/BF00122116.
The goal of this study was to investigate how an increase in the extracellular K+ (K0+) concentration immediately after fatigue affects the recovery of the resting potential, the twitch and tetanic contraction of frog sartorius muscle to further understand the role of K+ in the mechanism of fatigue. Resting potentials were measured with conventional microelectrodes. Twitch and tetanic contractions were elicited by field stimulation. All muscles were fatigued with tetanic contractions at a rate of one contraction per second for 3 min while being exposed to 3 mmole l-1 K0+. During fatigue development the resting potential decreased by 16 mV (control group and pH0 7.2, extracellular pH), while the decrease in the twitch force was 32.8%, compared to 79.3% for the tetanic force, and 84.6% for the maximum rate of force development of the tetanus. Fatigued muscles were also unable to maintain a plateau phase during a tetanus: force declined by 14.8% during this phase. During the recovery period under control conditions (3 mmole l-1 K0+), all four parameters returned to their pre-fatigue values, the recovery of the plateau phase was the fastest (10 min), while that of the twitch force was the slowest (80 min). When K0+ was increased to 7.5 or 9.5 mmole l-1 immediately after fatigue, the recovery rate of the tetanic force and plateau phase was reduced. The maximum rate of force development of the tetanus, however, recovered at a faster rate than control muscles. The recovery of the twitch force was also increased above that of control when K0+ was increased to 9.0 mmole l-1 (a concentration which maximally potentiates the twitch force of unfatigued muscle). Frog sartorius muscles were also tested at pH0 6.4, a pH0 which inhibits force recovery. At that pH0 the effects of K0+ were similar to those observed at pH0 7.2. It is concluded that the role of K+ in muscle fatigue is more complex and may not involve just a contribution to the decrease in force during fatigue development, but may also contribute to an increase in force development under some conditions.
本研究的目的是探究疲劳后即刻细胞外钾离子（K0+）浓度升高如何影响青蛙缝匠肌静息电位的恢复、单收缩和强直收缩，以进一步了解钾离子在疲劳机制中的作用。使用传统微电极测量静息电位。通过场刺激引发单收缩和强直收缩。所有肌肉在暴露于3 mmol l-1 K0+的情况下，以每秒一次收缩的频率进行强直收缩3分钟而疲劳。在疲劳发展过程中，静息电位下降了16 mV（对照组，细胞外pH值为7.2），而单收缩力下降了32.8%，强直收缩力下降了79.3%，强直收缩的最大力发展速率下降了84.6%。疲劳肌肉在强直收缩期间也无法维持平台期：在此阶段力下降了14.8%。在对照条件下（3 mmol l-1 K0+）的恢复期间，所有四个参数均恢复到疲劳前的值，平台期的恢复最快（10分钟），而单收缩力的恢复最慢（80分钟）。当疲劳后即刻将K0+增加到7.5或9.5 mmol l-1时，强直收缩力和平台期的恢复速率降低。然而，强直收缩的最大力发展速率比对照肌肉恢复得更快。当K0+增加到9.0 mmol l-1（该浓度可最大程度增强未疲劳肌肉的单收缩力）时，单收缩力的恢复也高于对照。青蛙缝匠肌也在pH值为6.4的条件下进行了测试，该pH值会抑制力的恢复。在该pH值下，K0+的作用与在pH值为7.2时观察到的作用相似。结论是，钾离子在肌肉疲劳中的作用更为复杂，可能不仅导致疲劳发展过程中力的下降，还可能在某些条件下促进力的发展增加。
