Does the sarcoplasmic reticulum function contribute to the decline of muscle contractile force following eccentric contraction ?

为了研究肌浆网（SR） Ca2+处理功能和肌膜兴奋性的改变是否会导致偏心收缩（ECC）后收缩力的丧失，我们检测了受ECC刺激的大鼠后肢肌肉的收缩力、SR功能和肌膜Na+-K+- atp酶活性。ECC导致大鼠力降低，SR释放Ca2+的能力受损，Na+-K+- atp酶活性降低。这些结果表明，ecc收缩肌肉产生的力可能在更大程度上受到SR Ca2+释放减少和肌膜兴奋性的影响。

To investigated whether the alterations in sarcoplasmic reticulum (SR) Ca2+handling function and excitability of sarcolemma would contribute to a loss of the contractile force following eccentric contraction (ECC), we examined contractile force, SR functions and sarcolemma Na+-K+-ATPase activity in ECC-stimulated rat hindlimb muscles. ECC resulted in force reductions, impaired capacity of Ca2+release by the SR and decreased Na+-K+-ATPase activity in rat. These results suggest that force developed by ECC-contracted muscle may be affected to a greater extent by diminished release of Ca2+from the SR and excitability of sarcolemma.