AdventHealth Translational Research Institute, Orlando, Florida.
Am J Physiol Cell Physiol. 2022 Aug 1;323(2):C606-C616. doi: 10.1152/ajpcell.00146.2022. Epub 2022 Jul 4.
The impact of aerobic training on human skeletal muscle cell (HSkMC) mitochondrial metabolism is a significant research gap, critical to understanding the mechanisms by which exercise augments skeletal muscle metabolism. We therefore assessed mitochondrial content and capacity in fully differentiated CD56 HSkMCs from lean active (LA) and sedentary individuals with obesity (OS) at baseline, as well as lean/overweight sedentary individuals (LOS) at baseline and following an 18-day aerobic training intervention. Participants had in vivo skeletal muscle PCr recovery rate by P-MRS (mitochondrial oxidative kinetics) and cardiorespiratory fitness (V̇o) assessed at baseline. Biopsies of the vastus lateralis were performed for the isolation of skeletal muscle stem cells. LOS individuals repeated all assessments posttraining. HSkMCs were evaluated for mitochondrial respiratory capacity by high-resolution respirometry. Data were normalized to two indices of mitochondrial content (CS activity and OXPHOS protein expression) and a marker of total cell count (quantity of DNA). LA individuals had significantly higher V̇o than OS and LOS-Pre training; however, no differences were observed in skeletal muscle mitochondrial capacity, nor in carbohydrate- or fatty acid-supported HSkMC respiratory capacity. Aerobic training robustly increased in vivo skeletal muscle mitochondrial capacity of LOS individuals, as well as carbohydrate-supported HSkMC respiratory capacity. Indices of mitochondrial content and total cell count were similar among the groups and did not change with aerobic training. Our findings demonstrate that bioenergetic changes induced with aerobic training in skeletal muscle in vivo are retained in HSkMCs in vitro without impacting mitochondrial content, suggesting that training improves intrinsic skeletal muscle mitochondrial capacity.
有氧运动训练对人类骨骼肌细胞（HSkMC）线粒体代谢的影响是一个重要的研究空白，对于理解运动增强骨骼肌代谢的机制至关重要。因此，我们在基线时评估了来自瘦活跃（LA）和肥胖久坐（OS）个体的完全分化的 CD56 HSkMC 中的线粒体含量和能力，以及基线时和 18 天有氧运动训练干预后瘦/超重久坐（LOS）个体的线粒体含量和能力。参与者通过 P-MRS（线粒体氧化动力学）和心肺功能（V̇o）评估了体内骨骼肌 PCr 恢复率。在基线时进行了股外侧肌活检以分离骨骼肌干细胞。LOS 个体在训练后重复所有评估。通过高分辨率呼吸测定法评估 HSkMC 的线粒体呼吸能力。数据归一化为线粒体含量的两个指数（CS 活性和 OXPHOS 蛋白表达）和总细胞计数的标志物（DNA 量）。LA 个体的 V̇o 明显高于 OS 和 LOS-训练前；然而，在骨骼肌线粒体容量方面没有观察到差异，也没有观察到碳水化合物或脂肪酸支持的 HSkMC 呼吸能力的差异。有氧运动训练强烈增加了 LOS 个体的体内骨骼肌线粒体容量，以及碳水化合物支持的 HSkMC 呼吸能力。线粒体含量和总细胞计数的指数在各组之间相似，并且不会随有氧运动训练而改变。我们的研究结果表明，有氧运动训练在体内骨骼肌中诱导的生物能变化在体外 HSkMC 中得以保留，而不会影响线粒体含量，这表明训练提高了内在的骨骼肌线粒体容量。
