Caffeine is a pharmacological agent that has been shown to enhance muscle contraction. The stimulatory effects of caffeine may be, in part, due to alterations in the skeletal muscle redox status. Specifically, caffeine administration to rats has been shown to rapidly, but transiently, decrease levels of skeletal muscle nitric oxide (NO) synthase. Decreased levels of NO could lead to elevated oxidative stress, since NO is a potent superoxide radical scavenger. We tested the hypothesis that acute caffeine administration would decrease muscle nitrosative stress, increase oxidative stress, and upregulate the expression of key antioxidant enzymes. Male Sprague Dawley rats received i.p. administration of caffeine (16 mg/kg; n=8) or vehicle (saline; n=8). Thirty minutes post injection the rats were anesthetized and the soleus muscles were harvested for analysis. No differences in oxidative injury (protein carbonyls) or nitrosative injury (3‐nitrotyrosine) were detected (p>0.05). Caffeine administration did not alter manganese superoxide dismutase or copper‐zinc superoxide dismutase protein levels, but resulted in a 50% increase in catalase protein levels (p<0.05). In summary, acute caffeine administration may upregulate skeletal muscle catalase expression by a mechanism independent of oxidative stress. Supported by Syracuse University SOE and APS UGSRF