Muscle regeneration is a process happening during the whole life of the human being, mostly relying on muscle stem cells (MuSC). MuSC are adult stem cells maintained quiescent in their niche (in between the muscle fiber and basal lamina) and able to be activated upon muscle injury. Their activation results in the exit from the G0 phase to re-enter the cell cycle and proliferate as myogenic progenitors called myoblasts. Once myoblasts reach a sufficient amount, they eventually differentiate and fuse to repair the damaged muscle fiber. However, a part of the myoblast population returns to the quiescent state to replenish the pool of MuSC for further injuries. The mechanisms of activation of human MuSC, together with the return into quiescence of myoblasts remain elusive. My thesis project aimed to better characterize these processes, with particular attention to the potential involvement of Ca2+ signals. Due to the impossibility to study those processes in vivo, we used an in vitro model based on primary human MuSC. We first extracted MuSC from muscle biopsy and let them proliferate as myoblasts. Once confluent, myoblasts can be differentiated in a medium poor in growth factors. Around 70% of myoblasts fuse to form large polynucleated cells called myotubes while the remaining cells stay mononucleated and acquire stemness characteristics. These cells are called reserve cells (RC) and are the in vitro pendant of MuSC. Interestingly, RC are in a quiescent state and can be activated by fetal calf serum (FCS) to re-enter the cell cycle and proliferate as myoblasts. Thus, this in vitro model allows us to recapitulate the process of return of quiescence of MuSC and their subsequent activation.