Department of Health Sciences, Program of Exercise Science, Bronx, CUNY Lehman College, New York, USA.
J Strength Cond Res. 2013 Jun;27(6):1720-30. doi: 10.1519/JSC.0b013e31828ddd53.
It has been well documented in the literature that resistance training can promote marked increases in skeletal muscle mass. Postexercise hypertrophic adaptations are mediated by a complex enzymatic cascade whereby mechanical tension is molecularly transduced into anabolic and catabolic signals that ultimately lead to a compensatory response, shifting muscle protein balance to favor synthesis over degradation. Myocellular signaling is influenced, in part, by the endocrine system. Various hormones have been shown to alter the dynamic balance between anabolic and catabolic stimuli in muscle, helping to mediate an increase or decrease in muscle protein accretion. Resistance training can have an acute impact on the postexercise secretion of several of these hormones including insulin-like growth factor, testosterone, and growth hormone (GH). Studies show that hormonal spikes are magnified after hypertrophy-type exercise that involves training at moderate intensities with shortened rest intervals as compared with high-intensity strength-oriented training. The observed positive relationship between anabolic hormones and hypertrophy-type training has led to the hormone hypothesis, which postulates that acute postexercise hormonal secretions mediate increases in muscle size. Several researchers have suggested that these transient hormonal elevations may be more critical to hypertrophic adaptations than chronic changes in resting hormonal concentrations. Theoretically, high levels of circulating hormones increase the likelihood of interaction with receptors, which may have particular hypertrophic importance in the postworkout period when muscles are primed for anabolism. Moreover, hormonal spikes may enhance intracellular signaling so that postexercise protein breakdown is rapidly attenuated and anabolic processes are heightened, thereby leading to a greater supercompensatory response. Although the hormone hypothesis has received considerable support in the literature, several researchers have questioned its veracity, with some speculating that the purpose of postexercise hormonal elevations is to mobilize fuel stores rather than promote tissue anabolism. Therefore, the purpose of this article will be to critically and objectively review the current literature, and then draw relevant conclusions as to the potential role of acute systemic factors on muscle protein accretion.
文献中已有大量记载表明，抗阻训练可显著促进骨骼肌量的增加。运动后肌肉发生的肥厚适应性变化是由一个复杂的酶级联反应介导的，机械张力在分子水平上转化为合成代谢和分解代谢信号，最终导致代偿性反应，使肌肉蛋白平衡向合成代谢倾斜，促进合成代谢而抑制分解代谢。肌细胞信号受内分泌系统的部分影响。已经有多种激素被证明可以改变肌肉中合成代谢和分解代谢刺激之间的动态平衡，有助于调节肌肉蛋白合成的增加或减少。抗阻训练可以对运动后几种激素的分泌产生急性影响，包括胰岛素样生长因子、睾酮和生长激素（GH）。研究表明，与高强度力量训练相比，中等强度、休息时间较短的肥厚型运动后，激素峰值会放大。观察到的合成代谢激素与肥厚型训练之间的正相关关系导致了激素假说的提出，该假说认为，运动后激素的急性分泌介导了肌肉大小的增加。一些研究人员认为，这些短暂的激素升高对于肥厚适应性比静息激素浓度的慢性变化更为关键。从理论上讲，循环激素水平升高增加了与受体相互作用的可能性，这在肌肉为合成代谢做好准备的运动后时期可能具有特殊的肥厚重要性。此外，激素峰可能增强细胞内信号传导，从而迅速减弱运动后蛋白质分解，并增强合成代谢过程，从而导致更大的超补偿反应。尽管激素假说在文献中得到了广泛的支持，但一些研究人员对其真实性提出了质疑，一些人推测运动后激素升高的目的是动员燃料储存，而不是促进组织合成代谢。因此，本文将批判性和客观地回顾当前的文献，并就急性全身因素对肌肉蛋白合成的潜在作用得出相关结论。
