Biology subjects

Schytz, C. T.

Publications and source records attributed to Schytz, C. T..

3 recordsLinked to original sources

bioRxiv2024

Effect of high-altitude exposure on skeletal muscle mitochondrial subcellular distribution, ultrastructure and respiration in sea-level residents

Endurance exercise performance is associated with a well-developed skeletal muscle mitochondrial network, which is composed of subsarcolemmal mitochondria interconnected with intermyofibrillar mitochondria bending around the myofibrils. High-altitude exposure is typically incorporated in elite sport training regimens, but little is known about how this network adapts to an environment characterised by tissue hypoxia. For this reason, we investigated how high-altitude exposure affects mitochondrial subcellular distribution, ultrastructure, respiratory control, and intrinsic mitochondrial respiratory capacity. Nine healthy and recreationally active sea-level residents (eight males and one female) resided at an altitude of 3454 m with biopsies collected from the vastus lateralis muscle before and after 7 and 28 days at high altitude. The muscular mitochondrial volume density (MitoVD) increased after high-altitude exposure, driven by an increase in the intermyofibrillar MitoVD. This was however accompanied by a decreased cristae surface area per skeletal muscle fibre volume (MuscularCD) because of a decline in the cristae surface area per mitochondrial volume (MitoCD). Despite a reduced MuscularCD, mass-specific maximal coupled respiration (OXPHOS_CII+CI+ETF) increased slightly, and was considerably elevated when normalised to MuscularCD, suggesting intrinsic adaptations to high altitude. The difference between cristae-specific OXPHOS_CII+CI+ETF and an associated cristae-specific leak respiration (Leak_CII+CI+ETF) indicated a markedly higher degree of coupling between the electron flow in the electron transport system and ATP production. As the effect size 95% confidence intervals includes trivial effects the results need to be substantiated. In conclusion, high-altitude exposure altered mitochondrial subcellular distribution, ultrastructure and induced intrinsic respiratory adaptations.

physiology↗

bioRxiv2023

Differential utilisation of subcellular skeletal muscle glycogen pools: A comparative analysis between 1 and 15 minutes of maximal exercise

Distinct subcellular pools of glycogen particles exist within skeletal muscle fibres, distributed both within and between myofibrils and can be found in proximity to, or at a distance from mitochondria. Their precise localisation may influence their degradation rate and role in muscle function. Here, we investigated how exercise at different intensities (1- and 15-min maximal exercise) with known variations in glycogenolytic rate and relative contribution from anaerobic metabolism affects the utilisation of the distinct pools. Further, we investigated how lowered carbohydrate and energy intake affected glycogen volume densities and the storage of glycogen particles (i.e., localisation, size, and number) and their subsequent utilisation during the exercises. Using a randomized, counterbalanced, cross-over design, participants performed two maximal cycle tests of either 1 (n=10) or 15 min (n=10), conducted following consumption of two distinct diets with either high or lowered carbohydrate and energy contents. Muscle biopsies from m. vastus lateralis were obtained before and after the exercises. Intermyofibrillar glycogen was preferentially utilised during the 1-min exercise, whereas intramyofibrillar glycogen was preferentially utilised during the 15-min exercise. The lowered carbohydrate and energy intake decreased the particle size across all subcellular pools and reduced the numerical density in the intramyofibrillar and subsarcolemmal pools, with no effects on the glycogen utilisation during the subsequent exercise. In conclusion, the distinct subcellular glycogen pools were differentially utilised during 1-min and 15-min maximal exercise. Additionally, lowered carbohydrate and energy consumption reduces particle size and numerical density, depending on subcellular localisation.

physiology↗

bioRxiv2023

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

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 (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.

physiology↗