Department of Human Nutrition, Foods, and Exercise, Virginia Tech, Blacksburg, VA, USA.
Department of Human Nutrition, Foods, and Exercise, Virginia Tech, Blacksburg, VA, USA; Metabolic Phenotyping Core, Virginia Tech, Blacksburg, VA, USA; Fralin Translational Obesity Research Center, Virginia Tech, Blacksburg, VA, USA.
Mol Metab. 2017 Dec;6(12):1597-1609. doi: 10.1016/j.molmet.2017.10.006. Epub 2017 Oct 21.
We tested the hypothesis that skeletal muscle of endurance-trained male runners would exhibit elevated autophagy and mitophagy markers, which would be associated with greater metabolic flexibility following a high-fat meal (HFM).
Muscle biopsies were collected to determine differences in autophagy and mitophagy protein markers and metabolic flexibility under fasting conditions and 4 h following a HFM between endurance-trained male runners (n = 10) and sedentary, non-obese controls (n = 9).
Maximal oxygen consumption (ml·kg·min) was approximately 50% higher (p < 0.05) in endurance-trained runners compared with sedentary controls (65.8 ± 2.3 and 43.1 ± 3.4, respectively). Autophagy markers were similar between groups. Mitophagy and mitochondrial dynamics protein markers were significantly higher in skeletal muscle of endurance-trained runners compared with sedentary controls in the fasted state, although unaffected by the HFM. Skeletal muscle metabolic flexibility was similar between groups when fasted (p > 0.05), but increased in response to the HFM in endurance-trained athletes only (p < 0.005). Key mitophagy markers, phospho-Pink1 and phospho-Parkin (r = 0.64, p < 0.005), and phospo-Parkin and phospho-Drp1 (r = 0.70, p < 0.05) were correlated only within the endurance-trained group. Autophagy and mitophagy markers were not correlated with metabolic flexibility.
In summary, mitophagy may be enhanced in endurance-trained runners based on elevated markers of mitophagy and mitochondrial dynamics. The HFM did not alter autophagy or mitophagy in either group. The absence of a relationship between mitophagy markers and metabolic flexibility suggests that mitophagy is not a key determinant of metabolic flexibility in a healthy population, but further investigation is warranted.
我们检验了这样一个假设，即经过耐力训练的男性跑步者的骨骼肌会表现出升高的自噬和线粒体自噬标志物，这与高脂肪餐后（HFM）的代谢灵活性增加有关。
在 HFM 后 4 小时内，收集肌肉活检以确定禁食条件下和 HFM 后耐力训练的男性跑步者（n=10）和久坐、非肥胖对照者（n=9）之间的自噬和线粒体自噬蛋白标志物和代谢灵活性的差异。
与久坐对照组相比，耐力训练跑步者的最大耗氧量（ml·kg·min）约高 50%（p<0.05）（分别为 65.8±2.3 和 43.1±3.4）。两组的自噬标志物相似。与久坐对照组相比，在禁食状态下，耐力训练跑步者的线粒体自噬和线粒体动力学蛋白标志物显著升高，但不受 HFM 的影响。两组在禁食时的肌肉代谢灵活性相似（p>0.05），但仅在耐力训练运动员中对 HFM 有反应（p<0.005）。关键的线粒体自噬标志物磷酸化 Pink1 和磷酸化 Parkin（r=0.64，p<0.005）和磷酸化 Parkin 和磷酸化 Drp1（r=0.70，p<0.05）仅在耐力训练组中相关。自噬和线粒体自噬标志物与代谢灵活性无关。
总之，基于线粒体自噬和线粒体动力学标志物的升高，耐力训练的跑步者可能会增强线粒体自噬。HFM 并未改变两组的自噬或线粒体自噬。线粒体自噬标志物与代谢灵活性之间没有关系表明，在健康人群中，线粒体自噬不是代谢灵活性的关键决定因素，但需要进一步研究。
