Grip force, EDL contractile properties, and voluntary wheel running after postdevelopmental myostatin depletion in mice
Grip force, EDL contractile properties, and voluntary wheel running after postdevelopmental myostatin depletion in mice
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DOI：
10.1152/japplphysiol.00300.2010
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发表时间：
2010-09-01
影响因子：
3.3
通讯作者：
Welle, Stephen
中科院分区：
文献类型：
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作者：
Personius, Kirkwood E.;Jayaram, Aditi;Welle, Stephen
Personius KE, Jayaram A, Krull D, Brown R, Xu T, Han B, Burgess K, Storey C, Shah B, Tawil R, Welle S. 小鼠发育后肌生长抑制素耗尽后的握力、EDL 收缩特性和自愿轮跑。 J Appl Physiol 109: 886-894, 2010。首次发表于 2010 年 7 月 1 日； doi:10.1152/japplphyol.00300.2010.-关于通过减少肌生长抑制素活性使肌肉异常变大是否会影响产生力量的能力或执行需要肌肉耐力的活动的能力，尚未达成共识。因此，我们检查了小鼠的握力、趾长伸肌 (EDL) 的收缩特性和随意轮跑，其中肌肉生长抑制素在正常肌肉发育后耗尽。在 4 个月大的小鼠中，诱导 Cre 重组酶活性以敲除肌肉生长抑制素基因的外显子 3，该外显子的两侧是 loxP 序列 (Mstn[f/f])。具有正常肌生长抑制素基因 (Mstn[w/w]) 的对照小鼠接受相同的 Cre 激活治疗。肌肉生长抑制素的消耗使所有检查的肌肉（腓肠肌、股四头肌、胫骨前肌、EDL、比目鱼肌、三头肌）的质量增加了大约 20-40%。在肌生长抑制素敲除后 2-22 周多次测量的握力，在肌生长抑制素缺陷小鼠中并不总是更大。 EDL 收缩特性在肌肉生长抑制素敲除后 7-13 个月测定。肌生长抑制素缺陷型肌肉的抽搐力往往更大（+24%；P = 0.09），而强直力并未持续升高（平均+11%；P = 0.36），尽管所有肌生长抑制素缺陷型小鼠的 EDL 质量均大于正常值（平均 + 36%；P < 0.001）。缺乏肌生长抑制素的肌肉中由偏心收缩引起的力不足大约是正常 EDL 肌肉的两倍（五次偏心收缩后分别为 31% 和 16%；P = 0.02）。在肌生长抑制素耗尽后的 12 周内，肌生长抑制素缺陷小鼠的跑步距离比对照小鼠少 19%（P < 0.01），这主要是因为每晚跑步次数减少，而不是跑步速度或跑步持续时间减少。在通过其他方式诱导肌肉肥大后，观察到比张力（力与质量之比）的降低和跑步的减少，这表明它们是通常与异常大的肌肉相关的特征，而不是肌生长抑制素缺乏的独特影响。
Personius KE, Jayaram A, Krull D, Brown R, Xu T, Han B, Burgess K, Storey C, Shah B, Tawil R, Welle S. Grip force, EDL contractile properties, and voluntary wheel running after postdevelopmental myostatin depletion in mice. J Appl Physiol 109: 886-894, 2010. First published July 1, 2010; doi:10.1152/japplphysiol.00300.2010.-There is no consensus about whether making muscles abnormally large by reducing myostatin activity affects force-generating capacity or the ability to perform activities requiring muscular endurance. We therefore examined grip force, contractile properties of extensor digitorum longus (EDL) muscles, and voluntary wheel running in mice in which myostatin was depleted after normal muscle development. Cre recombinase activity was induced to knock out exon 3 of the myostatin gene in 4-mo-old mice in which this exon was flanked by loxP sequences (Mstn[f/f]). Control mice with normal myostatin genes (Mstn[w/w]) received the same Cre-activating treatment. Myostatin depletion increased the mass of all muscles that were examined (gastrocnemius, quadriceps, tibialis anterior, EDL, soleus, triceps) by similar to 20-40%. Grip force, measured multiple times 2-22 wk after myostatin knockout, was not consistently greater in the myostatin-deficient mice. EDL contractile properties were determined 7-13 mo after myostatin knockout. Twitch force tended to be greater in myostatin-deficient muscles (+24%; P = 0.09), whereas tetanic force was not consistently elevated (mean +11%; P = 0.36), even though EDL mass was greater than normal in all myostatin-deficient mice (mean + 36%; P < 0.001). The force deficit induced by eccentric contractions was approximately twofold greater in myostatin-deficient than in normal EDL muscles (31% vs. 16% after five eccentric contractions; P = 0.02). Myostatin-deficient mice ran 19% less distance (P < 0.01) than control mice during the 12 wk following myostatin depletion, primarily because of fewer running bouts per night rather than diminished running speed or bout duration. Reduced specific tension (ratio of force to mass) and reduced running have been observed after muscle hypertrophy was induced by other means, suggesting that they are characteristics generally associated with abnormally large muscles rather than unique effects of myostatin deficiency.