Institute for Mental and Physical Health and Clinical Translation, Metabolic Research Unit, School of Medicine, Deakin University, Geelong, Australia.
Department of Sports Science and Clinical Biomechanics, University of Southern Denmark, Odense, Denmark.
J Physiol. 2023 Jul;601(14):2899-2915. doi: 10.1113/JP284394. Epub 2023 Apr 24.
Mitochondria are the cellular organelles responsible for resynthesising the majority of ATP. In skeletal muscle, there is an increased ATP turnover during resistance exercise to sustain the energetic demands of muscle contraction. Despite this, little is known regarding the mitochondrial characteristics of chronically strength-trained individuals and any potential pathways regulating the strength-specific mitochondrial remodelling. Here, we investigated the mitochondrial structural characteristics in skeletal muscle of strength athletes and age-matched untrained controls. The mitochondrial pool in strength athletes was characterised by increased mitochondrial cristae density, decreased mitochondrial size, and increased surface-to-volume ratio, despite similar mitochondrial volume density. We also provide a fibre-type and compartment-specific assessment of mitochondria morphology in human skeletal muscle, which reveals across groups a compartment-specific influence on mitochondrial morphology that is largely independent of fibre type. Furthermore, we show that resistance exercise leads to signs of mild mitochondrial stress, without an increase in the number of damaged mitochondria. Using publicly available transcriptomic data we show that acute resistance exercise increases the expression of markers of mitochondrial biogenesis, fission and mitochondrial unfolded protein responses (UPR ). Further, we observed an enrichment of the UPR in the basal transcriptome of strength-trained individuals. Together, these findings show that strength athletes possess a unique mitochondrial remodelling, which minimises the space required for mitochondria. We propose that the concurrent activation of markers of mitochondrial biogenesis and mitochondrial remodelling pathways (fission and UPR ) with resistance exercise may be partially responsible for the observed mitochondrial phenotype of strength athletes. KEY POINTS: Untrained individuals and strength athletes possess comparable skeletal muscle mitochondrial volume density. In contrast, strength athletes' mitochondria are characterised by increased cristae density, decreased size and increased surface-to-volume ratio. Type I fibres have an increased number of mitochondrial profiles with minor differences in the mitochondrial morphological characteristics compared with type II fibres. The mitochondrial morphology is distinct across the subcellular compartments in both groups, with subsarcolemmal mitochondria being bigger in size when compared with intermyofibrillar. Acute resistance exercise leads to signs of mild morphological mitochondrial stress accompanied by increased gene expression of markers of mitochondrial biogenesis, fission and mitochondrial unfolded protein response (UPR ).
线粒体是负责重新合成大部分 ATP 的细胞细胞器。在抗阻运动中,骨骼肌的 ATP 周转率增加,以维持肌肉收缩的能量需求。尽管如此,对于长期力量训练个体的线粒体特征以及任何潜在的调节力量特异性线粒体重塑的途径,人们知之甚少。在这里,我们研究了力量运动员和年龄匹配的未经训练的对照组骨骼肌中的线粒体结构特征。尽管线粒体体积密度相似,但力量运动员的线粒体池特征为线粒体嵴密度增加、线粒体体积减小和比表面积增加。我们还提供了人类骨骼肌中线粒体形态的纤维型和隔室特异性评估,结果表明,跨组的线粒体形态存在隔室特异性影响,而与纤维类型基本无关。此外,我们表明抗阻运动导致轻微的线粒体应激迹象,而不会增加受损线粒体的数量。利用公开可用的转录组数据,我们表明急性抗阻运动增加了线粒体生物发生、分裂和线粒体未折叠蛋白反应 (UPR) 的标志物的表达。此外,我们观察到力量训练个体的基础转录组中 UPR 的富集。综上所述,这些发现表明力量运动员具有独特的线粒体重塑,这最大限度地减少了线粒体所需的空间。我们提出,抗阻运动同时激活线粒体生物发生和线粒体重塑途径(分裂和 UPR)的标志物,可能部分解释了力量运动员观察到的线粒体表型。关键点:未经训练的个体和力量运动员具有相似的骨骼肌线粒体体积密度。相比之下,力量运动员的线粒体特征是嵴密度增加、体积减小和比表面积增加。与 II 型纤维相比,I 型纤维的线粒体形态特征有轻微差异,但具有更多的线粒体轮廓数量。线粒体形态在两组的亚细胞隔室中都有明显的差异,其中肌膜下的线粒体比肌纤维间的线粒体更大。急性抗阻运动导致轻微的形态学线粒体应激迹象,伴随着线粒体生物发生、分裂和线粒体未折叠蛋白反应 (UPR) 标志物的基因表达增加。