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Autophagy is a cleaning mechanism of the cell to get rid of its dysfunctional or aging components, especially the mitochondria, the main cellular energy factory (mitophagy). The degradation of these constituents also provides an alternative source of nutrients to the cell in the fasted state or during prolonged endurance exercise like ultra-trail. Autophagy helps maintain muscle mass and requires fine regulation since excessive or deficient activation is implicated in metabolic disorders (type 2 diabetes, obesity) and myopathies. Physical exercise is currently emerging as a potential physiological strategy to stimulate autophagy and mitophagy in muscle, although the exercise modalities and molecular mechanisms involved remain little explored in humans. By better understanding the role of autophagy and mitophagy in exercise-induced muscle remodeling in healthy subjects, adapted physical activity protocols could improve the quality of life of patients with impaired muscle function and structure.

Telomeres, markers of our biological age, are nucleoprotein structures protecting the ends of chromosomes. For many years, telomeres were considered to be transcriptionally silent. Nevertheless, it now appears that they are transcribed in TERRA. Telomere length and TERRA expression are negatively correlated: high levels of TERRA are associated with shorter telomeres. Damaged telomeres induce cell senescence and interfere with proper tissue renewal. While endurance training has many health benefits, there is currently no evidence that it regulates the cellular aging process in skeletal muscle. The aim of this work is to study the impact of endurance training on telomere transcription and cell senescence in skeletal muscle.

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