Sepsis is a general, uncontrolled and systemic inflammation due to an infection. In serious cases of sepsis (called septic choc) mortality can range between 40% and 50% and concerns 200.000 people in the USA every year. Nowadays patient management is getting better and mortality diminishes, however patients are facing more and more long-term sequelae. As a result, among survivors, half of the patients will suffer of acquired neuromyopathy, meaning an important muscle weakness which can be disabling for up to 5 years after hospitalization. Many studies showed that this muscle weakness involved 1) the impairment of muscular membrane excitability, 2) mitochondrial dysfunction leading to bioenergetic failure and oxidative stress and 3) proteolysis, mainly related to an activation of the ubiquitin-proteasome pathway. These mechanisms can be triggered by various factors, notably systemic inflammatory mediators, endocrine dysfunction, immobilization, drugs and electrolyte disturbances. We showed that in addition to these impairments the muscle stem cells (called satellite cells) were dysfunctional. Indeed in healthy situation muscle regeneration is very efficient. Upon muscle injury they are activated, they divide, multiply and fuse in order to regenerate muscle fibres. We have shown in mice that after a sepsis the satellite cells were impaired and that muscle regeneration was not occurring properly. This dysfunction was due to a decrease mitochondrial mass and a drop in ATP content triggering apoptosis upon activation of the satellite cells. We used Mesenchymal Stem Cell (MSCs) treatment after sepsis for their immunoregulatory and anti-apoptotic properties to reduce the noxious effect of sepsis on satellite cells. We showed that regeneration was significantly improved post-injury with decreased necrosis and fibrosis. The mitochondrial mass and ATP in the satellite cells were recovered and the systemic inflammation was reduced. The cellular mechanisms of MSCs rescue and the characterization of human SCs after sepsis are essential steps before being able to transfer this therapy to the clinics. Interestingly we have also observed that MSCs were able to transfer healthy mitochondrial material to impaired satellite cells to rescue them. At the functional level the force of septic mice increased when injected with MSCs. For this study we have two goals: First we want to understand by which mechanism(s) the mitochondrial material transfer occurs and secondly by collecting human muscle samples from septic patients we would like to isolate the satellite cells and characterise their state (genomic, metabolic and basic cellular behaviour) in order to assess their regenerative capacity. This will allow us to confirm the observation made in the mice models. This translational study will allow us to develop new therapies to avoid or cure the negative impact of sepsis on muscle stem cells and to a broader view on the acquired neuromyopathies in the intensive care units that concerns virtually all patients that stay bedridden and intubated for more than seven days at the hospital.