Contribution of impaired myofibril and ryanodine receptor function to prolonged low-frequency force depression after in situ stimulation in rat skeletal muscle
Contribution of impaired myofibril and ryanodine receptor function to prolonged low-frequency force depression after in situ stimulation in rat skeletal muscle
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DOI：
10.1007/s10974-015-9409-1
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发表时间：
2015-02
影响因子：
2.7
通讯作者：
D. Watanabe;Keita Kanzaki;Mai Kuratani;S. Matsunaga;N. Yanaka;M. Wada
中科院分区：
文献类型：
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作者：
D. Watanabe;Keita Kanzaki;Mai Kuratani;S. Matsunaga;N. Yanaka;M. Wada
本研究的目的是检查是否长期低频力抑郁症（PLFFD），发生在原位的结果降低肌原纤维钙敏感性和/或减少肌浆网（SR）钙释放。通过坐骨神经电刺激完整的大鼠腓肠肌，直到力降低至初始的约50%，并在刺激停止后30分钟解剖。在仅由IIB型纤维组成的浅表区域进行皮肤纤维和整个肌肉分析。在皮肤纤维（1与50 Hz）和整个肌肉（20与100 Hz）中，振动刺激显著降低了低频力与高频力的比值，分别为65%和73%。为了评估肌原纤维钙敏感性和ryanodine受体咖啡因敏感性的变化，皮肤纤维被激活的钙和咖啡因的解决方案，分别。疲劳肌肉的皮肤纤维显示咖啡因敏感性降低，肌原纤维Ca 2+敏感性增加。用2，2 ′-二硫代二吡啶和还原型谷胱甘肽处理疲劳肌纤维时，肌纤维Ca 2+敏感性的增加幅度小于休息肌纤维。在疲劳肌肉中，肌钙蛋白I的S-谷胱甘肽化增加，4-氯间甲酚诱导的次最大SR Ca 2+释放减少。这些研究结果表明，在PLFFD的早期阶段，发生在运动的动物和人类的快缩肌，肌钙蛋白I的S-谷胱甘肽化可能会减弱PLFFD通过增加肌原纤维Ca 2+的敏感性，在这种情况下，PLFFD可能归因于SR Ca 2+释放失败。
The aim of this study was to examine whether prolonged low-frequency force depression (PLFFD) that occurs in situ is the result of decreased myofibrillar Ca2+sensitivity and/or reduced sarcoplasmic reticulum (SR) Ca2+release. Intact rat gastrocnemius muscles were electrically stimulated via the sciatic nerve until force was reduced to ~50 % of the initial and dissected 30 min following the cessation of stimulation. Skinned fibre and whole muscle analyses were performed in the superficial region composed exclusively of type IIB fibres. Fatiguing stimulation significantly reduced the ratio of force at low frequency to that at high frequency to 65 % in skinned fibres (1 vs. 50 Hz) and 73 % in whole muscles (20 vs. 100 Hz). In order to evaluate changes in myofibrillar Ca2+sensitivity and ryanodine receptor caffeine sensitivity, skinned fibres were activated in Ca2+- and caffeine-containing solutions, respectively. Skinned fibres from fatigued muscles displayed decreased caffeine sensitivity together with increased myofibrillar Ca2+sensitivity. Treatment with 2,2′-dithiodipyridine and reduced glutathione induced a smaller increase in myofibrillar Ca2+sensitivity in fatigued than in rested fibres. In fatigued muscles,S-glutathionylation of troponin I was increased and submaximal SR Ca2+release, induced by 4-chloro-m-cresol, was decreased. These findings suggest that in the early stage of PLFFD that occurs in fast-twitch muscles of exercising animals and humans,S-glutathionylation of troponin I may attenuate PLFFD by increasing myofibrillar Ca2+sensitivity and that under such a circumstance, PLFFD may be ascribable to failure of SR Ca2+release.