Following initial spinal cord injury (SCI) a cascade of pathological events, including oxidative stress, leads to secondary injury. Glutathione (GSH) plays a critical role in oxidant scavenging. Maintenance of GSH concentrations after SCI lessens secondary injury, and improves recovery. Since glutamine promotes glutathione synthesis, this nonessential amino acid was examined for therapeutic potential. Denervation alters the expression of myosin heavy chain (MyHC) isoforms within skeletal muscles. The hypotheses of this study were that glutamine administration to SCI rats would lead to improved functional recovery and more preserved MyHC phenotypes in representative locomotor muscles. Male Wistar rats were divided into four groups: healthy, sham with laminectomy, laminectomized SCI untreated, and laminectomized SCI treated with glutamine. Functional performance was measured weekly for 6 weeks using Basso-Beattie-Bresnahan (BBB) scale and angle board methods. MyHC composition of rat soleus and extensor digitorum longus (EDL) muscles was determined using SDS-PAGE. Glutamine treated rats had significantly higher angle board scores (p<0.001) and BBB scores (p<0.01) than untreated SCI rats. Soleus of healthy rats contained 94% type 1 myosin isoform. Treated rats maintained 68%, which was significantly (p<0.001) greater than 28% in untreated rats. The EDL of healthy rats contained 55% type 2b myosin. There was a significant (p<0.001) decrease in this isoform following SCI, but no significant difference between treated and untreated groups. There were strong correlations between higher functional scores and more preserved MyHC phenotypes. Our findings suggest glutamine improves functional recovery and helps preserve myosin profile, by reducing secondary SCI thereby maintaining more nerves.