Abstract
Magnesium (Mg(2+)) is a key regulator of cellular biochemical processes and an essential cofactor in skeletal muscle physiology. Although Mg(2+) deficiency has been linked to reduced muscle strength, its role in the regulation of calcium (Ca(2+)) signaling and in inflammation remains incompletely understood. In this study, we examined the effects of Mg(2+) availability using the murine myoblast cell line C2C12. Cells were differentiated under low, normal, or high Mg(2+) conditions, and myotube formation, intracellular Ca(2+) fluxes, and resistance to inflammatory stimuli were assessed. Mg(2+) deficiency impaired myotube differentiation, while Mg(2+) supplementation preserved Ca(2+) response during stimulation and contributed to protect myotubes against inflammation-induced damage. Collectively, these findings highlight a dual role of Mg(2+) in sustaining functional performance under repeated stress and protecting myotubes against inflammatory injury. This study supports the importance of adequate dietary Mg(2+) intake as a potential strategy to mitigate muscle loss associated with aging and chronic inflammation.