Eurydice Lamirault

Sepsis is a systemic inflammatory response to infection, which in some cases can become excessive, leading to generalized inflammation. The evolution of this disease can lead to simultaneous failure of various organs essential to life, and to patients being admitted to intensive care. Deleterious effects on muscles will appear, contributing to weakness and muscle wasting. In the long term, this translates into reduced quality of life, prolonged rehabilitation and muscular atrophy, resulting in loss of strength and making daily activities difficult or impossible.

Muscular atrophy due to sepsis involves both intrinsic and extrinsic phenomena. The former are associated with a disturbance in the protein balance between excessive degradation (proteolysis) and insufficient production of muscle protein, leading to this loss of mass in patients. Extrinsic phenomena result from deregulation of stem cells and their microenvironment, impairing the muscle's capacity for repair and regeneration. While the former are well described, the kinetics of stem cell damage and its interaction with other cell types are poorly documented.

In the absence of in-depth knowledge of the pathophysiological mechanisms involved in muscle damage, few or no known therapeutic strategies are used to counteract this severe damage to striated skeletal muscle.

To alleviate this muscle wasting, neuromuscular electrical stimulation (ESNM) is being explored as a therapeutic alternative. This technique involves the controlled application of electrical currents at a low level of force, without muscle damage. In the literature, this technique for limiting sepsis-induced muscle damage is controversial, since no study has controlled the force produced by muscles in response to electrical stimulation, which is the only admissible criterion of efficacy. 

Our aim is therefore to apply a standardized ESNM protocol in a murine model of sepsis, and to demonstrate the functional, tissue and cellular effects.