The effect of antioxidants on sarcoplasmic reticulum function during muscle fatigue

第一个实验的目的是研究大鼠在跑步机跑到精疲力竭后，肌浆网（SR）利用腓肠肌和股外侧肌的浅表部分运动导致Ca^<2+>-隔离能力下降的原因。运动导致SR Ca^<2+>- atp酶活性和Ca^<2+>摄取率分别下降16%和34%。SR Ca^<2+>-ATPase蛋白中羰基含量增加了127%。在第二个实验中，验证了n -乙酰半胱氨酸（NAC）作为抗氧化剂之一可能通过调节SR Ca^<2+>处理能力来影响膈疲劳的假设。在没有NAG或NAG存在的情况下，以0.5次/秒的速度对大鼠横膈膜进行350毫秒的电刺激。在刺激开始后60秒及以后，nac处理的肌肉产生的力明显大于未处理的肌肉。在力降低到初始水平的50-80%的肌肉中，NAG治疗抑制了SR功能的降低。这些结果表明，SR Ca^<2+> - atp酶蛋白的氧化可能是SR Ca^<2+> -隔离能力下降的原因，而抗氧化剂诱导的SR功能下降的抑制可能是（至少部分地）延迟肌肉疲劳中期疲劳发展速度的原因。

The purpose of the first experiment was to examine a cause of exercise-induced decreases in Ca^<2+>-sequestering capacity by sarcoplasmic reticulum (SR) using the superficial portions of the gastrocnemius and vastus lateralis muscles of the rat after treadmill running to exhaustion. Exercise led to 16% and 34% decreases in SR Ca^<2+>-ATPase activity and Ca^<2+> uptake rate, respectively. The carbonyl group content in SR Ca^<2+>-ATPase protein was increased by 127%. In the second experiment, the hypothesis was tested that N-acetylcysteine (NAC) that is one of antioxidants may influence diaphragmic fatigue by modulating SR Ca^<2+> handling capacity. In the absence or presence of NAG, rat diaphragm was electrically stimulated with titanic trains (350 msec) delivered at 0.5 train/sec for various durations. At 60 sec after the onset of stimulation and beyond, force developed by NAC-treated muscle was significantly greater that that of non-treated muscle. In muscles where force was reduced to 50-80% of the initial level, treatment of NAG inhibited reductions in SR function. These results suggest that oxidation of SR Ca^<2+> -ATPase protein may account for decreases in Ca^<2+> -sequestering capacity by the SR and that antioxidant-induced inhibition of a decline in SR function may be responsible, at least partly, for a delay of the rate of fatigue development in the middle phase of muscular fatigue.