Can high-intensity training protect against exercise-induced oxidation of sarcoplasmic reticulum Ca^<2+>-ATPase?

细胞内游离Ca^2+浓度（[Ca^2+] f）在肌肉收缩和舒张中起着重要作用。在骨骼肌中，[Ca^2+]f的调节主要通过肌浆网（SR）释放和摄取Ca^2+的动力学来完成。虽然疲劳过程涉及多种因素和机制，但最近的证据表明，SR的功能障碍是肌肉疲劳的主要原因。我们先前观察到，SR功能的丧失可能至少部分归因于活性氧簇引起的蛋白质氧化，活性氧簇的产生在肌肉收缩期间升高。然而，目前还没有发表的数据来检验高强度训练是否可以防止急性运动引起的SR Ca^<2+>2+-ATP酶活性的恶化和Ca^<2+>-ATP酶的氧化。本研究旨在探讨大强度训练和/或单次运动对肌浆网Ca^<2+>-ATP酶功能和氧化的影响。我们在离体股外侧肌浅部进行了测量，结果表明，8周的跑步训练可引起肌浆网Ca^<2+>-ATP酶活性和Ca ^<2+>-ATP酶氧化的增加，但同时没有引起肌浆网Ca^<2+>-ATP酶活性和Ca^<2+>-ATP酶氧化的改变。释放率这些结果表明训练诱导的SR腔Ca^2+流出减少。尽管运动时间延长至力竭，但力竭运动引起的肌浆网Ca ^<2+>-摄取能力的降低和Ca^<2+>-ATP酶中羰基含量的增加在训练和未训练的肌肉之间没有差异。这些发现表明，高强度训练可能会保护Ca^<2+>-ATP酶免受剧烈肌肉收缩过程中发生的氧化修饰。

The cytosolic free Ca^<2+> concentration ([Ca^<2+>]_f) plays a central role in muscle contraction and relaxation. In skeletal muscle, the regulation of [Ca^<2+>]f is accomplished primarily by the kinetics of Ca^<2+> release and uptake by the sarcoplasmic reticulum (SR). Although the fatigue process involves multiple factors and mechanisms, recent evidence implies that functional impairment of the SR is a major contributor to muscle fatigue. We previously observed that a loss of SR function may be attributed, at least partly, to protein oxidation by reactive oxygen species, generation of which is elevated during muscle contraction. However, no published data presently exists that examines whether high-intensity training could protect against deteriorating SR Ca^<2+>2+-ATPase activity and oxidation of Ca^<2+>-ATPase with acute exercise. The purpose of this study was to investigate the influence of high-intensity training and/or a single bout exercise on SR function and oxidation of Ca^<2+>-ATPase.Our in vitro measures on the superficial region of the vastus lateralis revealed that 8 weeks of running training elicited an increase in SR Ca^<2+>-uptake rate without concomitant changes in SR Ca^<2+>-ATPase activity and Ca^<2+>-release rate. These results implicate training-induced decreases in Ca^<2+> efflux from the SR lumen. Despite the extension of the run time to exhaustion, no differences existed in exhaustive exercise-induced reductions in SR Ca^<2+>-uptake ability and increases in carbonyls contained in Ca^<2+>-ATPase between trained and untrained muscles. These findings suggest that high-intensity training might protect Ca^<2+>-ATPase enzyme against oxidative modification that occurs during vigorous muscle contraction.