University of Memphis, Department of Exercise and Sport Sciences, Memphis, TN 38152, USA.
Appl Physiol Nutr Metab. 2012 Feb;37(1):80-7. doi: 10.1139/h11-131. Epub 2012 Jan 5.
Power is critical to muscle performance, specifically in athletic populations. Mitogen-activated protein kinase (MAPK) pathways (extracellular signal-regulated protein kinase (ERK 1/2), p38, and c-Jun NH(2)-terminal kinase (JNK)) are intracellular signal transduction mechanisms that partially regulate exercise-induced skeletal muscle alterations. These pathways are highly responsive to exercise, but their reaction to high power, multi-joint resistance exercise is yet to be examined. Nine weightlifting-trained men performed 15 sets of three repetitions of a dynamic clean pull exercise at 85% of their one repetition maximum. Vastus lateralis biopsies were obtained prior to (pre) and after the 8th (mid) and 15th set (post) of exercise. Three subjects returned to serve as non-exercising controls for a similar sequence of biopsies (CON). The ratio of phosphorylated MAPK to total MAPK increased significantly for p38 (3.0 fold, p < 0.05) and JNK (2.4 fold, p < 0.05) by the mid biopsy. ERK 1/2 phosphorylation followed a similar trend (2.3 fold) (p = 0.052). The ratio of phosphorylation to total MAPK did not differ from mid to post biopsy. None of the pathways were phosphorylated above resting in the CON condition (p > 0.05), and thus the biopsy procedure itself did not account for the entire increase in MAPK phosphorylation during EX. These data indicate MAPK pathways are activated early and remain elevated throughout the duration of high power resistance exercise. These findings help describe the mechanisms partially responsible for chronic adaptations in response to high intensity, high power resistance training in humans.
力量对于肌肉表现至关重要，尤其是在运动员群体中。丝裂原活化蛋白激酶（MAPK）途径（细胞外信号调节蛋白激酶（ERK1/2）、p38 和 c-Jun NH2-末端激酶（JNK））是部分调节运动引起的骨骼肌变化的细胞内信号转导机制。这些途径对运动高度敏感，但它们对高功率、多关节抗阻运动的反应尚未得到检验。9 名举重训练的男性进行了 15 组 3 次重复的动态清洁拉运动，强度为 1 次最大重复的 85%。在运动前（pre）、第 8 组（mid）和第 15 组（post）后获取股外侧肌活检。3 名受试者作为类似活检序列的非运动对照（CON）返回。p38（3.0 倍，p<0.05）和 JNK（2.4 倍，p<0.05）的磷酸化 MAPK 与总 MAPK 的比值在 mid 活检时显著增加。ERK1/2 磷酸化也呈现类似趋势（2.3 倍）（p=0.052）。mid 到 post 活检时，磷酸化与总 MAPK 的比值没有差异。在 CON 条件下，没有任何途径的磷酸化高于静息状态（p>0.05），因此活检过程本身并没有解释 EX 期间 MAPK 磷酸化的全部增加。这些数据表明，MAPK 途径在高功率抗阻运动早期被激活，并在整个运动过程中保持升高。这些发现有助于描述部分负责高强度、高功率抗阻训练引起的慢性适应的机制。
