<jats:title>Abstract</jats:title><jats:p>A major consequence of muscular dystrophy is that increased membrane fragility leads to high calcium influx and results in muscle degeneration and myonecrosis. Prior reports have demonstrated that increased nitric oxide production via <jats:sc>L</jats:sc>‐arginine treatment of normal and <jats:italic>mdx</jats:italic> mice resulted in increased expression of utrophin and increased activation of muscle satellite cells, which could ameliorate the dystrophic pathology. We delivered <jats:sc>L</jats:sc>‐arginine to normal and <jats:italic>mdx</jats:italic> mice, and examined muscles for any functional changes associated with its administration. Treated <jats:italic>mdx</jats:italic> muscles were less susceptible to contraction‐induced damage and exhibited a rightward shift of the force–frequency relationship. Immunoblotting revealed increases in utrophin and γ‐sarcoglycan in the treated muscles. There was also a decrease in Evans blue dye uptake, indicating a reduction in myonecrosis. However, there was no decrease in serum creatine kinase or the proportion of central nuclei, nor any improvement in specific force. Together, these results show that <jats:sc>L</jats:sc>‐arginine treatment can be beneficial to <jats:italic>mdx</jats:italic> muscle function, perhaps through a combination of enhanced calcium handling and increased utrophin, thereby decreasing muscle degeneration. Muscle Nerve, 2005</jats:p>