Résumé
Regularly performed endurance exercise has a number of health benefits, including improvements in cardiovascular function, muscle metabolism, and increased work capacity. The increase in endurance is a result of greater oxygen delivery and extraction by the exercising muscle. Oxygen extraction is a result of an improved capillary-to-fiber ratio, as well as a higher mitochondrial content within muscle. The increase in mitochondrial content is a well-established and dramatic adaptation within the exercised muscle, but the molecular mechanisms underlying this change in muscle phenotype are just beginning to be clarified. An understanding of the cellular processes involved could help in the development of therapeutic applications other than exercise, and may help us better comprehend the pathology of mitochondrial diseases. This increase in mitochondrial content which occurs as a result of regular exercise is referred to as mitochondrial biogenesis. The process is complex because mitochondria are composed of proteins encoded by both nuclear and mitochondrial DNA (mtDNA). The major steps involved include: (1) signaling events leading to transcription, brought about by each exercise bout; (2) transcriptional regulation of nuclear-encoded genes encoding mitochondrial proteins, mainly mediated by the coactivator PGC-1α; (3) control of mitochondrial DNA gene expression by the transcription factor Tfam; (4) mitochondrial fission and fusion mechanisms; (5) import of nuclear-derived gene products into the mitochondrion via the protein import machinery; and (6) assembly of nuclear- and mitochondrially-encoded subunits into functional holoenzyme complexes.