Metabolic stress‐dependent regulation of the mitochondrial biogenic molecular response to high‐intensity exercise in human skeletal muscle

摘要

Key points class="unordered" style="list-style-type:disc" id="tjp13003-list-0001">Low‐volume high‐intensity exercise training promotes muscle mitochondrial adaptations that resemble those associated with high‐volume moderate‐intensity exercise training. These training‐induced mitochondrial adaptations stem from the cumulative effects of transient transcriptional responses to each acute exercise bout.However, whether metabolic stress is a key mediator of the acute molecular responses to high‐intensity exercise is still incompletely understood.Here we show that, by comparing different work‐matched low‐volume high‐intensity exercise protocols, more marked metabolic perturbations were associated with enhanced mitochondrial biogenesis‐related muscle mRNA responses.Furthermore, when compared with high‐volume moderate‐intensity exercise, only the low‐volume high‐intensity exercise eliciting severe metabolic stress compensated for reduced exercise volume in the induction of mitochondrial biogenic mRNA responses.The present results, besides improving our understanding of the mechanisms mediating exercise‐induced mitochondrial biogenesis, may have implications for applied and clinical research that adopts exercise as a means to increase muscle mitochondrial content and function in healthy or diseased individuals.