Increased mitochondrial surface area and cristae density in the skeletal muscle of strength athletes

Author:

Botella Javier1ORCID,Schytz Camilla T.2ORCID,Pehrson Thomas F.2,Hokken Rune2,Laugesen Simon2,Aagaard Per2,Suetta Charlotte3,Christensen Britt4,Ørtenblad Niels2ORCID,Nielsen Joachim2ORCID

Affiliation:

1. Institute for Mental and Physical Health and Clinical Translation, Metabolic Research Unit, School of Medicine Deakin University Geelong Australia

2. Department of Sports Science and Clinical Biomechanics University of Southern Denmark Odense Denmark

3. Geriatric Research Unit, Department of Geriatric and Palliative Medicine Copenhagen University Hospital, Bispebjerg and Frederiksberg Copenhagen Denmark

4. Department of Endocrinology and Internal Medicine, NBG/THG Aarhus University Hospital Aarhus Denmark

Abstract

AbstractMitochondria 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 (UPRmt). Further, we observed an enrichment of the UPRmt 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 UPRmt) with resistance exercise may be partially responsible for the observed mitochondrial phenotype of strength athletes. imageKey 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 (UPRmt).

Publisher

Wiley

Subject

Physiology

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