Effects of endurance training and acute exercise on sarcoplasmic reticulum function

本研究旨在探讨耐力训练和(或)一次急性运动对骨骼肌纤维肌浆网(SR)钙摄取和释放速率及钙激活的三磷酸腺苷酶(ATPase)活性的影响。经过10周的训练后，一半的训练和未训练的大鼠被进行中等强度的跑步，直到筋疲力尽。跑台训练使大鼠足底肌(PL)的肌浆网钙摄取率和肌浆网钙摄取率降低，而比目鱼肌(SOL)的肌浆网钙摄取率和肌浆网钙摄取率降低。力竭跑后即刻，双侧肌肉均出现SR功能障碍，其中SOL的变化更为明显。在PL中，急性运动仅导致未训练肌肉的钙摄取速率和钙ATP酶活性降低。在SOL的情况下，未经训练和训练的肌肉中的钙释放速率以及钙摄取速率和钙离子的ATPase活性均受到不利影响。在这些变化的程度上，受过训练的和未受过训练的SOL之间没有差异。然而，以每一次力竭时的Δ摄取或释放速率表示的钙摄取和释放速率的平均下降速率，在未经训练的SOL中大约是训练组的2倍。二硫苏糖醇的孵育未能恢复在训练的SOL和训练的SOL中观察到的降低的催化活性。这些发现表明，运动诱导的SR Ca；-ATPase蛋白和耐力训练可能能够延缓运动中SR功能的抑制率。

The purpose of this study was to examine the effect of endurance training and/or an acute bout of exercise on Ca^<2+> uptake and release rate and Ca^<2+>-stimulatated adenosine triphosphatase (ATPase) activity of sarcoplasmic reticulum (SR) in skeletal muscle fibers. Following 10 weeks of training, one-half of trained and untrained rats were subjected to moderate-intensity runs to exhaustion. A training program of treadmill running elicited depressions in SR Ca^<2+> uptake rate and Ca^<2+>-ATPase activity in the plantaris muscle (PL), but not in the soleus muscle (SOL). Immediately after exhaustive running, the dysfunction of SR occurred in both muscles, with more pronounced alterations being observed in SOL.In PL, acute exercise brought about reductions in Ca^<2+> uptake rate and Ca^<2+>-ATPase activity in only untrained muscles. In the case of SOL, Ca^<2+> release rate as well as Ca^<2+> uptake rate and Ca^<2+>-ATPase activity were adversely affected in both untrained and trained muscles. No differences existed between trained and untrained SOL with regard to the extent of these changes. However, the mean rates of the decline of Ca^<2+> uptake and release rates, expressed as Δ uptake or release rates per time to exhaustion, were approximately 2-fold higher in untrained SOL than in trained SOL.Incubation of dithiothreitol, a disulfide reducing agent, failed to restore the decreased catalytic activity observed in exercised SOL and PL.These findings suggest that exercise-induced decline in SR Ca^<2+>-ATPase may not be caused by an oxidation of sulfhydryl groups on SR Ca^<2+>-ATPase protein and that endurance training may be capable of delaying th depression rate of SR function that occurred during exercise.