Dupont-Versteegden E E, Houlé J D, Gurley C M, Peterson C A
Department of Geriatrics, University of Arkansas for Medical Sciences, Geriatric Research, Education, Clinical Center, McClellan Department of Veterans Affairs Hospital, Little Rock, Arkansas 72205, USA.
Am J Physiol. 1998 Oct;275(4):C1124-33. doi: 10.1152/ajpcell.1998.275.4.C1124.
Muscles of spinal cord-transected rats exhibit severe atrophy and a shift toward a faster phenotype. Exercise can partially prevent these changes. The goal of this study was to investigate early events involved in regulating the muscle response to spinal transection and passive hindlimb exercise. Adult female Sprague-Dawley rats were anesthetized, and a complete spinal cord transection lesion (T10) was created in all rats except controls. Rats were killed 5 or 10 days after transection or they were exercised daily on motor-driven bicycles starting at 5 days after transection and were killed 0.5, 1, or 5 days after the first bout of exercise. Structural and biochemical features of soleus and extensor digitorum longus (EDL) muscles were studied. Atrophy was decreased in all fiber types of soleus and in type 2a and type 2x fibers of EDL after 5 days of exercise. However, exercise did not appear to affect fiber type that was altered within 5 days of spinal cord transection: fibers expressing myosin heavy chain 2x increased in soleus and EDL, and extensive coexpression of myosin heavy chain in soleus was apparent. Activation of satellite cells was observed in both muscles of transected rats regardless of exercise status, evidenced by increased accumulation of MyoD and myogenin. Increased expression was transient, except for MyoD, which remained elevated in soleus. MyoD and myogenin were detected both in myofiber and in satellite cell nuclei in both muscles, but in soleus, MyoD was preferentially expressed in satellite cell nuclei, and in EDL, MyoD was more readily detectable in myofiber nuclei, suggesting that MyoD and myogenin have different functions in different muscles. Exercise did not affect the level or localization of MyoD and myogenin expression. Similarly, Id-1 expression was transiently increased in soleus and EDL upon spinal cord transection, and no effect of exercise was observed. These results indicate that passive exercise can ameliorate muscle atrophy after spinal cord transection and that satellite cell activation may play a role in muscle plasticity in response to spinal cord transection and exercise. Finally, the mechanisms underlying maintenance of muscle mass are likely distinct from those controlling myosin heavy chain expression.
脊髓横断大鼠的肌肉会出现严重萎缩，并向更快的表型转变。运动可以部分预防这些变化。本研究的目的是调查参与调节肌肉对脊髓横断和被动后肢运动反应的早期事件。成年雌性Sprague-Dawley大鼠被麻醉，除对照组外，所有大鼠均制造了完全性脊髓横断损伤（T10）。在横断后5天或10天处死大鼠，或者从横断后5天开始每天在电动自行车上运动，在第一次运动后0.5天、1天或5天处死大鼠。研究了比目鱼肌和趾长伸肌（EDL）的结构和生化特征。运动5天后，比目鱼肌所有纤维类型以及EDL的2a型和2x型纤维的萎缩均减轻。然而，运动似乎并未影响脊髓横断后5天内发生改变的纤维类型：比目鱼肌和EDL中表达肌球蛋白重链2x的纤维增加，并且比目鱼肌中肌球蛋白重链的广泛共表达明显。无论运动状态如何，在横断大鼠的两块肌肉中均观察到卫星细胞的激活，MyoD和生肌调节因子的积累增加证明了这一点。除了比目鱼肌中MyoD仍保持升高外，表达增加是短暂的。在两块肌肉的肌纤维和卫星细胞核中均检测到MyoD和生肌调节因子，但在比目鱼肌中，MyoD优先在卫星细胞核中表达，而在EDL中，MyoD在肌纤维细胞核中更容易检测到，这表明MyoD和生肌调节因子在不同肌肉中具有不同功能。运动并未影响MyoD和生肌调节因子表达的水平或定位。同样，脊髓横断后比目鱼肌和EDL中Id-1表达短暂增加，未观察到运动的影响。这些结果表明，被动运动可以改善脊髓横断后的肌肉萎缩，并且卫星细胞激活可能在响应脊髓横断和运动的肌肉可塑性中起作用。最后，维持肌肉质量的机制可能与控制肌球蛋白重链表达的机制不同。
