The role of plasma glutamine concentration and glutamine supplementation on immunosuppression was investigated in combat athletes. Twenty-three male athletes were randomly assigned to receive glutamine (21 g/day, n=12) or placebo (ovalbumin, n=11) for 10 days. Six athletes who did not lose weight served as controls. Athletes were assessed 21 days before (−21d), 1 day before (−1d) and 5 days after (+5d) a competition. Weight reduction was similar between glutamine (−8.2%± 4.1%) and placebo (−8.5%±2.4%) and negligible in control (−0.6%±1.4%). In both weight-loss groups, the majority of athletes reported symptoms of upper respiratory symptoms, as assessed by the Wisconsin upper respiratory symptom survey questionnaire. Only two athletes reported symptoms in the control group. Immune cell function remained unchanged throughout the study except for an increase in neutrophil phagocytic activity (placebo: −21d=5,251±2,986; −1d=17,428±22,374; +5d=21,125±21,934; glutamine: −21d=6,096±3,549; −1d=11,029±17,113; +5d=28,186±21,032 FI) and a minor change in monocyte phagocytic activity (placebo: −21d=4,421±3,634; −1d=3,329±6,283; +5d=3,243± 2,553; glutamine: −21d=4,051±3,186; −1d=3,106±2,625; +5d=4,981± 4,598) in both glutamine and placebo after weight loss. Plasma glutamine and cortisol remained unchanged across the study. creatine kinase levels were increased in placebo (−21d=125.2±54.1; −1d=187.2± 73.5; +5d=111.3±59.1 U/L) but not in glutamine (−21d=136.2±58.2; −1d= 168.8±65.0; +5d=129.7±64.0 U/L). Rapid weight loss increased the frequency and severity of infection symptoms, but this was neither associated with plasma glutamine depletion nor counteracted by glutamine supplementation.