McClung J M, Davis J M, Carson J A
University of South Carolina, Department of Exercise Science, 1300 Wheat Street, Columbia, SC 29208, USA.
Exp Physiol. 2007 Jan;92(1):219-32. doi: 10.1113/expphysiol.2006.035071. Epub 2006 Sep 21.
Resumption of normal muscle loading after a period of disuse initiates cellular processes related to mass accretion. The renewed loading also induces a significant amount of muscle damage and subsequent inflammation. Ovarian hormone depletion delays atrophied myofibre mass recovery. Ovarian hormones are also global regulators of immune system function. The purpose of this study was to determine whether ovarian hormone depletion-induced deficits in myofibre regrowth after disuse atrophy are related to the induction of muscle damage and the associated inflammatory response. We hypothesized that soleus muscle immune cell infiltration and inflammatory gene expression would be both accentuated and prolonged in ovarian hormone-depleted rats during the first week of recovery from disuse atrophy. Intact and ovariectomized (OVX) female rats were subjected to hindlimb suspension for 10 days and then returned to normal ambulation for a recovery period, the rats were killed and the soleus muscle removed for analysis. Although reloading increased both circulating creatine kinase and myofibre membrane disruption, there was no effect of ovarian hormones on these processes during recovery. Muscle neutrophil concentration was increased above baseline regardless of hormone status at days 1 and 3 of recovery; however, this increase was 43% greater at day 3 in the OVX group. Muscle ED1+ and ED2+ macrophage concentrations were increased during recovery in both groups. However, macropage concentrations remained elevated at day 7 of recovery in the OVX group, whereas they returned to control levels in the intact group. Cyclo-oxygenase-2, interleukin-6 and interleukin-1beta muscle mRNA expression increased similarly during recovery, regardless of ovarian hormone status. These results demonstrate that the initial myofibre damage and inflammatory gene expression induced during muscle recovery from disuse atrophy are independent of ovarian hormone status.
一段时间的废用后恢复正常的肌肉负荷会启动与质量增加相关的细胞过程。重新加载还会引发大量的肌肉损伤及随后的炎症。卵巢激素缺乏会延迟萎缩肌纤维质量的恢复。卵巢激素也是免疫系统功能的全局调节因子。本研究的目的是确定卵巢激素缺乏引起的废用性萎缩后肌纤维再生缺陷是否与肌肉损伤的诱导及相关的炎症反应有关。我们假设，在从废用性萎缩恢复的第一周，卵巢激素缺乏的大鼠比目鱼肌免疫细胞浸润和炎症基因表达会更加明显且持续时间更长。将完整和去卵巢（OVX）的雌性大鼠后肢悬吊10天，然后恢复正常行走进行恢复期，之后处死大鼠并取出比目鱼肌进行分析。尽管重新加载会增加循环肌酸激酶和肌纤维膜破坏，但在恢复过程中卵巢激素对这些过程没有影响。在恢复的第1天和第3天，无论激素状态如何，肌肉中性粒细胞浓度均高于基线水平；然而，在第3天，OVX组的这种增加幅度高出43%。两组在恢复过程中肌肉ED1+和ED2+巨噬细胞浓度均增加。然而，在恢复的第7天，OVX组巨噬细胞浓度仍保持升高，而完整组则恢复到对照水平。无论卵巢激素状态如何，恢复过程中环氧合酶-2、白细胞介素-6和白细胞介素-1β肌肉mRNA表达的增加情况相似。这些结果表明，废用性萎缩肌肉恢复过程中最初的肌纤维损伤和炎症基因表达与卵巢激素状态无关。
