Research Centre in Physical Activity, Health and Leisure, University of Porto, Portugal.
Mitochondrion. 2009 Nov;9(6):454-62. doi: 10.1016/j.mito.2009.08.005. Epub 2009 Aug 12.
The aim of the present work was to test the hypothesis that moderate endurance treadmill training ameliorates gastrocnemius mitochondrial bioenergetics and increases the tolerance to the calcium-induced mitochondrial permeability transition pore (MPTP) opening. Twelve adult (6-8 week old) male Wistar rats were randomly divided into two groups (n=6per group): sedentary and trained (14 week of endurance treadmill running, 60min/day). Several end-points for invitro gastrocnemius mitochondrial function including oxygen consumption, transmembrane electric potential and susceptibility to calcium-induced MPTP opening were evaluated. Caspase-9 activity was measured in the intact tissue. Endurance training induced significant increases in state 3 and in respiratory control ratio both with complex I and II-linked substrates (malate+pyruvate and succinate, respectively). Increased CCCP-induced uncoupled respiration with succinate as substrate was also observed (p<0.05). No differences were found regarding state 4 and ADP/O ratio with both substrates. In addition, training significantly decreased the phosphorylative lag phase, whereas no changes were observed on maximal transmembrane electric potential, ADP-induced depolarization and repolarization potential (p<0.05). Interestingly and as opposed to our hypothesis, muscle mitochondria isolated from trained rats were more susceptible to MPTP induction by calcium, although in an initial phase muscle mitochondria isolated from trained rats had an increased calcium uptake. Interestingly, we also verified that endurance training increased the activity of caspase 9. The data obtained confirms that endurance training results in a general improvement in the gastrocnemius mitochondrial respiratory function, although mitochondrial and cellular alterations during training also result in increased calcium-induced MPTP opening.
即中等强度的耐力跑步机训练可改善比目鱼肌线粒体生物能学，并提高对钙诱导的线粒体通透性转换孔（MPTP）开放的耐受性。12 只成年（6-8 周龄）雄性 Wistar 大鼠被随机分为两组（每组 n=6）：安静组和训练组（14 周耐力跑步机跑步，每天 60 分钟）。评估了离体比目鱼肌线粒体功能的多个终点，包括耗氧量、跨膜电势和对钙诱导的 MPTP 开放的敏感性。在完整组织中测量了 caspase-9 活性。耐力训练显著增加了状态 3 和呼吸控制比，两者均与复合物 I 和 II 连接的底物（苹果酸+丙酮酸和琥珀酸）有关。还观察到 CCCP 诱导的与琥珀酸作为底物的解偶联呼吸增加（p<0.05）。两种底物的状态 4 和 ADP/O 比值均无差异。此外，训练显著缩短了磷酸化滞后期，而最大跨膜电势、ADP 诱导的去极化和复极化电势均无变化（p<0.05）。有趣的是，与我们的假设相反，尽管来自训练大鼠的肌肉线粒体在初始阶段具有增加的钙摄取，但它们对钙诱导的 MPTP 诱导更为敏感。有趣的是，我们还证实了耐力训练增加了 caspase 9 的活性。所得数据证实，耐力训练导致比目鱼肌线粒体呼吸功能的普遍改善，尽管训练期间的线粒体和细胞改变也导致钙诱导的 MPTP 开放增加。
