Mechanisms of Retarded Recovery of Muscular Fatigue After Vigorous Contraction

肌浆网（SR）是所有肌细胞膜中的一种膜结构，它紧密地包围着每一个肌原纤维，在调节细胞内游离Ca^2+浓度方面起着关键作用。本研究旨在阐明剧烈收缩后肌肉疲劳恢复迟缓的潜在机制，重点关注SR对Ca^2+处理能力的变化。结果：1.电刺激引起的后肢骨骼肌重复性收缩，在刺激1 min和5 min时，腓肠肌浅层和深层SR Ca^<2+>-ATP酶活性分别降低//，比目鱼肌活性无变化.刺激5分钟后恢复30分钟，可使GS肌浆网Ca^<2+>-ATP酶活性的降低程度减轻。然而，在该时间点，酶中所含的羰基含量 关于我们 e和异硫氰酸荧光素（FITC）结合酶保持增加和减少，分别3。提取糖原从SR膜通过处理与葡糖淀粉酶诱发减少糖原磷酸化酶的SR和升高的FITC结合。然而，这些变化并不伴随着SR Ca^<2+>-ATP酶催化活性的变化，这些发现并不意味着蛋白质的氧化修饰，核苷酸结合结构域的结构改变或糖原的消耗是导致收缩诱导的SR Ca ^2+处理能力下降的原因。肌浆网Ca^<2+>-ATP酶活性和/或寡聚化程度的不同可以解释肌浆网Ca ^<2 +>-处理能力的不同恢复率。少

The sarcoplasmic reticulum (SR), a membrane structure in all mu grip evils that closely surrounds each myofibril, plays a critical role in the regulation of intracellular free Ca^<2+> concentration. The present study was undertaken to address the mechanisms underlying retarded recovery of muscular fatigue after vigorous contraction, with focus on changes in the Ca^<2+>-handling ability of the SR Experiments conducted with rat skeletal muscles provided the findings described below.1. Repetitive muscle contractions hind limb skeletal muscles induced by electric nerve stimulation caused //depressions in SR Ca^<2+>-ATPase activity in the superficial (GS) and deep regions of the gastrocnemius at 1 and 5 min of stimulation, respectively and 2/no changes in the activity in the soleus.2. Thirty-min recovery after 5-min stimulation resulted in restorations of contraction-induced decreases in SR Ca^<2+>-ATPase activity in GS. However, at this time point, a carbonyl content comprised in the enzym … More e and a fluorescein isothiocyanate (FITC) binding to the enzyme remained increased and decreased, respectively3. Extraction of glycogen from the SR membrane by treatment with glucoamylase evoked decreases in glycogen phosphorylase on the SR and elevations of FITC binding. However, these alterations were not accompanied by changes in the catalytic activity of SR Ca^<2+>-ATPase.These findings do not implicate oxidative modifications of protein, structural alterations to the nucleotide-binding domain or depletion of glycogen as a contributor to contraction-induced depressions in the Ca^<2+>-handling ability of the SR It has previously been shown that the rate of restoration of the impaired SR Ca-uptake capacity induced by vigorous muscle contraction varies among different contraction modes, even when immediately after the cessation of contraction, the extent of the depression in SR Ca^<2+>-uptake capacity is similar The distinct restoration rate of SR Ca^<2+>-handling capacity could be explained by the varied degrees of protease activation and/or of oligomerization of SR Ca^<2+-> ATPase. Less