Department of Physiology and Biochemistry, Faculty of Rehabilitation, University School of Physical Education, Krakow, Poland.
Exp Physiol. 2012 Mar;97(3):386-99. doi: 10.1113/expphysiol.2011.062992. Epub 2011 Dec 23.
In this study, we hypothesized that 5 weeks of cycling endurance training can decrease the magnitude of the non-proportional increase in oxygen uptake (V(O(2))) to power output relationship (V(O(2)) 'excess') at exercise intensities exceeding the lactate threshold (LT). Ten untrained, physically active men performed a bout of incremental cycling exercise until exhaustion before and after training. The mitochondrial DNA copy number, myosin heavy chain composition and content of uncoupling protein 3 and sarcoplasmic reticulum Ca(2+)-ATPases (SERCAs) were analysed in muscle biopsies taken from vastus lateralis before and after training. The training resulted in an enhancement of the power-generating capabilities at maximal oxygen uptake (V(O(2)max)) by ∼7% (P = 0.002) despite there being no changes in V(O(2)max) (P = 0.49). This effect was due to a considerable reduction in the magnitude of the V(O(2)) 'excess' (P < 0.05) above the LT. A decrease in plasma ammonia concentration was found during exercise after training (P < 0.05). A downregulation of SERCA2 in vastus lateralis (P = 0.006) was observed after training. No changes in myosin heavy chain composition, selected electron transport chain proteins, uncoupling protein 3 or the mitochondrial DNA copy number (P > 0.05) were found after training. We conclude that the training-induced increase in power-generating capabilities at V(O(2)max) was due to attenuation of the V(O(2)) 'excess' above the LT. This adaptive response seems to be related to the improvement of muscle metabolic stability, as judged by a lowering of plasma ammonia concentration. The enhancement of muscle metabolic stability after training could be caused by a decrease in ATP usage at a given power output owing to downregulation of SERCA2 pumps.
在这项研究中，我们假设 5 周的自行车耐力训练可以减少超过乳酸阈（LT）的运动强度下摄氧量（V（O2））与功率输出关系（V（O2）过剩）的不成比例增加幅度。10 名未经训练的、身体活跃的男性在训练前后进行了一次递增式自行车运动，直到力竭。在训练前后，从股外侧肌中提取肌肉活检，分析线粒体 DNA 拷贝数、肌球蛋白重链组成、解偶联蛋白 3 和肌浆网 Ca2+-ATP 酶（SERCA）的含量。训练导致最大功率摄氧量（V（O2）max）下的功率产生能力提高了约 7%（P = 0.002），尽管 V（O2）max 没有变化（P = 0.49）。这种效果是由于 LT 以上 V（O2）过剩幅度的显著降低（P < 0.05）。训练后，运动时血浆氨浓度降低（P < 0.05）。训练后股外侧肌中 SERCA2 的下调（P = 0.006）。训练后，肌球蛋白重链组成、选定的电子传递链蛋白、解偶联蛋白 3 或线粒体 DNA 拷贝数没有变化（P > 0.05）。我们得出结论，V（O2）max 下功率产生能力的训练诱导增加是由于 LT 以上 V（O2）过剩的衰减。这种适应性反应似乎与肌肉代谢稳定性的改善有关，这可以从血浆氨浓度的降低来判断。由于 SERCA2 泵的下调，给定功率输出下 ATP 利用率的降低可能导致训练后肌肉代谢稳定性的增强。
