White S H, Wohlgemuth S, Li C, Warren L K
J Anim Sci. 2017 Sep;95(9):4078-4084. doi: 10.2527/jas2017.1919.
Exercise is known to promote mitochondrial biogenesis in skeletal muscle as well as enhance mitochondrial function and efficiency in human and rodent models. These adaptations help to decrease exercise-associated production of reactive oxygen species, which can negatively affect health and performance if antioxidant mechanisms are overwhelmed. Little is known about the adaptations of mitochondria in response to exercise training in the growing horse or if supplementation with a dietary antioxidant can improve mitochondrial function. To evaluate the separate and combined effects of selenium (Se) supplementation, training, and an acute strenuous exercise bout on mitochondrial adaptations in young horses, 30 American Quarter Horse yearlings were randomly assigned to an exercise training group or a no-training group and, within each group, received either 0.1 or 0.3 mg Se/kg DM for 14 wk. The study was split into 2 phases (wk 0 to 8 and wk 9 to 14), with half of the trained horses switched to the opposite dietary treatment in Phase 2. At the end of each phase, all horses underwent a 120-min submaximal exercise test (SET; SET 1 and SET 2). Biopsies of the middle gluteal muscle were collected before and after each phase of the study and in response to each SET and analyzed for markers of mitochondrial number and function. At rest, horses receiving 0.3 mg Se/kg DM had higher citrate synthase activity ( = 0.021) than horses receiving 0.1 mg Se/kg DM, indicating higher mitochondrial content. In contrast, cytochrome oxidase (CCO) activity was not affected by dietary Se overall, but horses that were dropped from 0.3 mg Se/kg DM to 0.1 mg Se/kg DM during Phase 2 showed a decrease ( = 0.034) in integrated CCO activity from wk 9 to 14, suggesting impaired mitochondrial function. Mitochondrial enzyme activities were unaffected by an acute, strenuous exercise bout (SET 1 and SET 2). Our relatively low-intensity exercise training protocol did not appear to induce functional mitochondrial adaptations. However, elevated dietary Se may impart beneficial effects on mitochondrial biogenesis during growth and training. A more strenuous exercise training protocol should be investigated to determine the potential benefits of elevated dietary Se for elite equine athletes.
众所周知,运动可促进骨骼肌中的线粒体生物合成,并增强人类和啮齿动物模型中的线粒体功能及效率。这些适应性变化有助于减少运动相关的活性氧生成,如果抗氧化机制不堪重负,活性氧会对健康和表现产生负面影响。关于成长中的马匹线粒体对运动训练的适应性变化,或者补充膳食抗氧化剂是否能改善线粒体功能,目前所知甚少。为了评估补充硒(Se)、训练以及一次急性剧烈运动对幼马线粒体适应性变化的单独及联合影响,30匹美国四分之一马一岁驹被随机分为运动训练组或非训练组,且在每组内,分别给予0.1或0.3毫克硒/千克干物质,持续14周。该研究分为两个阶段(第0至8周和第9至14周),在第二阶段,一半训练马改为相反的膳食处理。在每个阶段结束时,所有马匹都进行了一次120分钟的次最大运动测试(SET;SET 1和SET 2)。在研究的每个阶段前后以及每次SET前后,采集臀中肌活检样本,并分析线粒体数量和功能的标志物。休息时,接受0.3毫克硒/千克干物质的马匹比接受0.1毫克硒/千克干物质的马匹具有更高的柠檬酸合酶活性(P = 0.021),表明线粒体含量更高。相比之下,细胞色素氧化酶(CCO)活性总体上不受膳食硒的影响,但在第二阶段从0.3毫克硒/千克干物质降至0.1毫克硒/千克干物质的马匹,其从第9周至14周的综合CCO活性出现下降(P = 0.034),表明线粒体功能受损。线粒体酶活性不受急性剧烈运动(SET 1和SET 2)的影响。我们相对低强度的运动训练方案似乎并未诱导功能性线粒体适应性变化。然而,增加膳食硒可能在生长和训练期间对线粒体生物合成产生有益影响。应研究更剧烈的运动训练方案,以确定增加膳食硒对精英马术运动员的潜在益处。