Cluster analysis tests the importance of myogenic gene expression during myofiber hypertrophy in humans
Cluster analysis tests the importance of myogenic gene expression during myofiber hypertrophy in humans
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DOI：
10.1152/japplphysiol.00024.2007
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发表时间：
2007-06-01
影响因子：
3.3
通讯作者：
Cross, James M.
中科院分区：
文献类型：
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作者：
Bamman, Marcas M.;Petrella, John K.;Cross, James M.
我们应用 K 均值聚类分析来检验以下假设：已知调节蛋白质合成和卫星细胞活性的肌肉特异性因子在 66 名经历极端、中度和失败肌纤维肥大的人类受试者中进行渐进性阻力训练（PRT，16 周）期间会差异表达。在基线 (T1) 以及第一次 (T2) 和最后一次 (T3) 负荷回合后 24 小时收集的肌肉活检中评估 IGF-I 亚型 Ea (IGF-IEa)、机械生长因子 (MGF、IGF-IEc)、肌细胞生成素和 MyoD 的肌肉 mRNA 表达，这些受试者来自先前未经训练的受试者，这些受试者分为极端反应者 (Xtr, n = 17)、中等反应者 (Mod, n = 32），以及基于平均肌纤维肥大的无反应者（Non，n = 17）。 Xtr 中的肌纤维生长平均为 2,475 μ m(2)，Mod 中为 1, 111 μ m(2)，Non 中为 - 16 μ m(2)。主要训练效果显示所有成绩单均有所增加（46-83%，P < 0.005）。对于整个队列，IGF-IEa。 MGF 和肌细胞生成素 mRNA 在 T2 时上调（P < 0.05），而 MyoD 直到 T3 才显着增加（P < 0.001）。在簇内，MGF 和肌生成素上调在 Xtr（126% 和 65%）和 Mod（73% 和 41%）中表现强劲，而在 Non 中没有变化。虽然到 T3 在所有簇中都很显着，但 IGF-IEa 在 Xtr 中增加最多（105%），在 Non 中增加最少（44%）。尽管 MyoD 表达总体增加，但未检测到簇内的变化。我们首次揭示，MGF 和肌细胞生成素转录物在经历不同程度的 PRT 介导的肌纤维肥大的受试者中存在差异表达。数据强烈表明，这些基因的负载介导诱导可能会在 PRT 期间启动促进肌纤维生长所需的重要作用，而 MyoD 的作用尚不清楚。
We applied K-means cluster analysis to test the hypothesis that muscle-specific factors known to modulate protein synthesis and satellite cell activity would be differentially expressed during progressive resistance training (PRT, 16 wk) in 66 human subjects experiencing extreme, modest, and failed myofiber hypertrophy. Muscle mRNA expression of IGF-I isoform Ea (IGF-IEa), mechanogrowth factor (MGF, IGF-IEc), myogenin, and MyoD were assessed in muscle biopsies collected at baseline (T1) and 24 h after the first (T2) and last (T3) loading bouts from previously untrained subjects clustered as extreme responders (Xtr, n = 17), modest responders (Mod, n = 32), and nonresponders (Non, n = 17) based on mean myofiber hypertrophy. Myofiber growth averaged 2,475 mu m(2) in Xtr, 1, 111 mu m(2) in Mod, and - 16 mu m(2) in Non. Main training effects revealed increases in all transcripts (46-83%, P < 0.005). For the entire cohort, IGF-IEa. MGF, and myogenin mRNAs were upregulated by T2 (P < 0.05), while MyoD did not increase significantly until T3 (P < 0.001). Within clusters, MGF and myogenin upregulation was robust in Xtr (126% and 65%) and Mod (73% and 41%) vs. no changes in Non. While significant in all clusters by T3, IGF-IEa increased most in Xtr (105%) and least in Non (44%). Although MyoD expression increased overall, no changes within clusters were detected. We reveal for the first time that MGF and myogenin transcripts are differentially expressed in subjects experiencing varying degrees of PRT-mediated myofiber hypertrophy. The data strongly suggest the load-mediated induction of these genes may initiate important actions necessary to promote myofiber growth during PRT, while the role of MyoD is less clear.