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

细胞内游离钙离子浓度([Ca^&lt；2+&gt；]f)在肌肉收缩和松弛中起着核心作用。在骨骼肌中，[Ca~(2+)]f的调节主要是通过肌浆网(SR)释放和摄取Ca~(2+)的动力学来完成的。虽然疲劳过程涉及多个因素和机制，但最近的证据表明，SR的功能障碍是导致肌肉疲劳的主要因素。我们以前观察到，SR功能的丧失可能至少部分归因于由活性氧物种引起的蛋白质氧化，在肌肉收缩过程中，活性氧物种的生成增加。然而，目前还没有公开的数据来检验高强度训练是否可以防止急性运动时SR Ca^&lt；2+&gt；2+-ATPase活性的恶化和Ca^&lt；2+&gt；-ATPase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功能和钙-ATP酶氧化的影响。我们在股外侧肌浅层进行的体外测量显示，8周的跑步训练增加了肌浆网钙摄取速率，但对肌浆网钙摄取速率和钙释放速率无明显影响。这些结果表明，训练导致SR管腔内Ca~(2+)流出减少。尽管跑到力竭的时间延长了，但训练和未训练的肌肉在力竭运动引起的肌浆网钙摄取能力的降低和钙离子-ATPase中的羰基增加方面没有差异。这些发现表明，高强度训练可能保护Ca^&lt；2+-ATPase酶不受肌肉剧烈收缩时发生的氧化修饰的影响。

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.