Ramos S V, Turnbull P C, MacPherson R E K, LeBlanc P J, Ward W E, Peters S J
Center for Bone and Muscle Health, Brock University, St Catharines, Ontario, Canada; Department of Kinesiology, Brock University, St Catharines, Ontario, Canada.
Exp Physiol. 2015 Apr 1;100(4):450-62. doi: 10.1113/expphysiol.2014.084434. Epub 2015 Mar 21.
What is the central question of this study? The aim was to determine whether mitochondrial protein content of perilipin 3 (PLIN3) and perilipin 5 (PLIN5) is increased following endurance training and whether mitochondrial PLIN5 protein is increased to a greater extent in endurance-trained rats when compared with sedentary rats following acute contraction. What is the main finding and its importance? Mitochondrial PLIN3 but not PLIN5 protein was increased in endurance-trained compared with sedentary rats, suggesting a mitochondrial role for PLIN3 due to chronic exercise. Contrary to our hypothesis, acute mitochondrial PLIN5 protein was similar in both sedentary and endurance-trained rats. Endurance training results in an increased association between skeletal muscle lipid droplets and mitochondria. This association is likely to be important for the expected increase in intramuscular fatty acid oxidation that occurs with endurance training. The perilipin family of lipid droplet proteins, PLIN(2-5), are thought to play a role in skeletal muscle lipolysis. Recently, results from our laboratory demonstrated that skeletal muscle mitochondria contain PLIN3 and PLIN5 protein. Furthermore, 30 min of stimulated contraction induces an increased mitochondrial PLIN5 content. To determine whether mitochondrial content of PLIN3 and PLIN5 is altered with endurance training, Sprague-Dawley rats were randomized into sedentary or endurance-trained groups for 8 weeks of treadmill running followed by an acute (30 min) sciatic nerve stimulation to induce lipolysis. Mitochondrial PLIN3 protein was ∼1.5-fold higher in red gastrocnemius of endurance-trained rats compared with sedentary animals, with no change in mitochondrial PLIN5 protein. In addition, there was an increase in plantaris intramuscular lipid storage. Acute electrically stimulated contraction in red gastrocnemius from sedentary and endurance-trained rats resulted in a similar increase of mitochondrial PLIN5 between these two groups, with no net change in PLIN3 in either group. Plantaris intramuscular lipid content decreased to a similar extent in sedentary and endurance-trained rats. These results suggest that while total mitochondrial PLIN5 content is not altered by endurance training, PLIN5 does have an acute role in the mitochondrial fraction during muscle contraction. Conversely, mitochondrial PLIN3 does not change acutely with muscle contraction, but PLIN3 content was increased following endurance training, indicating a role in chronic adaptations of skeletal muscle.
本研究的核心问题是什么?目的是确定耐力训练后脂滴包被蛋白3(PLIN3)和脂滴包被蛋白5(PLIN5)的线粒体蛋白含量是否增加,以及与久坐不动的大鼠在急性收缩后相比,耐力训练的大鼠中线粒体PLIN5蛋白增加的程度是否更大。主要发现及其重要性是什么?与久坐不动的大鼠相比,耐力训练的大鼠线粒体PLIN3蛋白增加,而PLIN5蛋白未增加,这表明由于长期运动PLIN3在线粒体中发挥作用。与我们的假设相反,久坐不动的大鼠和耐力训练的大鼠急性线粒体PLIN5蛋白相似。耐力训练导致骨骼肌脂滴与线粒体之间的关联增加。这种关联可能对耐力训练时预期的肌肉内脂肪酸氧化增加很重要。脂滴蛋白的脂滴包被蛋白家族PLIN(2 - 5)被认为在骨骼肌脂解中起作用。最近,我们实验室的结果表明骨骼肌线粒体含有PLIN3和PLIN5蛋白。此外,30分钟的刺激收缩会导致线粒体PLIN5含量增加。为了确定耐力训练是否会改变PLIN3和PLIN5的线粒体含量,将Sprague-Dawley大鼠随机分为久坐不动组或耐力训练组,进行8周的跑步机跑步,然后进行急性(30分钟)坐骨神经刺激以诱导脂解。与久坐不动的动物相比,耐力训练的大鼠红色腓肠肌中线粒体PLIN3蛋白高约1.5倍,线粒体PLIN5蛋白无变化。此外,比目鱼肌内脂质储存增加。久坐不动的大鼠和耐力训练的大鼠红色腓肠肌急性电刺激收缩导致两组之间线粒体PLIN5有类似增加,两组中PLIN3均无净变化。久坐不动的大鼠和耐力训练的大鼠比目鱼肌内脂质含量下降程度相似。这些结果表明,虽然耐力训练不会改变线粒体PLIN5的总含量,但PLIN5在肌肉收缩期间的线粒体部分中确实具有急性作用。相反,线粒体PLIN3不会随肌肉收缩而急性变化,但耐力训练后PLIN3含量增加,表明其在骨骼肌慢性适应中起作用。