INTRACELLULAR CALCIUM AND FORCE IN SINGLE-MOUSE MUSCLE-FIBERS FOLLOWING REPEATED CONTRACTIONS WITH STRETCH

INTRACELLULAR CALCIUM AND FORCE IN SINGLE-MOUSE MUSCLE-FIBERS FOLLOWING REPEATED CONTRACTIONS WITH STRETCH
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DOI:
10.1113/jphysiol.1995.sp020943
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发表时间:
1995-10-01
影响因子:
5.5
通讯作者:
ALLEN, DG
ALLEN, DG
中科院分区:
医学1区
文献类型:
--
作者:
BALNAVE, CD;ALLEN, DG

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1. 肌浆游离Ca2+浓度([Ca2+](i))的作用在减少肌肉力收缩与拉伸后,研究了单个纤维从小鼠脚趾肌。对于10次破伤风(议定书I),肌肉纤维被拉伸至其最佳长度(L(0))的25%;对于10次和30次破伤风(议定书II),肌肉纤维被拉伸至L(0)的50%。Indo-1。[Ca2+](i).2。在每个方案中,拉伸序列与等距控制进行比较;拉伸系列总是导致肌肉性能比等距控制更大的变化。观察到的变化是(i)破伤风力减少,(ii)破伤风[Ca2+]减少(i), (iii)静息[Ca2+]增加(i)和(iv)低刺激频率(30和50 Hz)与高刺激频率(100 Hz)相比,力的相对减少更大。这些变化维持了60分钟。拉伸静止的肌纤维对随后的[Ca2+](i)或力没有影响。按照方案一,10毫米咖啡因使强直性恢复到拉伸前的水平。在拉伸前后构建了强直性[Ca2+](i)与力曲线,结果表明,拉伸后肌纤维的最大Ca2+激活力和Ca2+敏感性均与对照组无显著差异。因此,力的减少似乎是破伤风[Ca2+](i)减少的结果。方案二中更严格的拉伸方案导致了比方案一更大的力量减少。10毫摩尔咖啡因并没有恢复控制力。拉伸前后[Ca2+](i)-力关系的比较表明,强直性力的降低是由强直性[C2+](i)的降低、最大Ca2+激活力的降低和Ca2+敏感性的降低共同引起的。在两种方案下,静息[Ca2+](i)显示出持续至少60分钟的小幅上升。这种升高的[Ca2+](i)与肌浆网Ca2+泵泵率的降低有关。这项研究表明,减少Ca2+释放和降低Ca2+敏感性有助于减少单个哺乳动物肌肉纤维在积极拉伸后的发力能力。
1. The role of the myoplasmic free Ca2+ concentration ([Ca2+](i)) in the reduction of muscle force following contractions with stretch was investigated in single fibres from mouse toe muscle. Muscle fibres were either stretched by 25% of their optimum length (L(0)) for ten tetani (Protocol I) or stretched by 50% of L(0) for betsveen ten and thirty tetani (Protocol II). Indo-1. was used to measure [Ca2+](i).2. In each protocol the stretch series was compared with isometric controls; the stretch series always resulted in greater changes in muscle properties than in the isometric controls. The observed changes were (i) reduced tetanic force, (ii) reduced tetanic [Ca2+](i), (iii) increased resting [Ca2+](i) and (iv) the greater relative reduction in force at low stimulus frequencies (30 and 50 Hz) compared with high (100 Hz). These changes were maintained for up to 60 min.3. Stretching a resting muscle fibre had no effect on the subsequent [Ca2+](i) or force.4. Following Protocol I 10 mM caffeine restored tetanic force to pre-stretch levels. Tetanic [Ca2+](i) vs. force curves were constructed pre- and post-stretch and showed that neither the maximum Ca2+-activated force nor the Ca2+ sensitivity of the muscle fibres post-stretch was significantly different from control. The force reduction, therefore, appears to be the result of reduced tetanic [Ca2+](i).5. The more severe stretching regimen of Protocol II resulted in a much greater reduction in force than Protocol I. Ten millimolar caffeine did not restore control force. Comparison of the [Ca2+](i)-force relationships pre- and post-stretch showed that the reduction in tetanic force was caused by a combination of a reduced tetanic [C2+](i), reduced maximum Ca2+-activated force and reduced Ca2+ sensitivity.6. Following both protocols the resting [Ca2+](i) showed a small rise which persisted for at least 60 min. This elevated [Ca2+](i) was associated with a reduction in the pump rate of the sarcoplasmic reticulum Ca2+ pump.7. This study establishes that reduced Ca2+ release and reduced Ca2+ sensitivity contribute to the reduction in force generating capacity of single mammalian muscle fibres following active stretches.