Cardinale Daniele A, Lilja Mats, Mandić Mirko, Gustafsson Thomas, Larsen Filip J, Lundberg Tommy R
Åstrand Laboratory, The Swedish School of Sport and Health Sciences, Stockholm, Sweden.
Elite Performance Centre, Bosön-Swedish Sports Confederation, Lidingö, Sweden.
Front Physiol. 2017 Dec 19;8:1074. doi: 10.3389/fphys.2017.01074. eCollection 2017.
The current study aimed to examine the effects of resistance exercise with concomitant consumption of high vs. low daily doses of non-steroidal anti-inflammatory drugs (NSAIDs) on mitochondrial oxidative phosphorylation in skeletal muscle. As a secondary aim, we compared the effects of eccentric overload with conventional training. Twenty participants were randomized to either a group taking high doses (3 × 400 mg/day) of ibuprofen (IBU; 27 ± 5 year; = 11) or a group ingesting a low dose (1 × 75 mg/day) of acetylsalicylic acid (ASA; 26 ± 4 year; = 9) during 8 weeks of supervised knee extensor resistance training. Each of the subject's legs were randomized to complete the training program using either a flywheel (FW) device emphasizing eccentric overload, or a traditional weight stack machine (WS). Maximal mitochondrial oxidative phosphorylation (CI+II) from permeabilized skeletal muscle bundles was assessed using high-resolution respirometry. Citrate synthase (CS) activity was assessed using spectrophotometric techniques and mitochondrial protein content using western blotting. After training, CI+II decreased ( < 0.05) in both IBU (23%) and ASA (29%) with no difference across medical treatments. Although CI+II decreased in both legs, the decrease was greater (interaction = 0.015) in WS (33%, = 0.001) compared with FW (19%, = 0.078). CS activity increased ( = 0.027) with resistance training, with no interactions with medical treatment or training modality. Protein expression of ULK1 increased with training in both groups ( < 0.001). The increase in quadriceps muscle volume was not correlated with changes in CI+II ( = 0.16). These results suggest that 8 weeks of resistance training with co-ingestion of anti-inflammatory drugs reduces mitochondrial function but increases mitochondrial content. The observed changes were not affected by higher doses of NSAIDs consumption, suggesting that the resistance training intervention was the prime mediator of the decreased mitochondrial phosphorylation. Finally, we noted that flywheel resistance training, emphasizing eccentric overload, rescued some of the reduction in mitochondrial function seen with conventional resistance training.
本研究旨在探讨在进行抗阻训练的同时，每日服用高剂量与低剂量非甾体抗炎药（NSAIDs）对骨骼肌线粒体氧化磷酸化的影响。作为次要目的，我们比较了离心超负荷训练与传统训练的效果。20名参与者被随机分为两组，一组在为期8周的有监督的伸膝抗阻训练期间服用高剂量（3×400毫克/天）布洛芬（IBU；年龄27±5岁；n = 11），另一组摄入低剂量（1×75毫克/天）乙酰水杨酸（ASA；年龄26±4岁；n = 9）。每位受试者的双腿被随机分配，使用强调离心超负荷的飞轮（FW）装置或传统的配重器械（WS）完成训练计划。使用高分辨率呼吸测定法评估透化骨骼肌束的最大线粒体氧化磷酸化（CI+II）。使用分光光度技术评估柠檬酸合酶（CS）活性，使用蛋白质印迹法评估线粒体蛋白含量。训练后，IBU组（23%）和ASA组（29%）的CI+II均下降（P<0.05），不同药物治疗之间无差异。虽然双腿的CI+II均下降，但与FW组（19%，P = 0.078）相比，WS组下降幅度更大（交互作用P = 0.015）（33%，P = 0.001）。抗阻训练使CS活性增加（P = 0.027），与药物治疗或训练方式无交互作用。两组训练后ULK1的蛋白表达均增加（P<0.001）。股四头肌体积的增加与CI+II的变化无相关性（P = 0.16）。这些结果表明，在服用抗炎药物的同时进行8周抗阻训练会降低线粒体功能，但会增加线粒体含量。观察到的变化不受高剂量NSAIDs摄入的影响，表明抗阻训练干预是线粒体磷酸化降低的主要介导因素。最后，我们注意到强调离心超负荷的飞轮抗阻训练挽救了一些传统抗阻训练中出现的线粒体功能下降。
