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急性抗阻运动训练不会增强高水平运动员或未经训练的老年人的线粒体重塑。

Acute resistance exercise training does not augment mitochondrial remodelling in master athletes or untrained older adults.

作者信息

Marshall Ryan Neil, McKendry James, Smeuninx Benoit, Seabright Alex Peter, Morgan Paul T, Greig Carolyn, Breen Leigh

机构信息

School of Sport, Exercise, and Rehabilitation Sciences, University of Birmingham, Birmingham, United Kingdom.

MRC-Versus Arthritis Centre for Musculoskeletal Ageing Research, Birmingham, United Kingdom.

出版信息

Front Physiol. 2023 Jan 4;13:1097988. doi: 10.3389/fphys.2022.1097988. eCollection 2022.

Abstract

Ageing is associated with alterations to skeletal muscle oxidative metabolism that may be influenced by physical activity status, although the mechanisms underlying these changes have not been unraveled. Similarly, the effect of resistance exercise training (RET) on skeletal muscle mitochondrial regulation is unclear. Seven endurance-trained masters athletes ([MA], 74 ± 3 years) and seven untrained older adults ([OC]. 69 ± 6 years) completed a single session of knee extension RET (6 x 12 repetitions, 75% 1-RM, 120-s intra-set recovery). Vastus lateralis muscle biopsies were collected pre-RET, 1 h post-RET, and 48h post-RET. Skeletal muscle biopsies were analyzed for citrate synthase (CS) enzyme activity, mitochondrial content, and markers of mitochondrial quality control immunoblotting. Pre-RET CS activity and protein content were ∼45% ( < .001) and ∼74% greater in MA compared with OC ( = .006). There was a significant reduction (∼18%) in CS activity 48 h post-RET ( < .05) in OC, but not MA. Pre-RET abundance of individual and combined mitochondrial electron transport chain (ETC) complexes I-V were significantly greater in MA compared with OC, as were markers of mitochondrial fission and fusion dynamics (p-DRP-1, p-MFF, OPA-1 & FIS-1, < .05 for all). Moreover, MA displayed greater expression of p-AMPK, PGC1α, TFAM, and SIRT-3 ( < .05 for all). Notably, RET did not alter the expression of any marker of mitochondrial content, biogenesis, or quality control in both OC and MA. The present data suggest that long-term aerobic exercise training supports superior skeletal muscle mitochondrial density and protein content into later life, which may be regulated by greater mitochondrial quality control mechanisms and supported superior fission-fusion dynamics. However, a single session of RET is unable to induce mitochondrial remodelling in the acute (1h post-RET) and delayed (48 h post-RET) recovery period in OC and MA.

摘要

衰老与骨骼肌氧化代谢的改变有关,这种改变可能受身体活动状态的影响,尽管这些变化背后的机制尚未完全阐明。同样,抗阻运动训练(RET)对骨骼肌线粒体调节的影响也尚不清楚。七名耐力训练的老年运动员([MA],74±3岁)和七名未经训练的老年人([OC],69±6岁)完成了一次膝关节伸展抗阻运动训练(6组,每组12次重复,75%的1次最大重复量,组间恢复120秒)。在抗阻运动训练前、训练后1小时和训练后48小时采集股外侧肌活检样本。对骨骼肌活检样本进行柠檬酸合酶(CS)酶活性、线粒体含量以及线粒体质量控制免疫印迹标志物的分析。与OC组相比,MA组抗阻运动训练前的CS活性和蛋白含量分别高出约45%(P<0.001)和约74%(P = 0.006)。OC组在抗阻运动训练后48小时CS活性显著降低(约18%)(P<0.05),而MA组未出现此情况。与OC组相比,MA组抗阻运动训练前单个及组合的线粒体电子传递链(ETC)复合体I-V的丰度显著更高,线粒体分裂和融合动力学标志物(p-DRP-1、p-MFF、OPA-1和FIS-1)也是如此(所有P<0.05)。此外,MA组p-AMPK、PGC1α、TFAM和SIRT-3的表达更高(所有P<0.05)。值得注意的是,抗阻运动训练并未改变OC组和MA组中线粒体含量、生物发生或质量控制的任何标志物的表达。目前的数据表明,长期有氧运动训练可使晚年骨骼肌线粒体密度和蛋白含量保持在较高水平,这可能受更强的线粒体质量控制机制调节,并得益于更优的分裂-融合动力学。然而,一次抗阻运动训练无法在OC组和MA组的急性恢复期(抗阻运动训练后1小时)和延迟恢复期(抗阻运动训练后48小时)诱导线粒体重塑。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/754f/9846504/544af887c68b/fphys-13-1097988-g001.jpg

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