Interactions between intracellular calcium and phosphate in intact mouse muscle during fatigue
Interactions between intracellular calcium and phosphate in intact mouse muscle during fatigue
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DOI：
10.1152/japplphysiol.01404.2010
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发表时间：
2011-08-01
影响因子：
3.3
通讯作者：
Rudolf, R.
中科院分区：
文献类型：
--
作者：
Allen, D. G.;Clugston, E.;Rudolf, R.
研究了麻醉小鼠完整胫骨前肌的疲劳情况。远端肌腱被分离并连接到力传感器，同时血流继续正常进行。用直接施加到肌肉表面的电极刺激肌肉，并通过重复（每 4 秒 1 次）、短暂（0.4 秒）、最大（100 Hz 刺激频率）破伤风来疲劳。力单调下降至初始值的 49 +/- 5%，半衰期为 36 +/- 5 秒，4 分钟后恢复至 86 +/- 4%。通过 P-31-NMR 对肌肉的高氯酸提取物测量细胞内磷酸盐浓度 ([P-i])。 [P-i] 在疲劳期间从 7.6 +/- 1.7 增加到 16.0 +/- 1.6 mmol/kg 肌肉湿重，并在恢复期间恢复到控制。实验前2周，用质粒已在肌肉中转染的骆驼测量细胞内Ca2+。 Yellow Cameleon 2 用于测量肌浆 Ca2+，D1ER 用于测量肌浆网 (SR) Ca2+。破伤风期间肌浆Ca2+在疲劳期间稳步下降，并在4分钟内完全恢复。 SR Ca2+ 在疲劳期间也单调下降，并在休息后显示出部分恢复。这些结果表明，力量下降的初始阶段伴随着[P-i]的上升和破伤风肌浆Ca2+的减少。我们认为这两种变化都会导致疲劳。破伤风肌浆 Ca2+ 下降的一个可能原因是 SR 中 CaPi 的沉淀。
Fatigue was studied in intact tibialis anterior muscle of anesthetized mice. The distal tendon was detached and connected to a force transducer while blood flow continued normally. The muscle was stimulated with electrodes applied directly to the muscle surface and fatigued by repeated (1 per 4 s), brief (0.4 s), maximal (100-Hz stimulation frequency) tetani. Force declined monotonically to 49 +/- 5% of the initial value with a half time of 36 +/- 5 s and recovered to 86 +/- 4% after 4 min. Intracellular phosphate concentration ([P-i]) was measured by P-31-NMR on perchloric acid extracts of muscles. [P-i] increased during fatigue from 7.6 +/- 1.7 to 16.0 +/- 1.6 mmol/kg muscle wet wt and returned to control during recovery. Intracellular Ca2+ was measured with cameleons whose plasmids had been transfected in the muscle 2 wk before the experiment. Yellow cameleon 2 was used to measure myoplasmic Ca2+, and D1ER was used to measure sarcoplasmic reticulum (SR) Ca2+. The myoplasmic Ca2+ during tetani declined steadily during the period of fatigue and showed complete recovery over 4 min. The SR Ca2+ also declined monotonically during fatigue and showed a partial recovery with rest. These results show that the initial phase of force decline is accompanied by a rise in [P-i] and a reduction in the tetanic myoplasmic Ca2+. We suggest that both changes contribute to the fatigue. A likely cause of the decline in tetanic myoplasmic Ca2+ is precipitation of CaPi in the SR.