Korea Institute of Sport Science, San223-19, Gongneung-2DongNowon-gu, Seoul 139-242, South Korea.
BMC Musculoskelet Disord. 2012 Oct 30;13:211. doi: 10.1186/1471-2474-13-211.
Although muscle dysfunction caused by unfamiliar lengthening contraction is one of most important issues in sports medicine, there is little known about the molecular events on regeneration process. The purpose of this study was to investigate the temporal and spatial expression patterns of myogenin, myoD, pax7, and myostatin after acute lengthening contraction (LC)-induced injury in the rat hindlimb.
We employed our originally developed device with LC in rat gastrocnemius muscle (n = 24). Male Wistar rats were anesthetized with isoflurane (aspiration rate, 450 ml/min, concentration, 2.0%). The triceps surae muscle of the right hindlimb was then electrically stimulated with forced isokinetic dorsi-flexion (180°/sec and from 0 to 45°). Tissue contents of myoD, myogenin, pax7, myostatin were measured by western blotting and localizations of myoD and pax7 was measured by immunohistochemistry. After measuring isometric tetanic torque, a single bout of LC was performed in vivo.
The torque was significantly decreased on days 2 and 5 as compared to the pre-treatment value, and recovered by day 7. The content of myoD and pax7 showed significant increases on day 2. Myogenin showed an increase from day 2 to 5. Myostatin on days 5 and 7 were significantly increased. Immunohistochemical analysis showed that myoD-positive/pax7-positive cells increased on day 2, suggesting that activated satellite cells play a role in the destruction and the early recovery phases.
We, thus, conclude that myogenic events associate with torque recovery after LC-induced injury.
尽管不熟悉的牵伸收缩引起的肌肉功能障碍是运动医学中最重要的问题之一，但对于再生过程中的分子事件知之甚少。本研究的目的是研究急性牵伸收缩（LC）诱导的大鼠后肢腓肠肌损伤后肌生成素、MyoD、Pax7 和肌肉生长抑制素的时空表达模式。
我们使用我们最初开发的设备在大鼠腓肠肌中进行 LC（n = 24）。雄性 Wistar 大鼠用异氟烷麻醉（吸气量 450 ml/min，浓度 2.0%）。然后用强制等速背屈（180°/秒，0 至 45°）电刺激后肢三头肌。通过 Western blot 测量 MyoD、肌生成素、Pax7 的组织含量，并通过免疫组织化学测量 MyoD 和 Pax7 的定位。测量等长强直扭矩后，在体内进行单次 LC。
与预处理值相比，第 2 天和第 5 天的扭矩显着降低，第 7 天恢复。第 2 天 MyoD 和 Pax7 的含量显着增加。肌生成素从第 2 天增加到第 5 天。第 5 天和第 7 天的肌肉生长抑制素显着增加。免疫组织化学分析显示，第 2 天 MyoD 阳性/Pax7 阳性细胞增加，提示激活的卫星细胞在破坏和早期恢复阶段发挥作用。
因此，我们得出结论，肌生成事件与 LC 诱导损伤后的扭矩恢复有关。
