Exercise Metabolism Group, School of Medical Sciences, RMIT University, PO Box 71, Bundoora, VIC 3083, Australia.
Exp Physiol. 2010 Feb;95(2):351-8. doi: 10.1113/expphysiol.2009.049353. Epub 2009 Oct 23.
We have previously demonstrated that well-trained subjects who completed a 3 week training programme in which selected high-intensity interval training (HIT) sessions were commenced with low muscle glycogen content increased the maximal activities of several oxidative enzymes that promote endurance adaptations to a greater extent than subjects who began all training sessions with normal glycogen levels. The aim of the present study was to investigate acute skeletal muscle signalling responses to a single bout of HIT commenced with low or normal muscle glycogen stores in an attempt to elucidate potential mechanism(s) that might underlie our previous observations. Six endurance-trained cyclists/triathletes performed a 100 min ride at approximately 70% peak O(2) uptake (AT) on day 1 and HIT (8 x 5 min work bouts at maximal self-selected effort with 1 min rest) 24 h later (HIGH). Another six subjects, matched for fitness and training history, performed AT on day 1 then 1-2 h later, HIT (LOW). Muscle biopsies were taken before and after HIT. Muscle glycogen concentration was higher in HIGH versus LOW before the HIT (390 +/- 28 versus 256 +/- 67 micromol (g dry wt)(1)). After HIT, glycogen levels were reduced in both groups (P < 0.05) but HIGH was elevated compared with LOW (229 +/- 29 versus 124 +/- 41 micromol (g dry wt)(1); P < 0.05). Phosphorylation of 5 AMP-activated protein kinase (AMPK) increased after HIT, but the magnitude of increase was greater in LOW (P < 0.05). Despite the augmented AMPK response in LOW after HIT, selected downstream AMPK substrates were similar between groups. Phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) was unchanged for both groups before and after the HIT training sessions. We conclude that despite a greater activation AMPK phosphorylation when HIT was commenced with low compared with normal muscle glycogen availability, the localization and phosphorylation state of selected downstream targets of AMPK were similar in response to the two interventions.
我们之前已经证明，经过 3 周的高强度间歇训练（HIT）培训计划，其中选择的 HIT 课程开始时肌肉糖原含量较低，与开始所有训练课程时糖原水平正常的受试者相比，能够更大程度地提高几种促进耐力适应的氧化酶的最大活性。本研究的目的是研究在低或正常肌肉糖原储备下开始单次 HIT 对急性骨骼肌信号转导的影响，试图阐明可能是我们之前观察结果的潜在机制。六名耐力训练的自行车手/三项全能运动员在第 1 天以大约 70%的峰值 O2 摄取（AT）进行了 100 分钟的骑行，然后在第 2 天（HIGH）进行了 24 小时的 HIT（8 x 5 分钟的工作回合，最大自选择努力，1 分钟休息）。另外六名在体能和训练历史上相匹配的受试者在第 1 天进行了 AT，然后在 1-2 小时后进行了 HIT（LOW）。在 HIT 前后采集了肌肉活检。在 HIT 之前，HIGH 中的肌肉糖原浓度高于 LOW（390 +/- 28 对 256 +/- 67 umol（g 干重）（1））。HIT 后，两组的糖原水平均降低（P < 0.05），但 HIGH 高于 LOW（229 +/- 29 对 124 +/- 41 umol（g 干重）（1）；P < 0.05）。HIT 后 5-AMP 激活蛋白激酶（AMPK）的磷酸化增加，但 LOW 中的增加幅度更大（P < 0.05）。尽管 HIT 后 LOW 中的 AMPK 反应增强，但 AMPK 的选定下游底物在两组之间相似。在 HIT 训练前后，两组的 p38 丝裂原激活蛋白激酶（p38 MAPK）磷酸化均无变化。我们得出的结论是，尽管在 HIT 开始时肌肉糖原可用性较低时，AMPK 磷酸化的激活幅度更大，但在两种干预措施下，AMPK 的选定下游靶标的定位和磷酸化状态相似。
