Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada.
Am J Physiol Endocrinol Metab. 2010 Aug;299(2):E180-8. doi: 10.1152/ajpendo.00073.2010. Epub 2010 May 18.
Fatty acid oxidation is highly regulated in skeletal muscle and involves several sites of regulation, including the transport of fatty acids across both the plasma and mitochondrial membranes. Transport across these membranes is recognized to be primarily protein mediated, limited by the abundance of fatty acid transport proteins on the respective membranes. In recent years, evidence has shown that fatty acid transport proteins move in response to acute and chronic perturbations; however, in human skeletal muscle the localization of fatty acid transport proteins in response to training has not been examined. Therefore, we determined whether high-intensity interval training (HIIT) increased total skeletal muscle, sarcolemmal, and mitochondrial membrane fatty acid transport protein contents. Ten untrained females (22 +/- 1 yr, 65 +/- 2 kg; .VO(2peak): 2.8 +/- 0.1 l/min) completed 6 wk of HIIT, and biopsies from the vastus lateralis muscle were taken before training, and following 2 and 6 wk of HIIT. Training significantly increased maximal oxygen uptake at 2 and 6 wk (3.1 +/- 0.1, 3.3 +/- 0.1 l/min). Training for 6 wk increased FAT/CD36 at the whole muscle (10%) and mitochondrial levels (51%) without alterations in sarcolemmal content. Whole muscle plasma membrane fatty acid binding protein (FABPpm) also increased (48%) after 6 wk of training, but in contrast to FAT/CD36, sarcolemmal FABPpm increased (23%), whereas mitochondrial FABPpm was unaltered. The changes on sarcolemmal and mitochondrial membranes occurred rapidly, since differences (< or =2 wk) were not observed between 2 and 6 wk. This is the first study to demonstrate that exercise training increases fatty acid transport protein content in whole muscle (FAT/CD36 and FABPpm) and sarcolemmal (FABPpm) and mitochondrial (FAT/CD36) membranes in human skeletal muscle of females. These results suggest that increases in skeletal muscle fatty acid oxidation following training are related in part to changes in fatty acid transport protein content and localization.
脂肪酸氧化在骨骼肌中受到高度调节,涉及几个调节部位,包括脂肪酸穿过血浆和线粒体膜的运输。这些膜的运输被认为主要是由蛋白质介导的,受到相应膜上脂肪酸转运蛋白丰度的限制。近年来,有证据表明脂肪酸转运蛋白会对急性和慢性干扰做出反应;然而,在人类骨骼肌中,训练对脂肪酸转运蛋白的定位尚未被检测到。因此,我们确定高强度间歇训练(HIIT)是否会增加骨骼肌总、肌浆膜和线粒体膜脂肪酸转运蛋白的含量。10 名未经训练的女性(22 ± 1 岁,65 ± 2 kg;.VO 2peak :2.8 ± 0.1 l/min)完成了 6 周的 HIIT,股外侧肌活检分别在训练前、训练 2 周和 6 周后采集。训练使 2 周和 6 周时的最大摄氧量显著增加(3.1 ± 0.1、3.3 ± 0.1 l/min)。6 周的训练使整个肌肉(10%)和线粒体水平(51%)的 FAT/CD36 增加,而肌浆膜含量没有变化。6 周的训练后,整个肌肉的血浆膜脂肪酸结合蛋白(FABPpm)也增加了(48%),但与 FAT/CD36 不同的是,肌浆膜 FABPpm 增加了(23%),而线粒体 FABPpm 没有变化。肌浆膜和线粒体膜的变化很快,因为在 2 周和 6 周之间没有观察到差异(<或=2 周)。这是第一项研究表明,运动训练增加了女性骨骼肌中整个肌肉(FAT/CD36 和 FABPpm)和肌浆膜(FABPpm)以及线粒体(FAT/CD36)膜的脂肪酸转运蛋白含量。这些结果表明,训练后骨骼肌脂肪酸氧化的增加部分与脂肪酸转运蛋白含量和定位的变化有关。