Dupont-Versteegden E E, Murphy R J, Houlé J D, Gurley C M, Peterson C A
Department of Geriatrics, University of Arkansas for Medical Sciences, and Central Arkansas Veterans Health Care System, Little Rock, Arkansas 72205, USA.
Am J Physiol. 1999 Sep;277(3):C589-97. doi: 10.1152/ajpcell.1999.277.3.C589.
In this study, possible mechanisms underlying soleus muscle atrophy after spinal cord transection and attenuation of atrophy with cycling exercise were studied. Adult female Sprague-Dawley rats were divided into three groups; in two groups the spinal cord was transected by a lesion at T10. One group was transected and killed 10 days later, and another group was transected and exercised for 5 days starting 5 days after transection. The third group served as an uninjured control. All animals received a continuous-release 5'-bromo-2'-deoxyuridine pellet 10 days before they were killed. Transection alone and transection with exercise lead to activation of satellite cells, but only the exercise group showed a trend toward an increase in the number of proliferating satellite cells. In all cases the number of activated satellite cells was significantly higher than the number that divided. Although the number of cells undergoing proliferation increased with exercise, no increase in fusion of satellite cells into muscle fibers was apparent. Spinal cord transection resulted in a 25% decrease in myonuclear number, and exercise was not associated with a restoration of myonuclear number. The number of apoptotic nuclei was increased after transection, and exercise attenuated this increase. However, the decrease in apoptotic nuclei with exercise did not significantly affect myonuclear number. We conclude that apoptotic nuclear loss likely contributes to loss of nuclei during muscle atrophy associated with spinal cord transection and that exercise can maintain muscle mass, at least in the short term, without restoration of myonuclear number.
在本研究中，我们探究了脊髓横断后比目鱼肌萎缩的潜在机制以及骑行运动对萎缩的缓解作用。成年雌性Sprague-Dawley大鼠被分为三组；其中两组在T10水平进行脊髓横断损伤。一组横断后10天处死，另一组横断后5天开始运动，持续运动5天。第三组作为未受伤的对照组。所有动物在处死前10天植入缓释型5'-溴-2'-脱氧尿苷微丸。单纯横断组和横断运动组均导致卫星细胞激活，但只有运动组显示出增殖卫星细胞数量有增加的趋势。在所有情况下，激活的卫星细胞数量均显著高于分裂的卫星细胞数量。虽然运动使增殖细胞数量增加，但卫星细胞融合到肌纤维中的现象并未明显增加。脊髓横断导致肌核数量减少25%，运动并未使肌核数量恢复。横断后凋亡核数量增加，运动减轻了这种增加。然而，运动导致的凋亡核减少对肌核数量没有显著影响。我们得出结论，凋亡性核丢失可能是脊髓横断相关肌肉萎缩过程中核丢失的原因，并且运动至少在短期内可以维持肌肉质量，而无需恢复肌核数量。
