Exosome regulation by physical activity and hypoxia
Exercise exerts its systemic effects partly by cross talk between organs that release molecules into the bloodstream called “exerkines”. Exerkines may be carried as cargo inside extracellular vesicles, and more particularly by the so-called exosomes, that are released by different secretory cell and have emerged as a mechanism for intercellular communication and health improvement. Exosomes have been found to be released following a single bout of exercise as well as after exercise training, inducing changes in exosome plasma concentrations, markers, and cargoes. How exercise in hypoxia modulate the secretion and/or content of exosomes is not known. The aim of this project is to investigate the amount and the content of exosomes released after different exercise paradigms in hypoxic conditions in human.
Targeting skeletal muscle by physical activity to treat metabolic dysfunction-associated fatty liver disease
In preclinical models and in subjects with metabolic dysfunction-associated fatty liver disease (MAFLD), muscle fat is associated with a progressive liver disease (NASH) and adverse MAFLD-associated features. We hypothesize the development and the operation of a skeletal muscle to-liver axis in the pathogenesis of NASH. The aim of the project is to test if ‘inadequate’ lipid accumulation within myocytes modifies muscle transcriptome, secretome and/or exosome release or content and whether those changes could directly or indirectly affect distant organs. Hence physical training that will mitigate muscle fat storage should abrogate the signature and limit liver disease progression.
Effects of hypoxia on the regulation of satellite cells
Satellite cells are muscle stem cells that once activated, proliferate, and differentiate into myocytes that finally fuse with an existing myofiber to regenerate or increase its mass. This process is called ‘myogenesis’. Satellite cell activation can be modulated by exercise and by hypoxia. The purpose of this project is to elucidate whether or not satellite cells are regulated in a different way in response to an eccentric exercise in hypoxia comparing to normoxia. In addition, we will investigate potential differences in satellite cell activation between environmental normobaric hypoxia and local hypoxia induced by blood flow restriction, two methods used to reach hypoxia at sea level.
Heat pre-conditioning and mitokine potential to limit muscle atrophy
Disuse muscle atrophy is a serious medical condition resulting from inactivity after injury, bed rest, cast immobilization, surgery or even exposure to microgravity such as space flights. Heat stress activates several signaling pathways related to mitochondrial gene expression and promotes mitochondrial adaptations such as increased mitochondrial content and oxidative capacity. Yet, the effect of heat stress on the release of small molecules by mitochondria, the so-called mitokines, is not clear. Heat stress is increasingly being used as an adjuvant physical therapy, and has shown to confer numerous health benefits. This study aims at understanding the role of mitokines and heat stress in disuse muscle atrophy and their utility as therapeutic or protective agents in a human and myogenic cell culture model. Another purpose is to investigate if heat stress affects the release of mitokines.
