Lee Sukho, Barton Elisabeth R, Sweeney H Lee, Farrar Roger P
Department of Kinesiology, University of Texas, Austin 78712, USA.
J Appl Physiol (1985). 2004 Mar;96(3):1097-104. doi: 10.1152/japplphysiol.00479.2003.
Muscle hypertrophy is the product of increased drive through protein synthetic pathways and the incorporation of newly divided satellite cells. Gains in muscle mass and strength can be achieved through exercise regimens that include resistance training. Increased insulin-like growth factor-I (IGF-I) can also promote hypertrophy through increased protein synthesis and satellite cell proliferation. However, it is not known whether the combined effect of IGF-I and resistance training results in an additive hypertrophic response. Therefore, rats in which viral administration of IGF-I was directed to one limb were subjected to ladder climbing to test the interaction of each intervention on muscle mass and strength. After 8 wk of resistance training, a 23.3% increase in muscle mass and a 14.4% increase in peak tetanic tension (P(o)) were observed in the flexor hallucis longus (FHL). Viral expression of IGF-I without resistance training produced a 14.8% increase in mass and a 16.6% increase in P(o) in the FHL. The combined interventions produced a 31.8% increase in muscle mass and a 28.3% increase in P(o) in the FHL. Therefore, the combination of resistance training and overexpression of IGF-I induced greater hypertrophy than either treatment alone. The effect of increased IGF-I expression on the loss of muscle mass associated with detraining was also addressed. FHL muscles treated with IGF-I lost only 4.8% after detraining, whereas the untreated FHL lost 8.3% muscle mass. These results suggest that a combination of resistance training and overexpression of IGF-I could be an effective measure for attenuating the loss of training-induced adaptations.
肌肉肥大是蛋白质合成途径驱动力增加以及新分裂卫星细胞融合的产物。通过包括抗阻训练在内的运动方案可以实现肌肉质量和力量的增加。胰岛素样生长因子-I(IGF-I)增加也可通过增加蛋白质合成和卫星细胞增殖来促进肥大。然而,IGF-I与抗阻训练的联合作用是否会导致相加的肥大反应尚不清楚。因此,将通过病毒给予IGF-I的大鼠一侧肢体进行爬梯训练,以测试每种干预措施对肌肉质量和力量的相互作用。抗阻训练8周后,拇长屈肌(FHL)的肌肉质量增加了23.3%,强直收缩峰值张力(P(o))增加了14.4%。未经抗阻训练的IGF-I病毒表达使FHL的质量增加了14.8%,P(o)增加了16.6%。联合干预使FHL的肌肉质量增加了31.8%,P(o)增加了28.3%。因此,抗阻训练与IGF-I过表达的联合诱导的肥大比单独任何一种治疗都更大。还研究了IGF-I表达增加对与废用训练相关的肌肉质量损失的影响。用IGF-I处理的FHL肌肉在废用训练后仅损失了4.8%,而未处理的FHL肌肉损失了8.3%的肌肉质量。这些结果表明,抗阻训练与IGF-I过表达的联合可能是减轻训练诱导适应性丧失的有效措施。