496 International Journal of Sport Nutrition and Exercise Metabolism, 20, 2010, 496-506 © 2010 Human Kinetics, Inc. Effect of 6 Weeks of n-3 Fatty-Acid Supplementation on Oxidative Stress in Judo Athletes Edith Filaire, Alain Massart, Hugues Portier, Matthieu Rouveix, Fatima Rosado, Anne S. Bage, Mylène Gobert, and Denys Durand The aim of this investigation was to assess the effects of 6 wk of eicosapentanoic acid (EPA) and docosahexa- noic acid (DHA) supplementation on resting and exercise-induced lipid peroxidation and antioxidant status in judoists. Subjects were randomly assigned to receive a placebo or a capsule of polyunsaturated fatty acids (PUFAs; 600 mg EPA and 400 mg DHA). Blood samples were collected in preexercise and postexercise con- ditions (judo-training session), both before and after the supplementation period. The following parameters were analyzed: α-tocopherol, retinol, lag phase , maximum rate of oxidation (R max ) during the propagating chain reaction, maximum amount of conjugated dienes (CD max ) accumulated after the propagation phase, nitric oxide (NO) and malondyaldehide (MDA) concentrations, salivary glutathione peroxidase activity, and the lipid proile. Dietary data were collected using a 7-day dietary record. A signiicant interaction effect between supplementation and time (p < .01) on triglycerides was noted, with values signiicantly lower in the n-3 long-chain-PUFA (LCPUFA) group after supplementation than in the placebo group. Signiicant interaction effects between supplementation and time on resting MDA concentrations and R max were found (p = .03 and p = .04, respectively), with elevated values in the n-3 LCPUFA group after supplementation and no change in the placebo group’s levels. The authors observed a signiicantly greater NO and oxidative-stress increase with exercise (MDA, R max , CD max , and NO) in the n-3 LCPUFA group than with placebo. No main or interaction effects were found for retinol and α-tocopherol. These results indicate that supplementation with n-3 LCPUFAs signiicantly increased oxidative stress at rest and after a judo-training session. Keywords: nutrition, exercise, omega-3 fatty acids, oxidative stress Oxidative stress is a state of disturbed balance between reactive oxygen species (ROS) and reactive nitrogen species (RNS) on one hand and antioxidant defenses on the other. Powers, Smuder, Kavazis, and Hudson (2010) deined oxidative stress as a disturbance in the redox balance in cells in favor of oxidants, with this imbalance resulting in oxidative damage to cellular components. During increased oxygen utilization, as occurs during strenuous exercise, the rate of ROS pro- duction may overwhelm the body’s capacity to detoxify them, which can lead to increased oxidative stress and subsequent lipid peroxidation. In addition, strenuous physical exercise is associated with an increase in body temperature, which increases the rate of free-radical production (Altan, Pabuccuoglu, Altan, Konyalioglu, & Bayraktar, 2003). Growing evidence indicates that ROS and RNS contribute to muscle fatigue (Ferreira & Reid, 2008), and several mechanisms including DNA damage, lipid peroxidation, protein damage, oxidation of important enzymes, and stimulation of proinlam- matory cytokine release have also been implicated in the tissue damage by ROS (Finkel, 2001). Antioxidant enzymes (catalase, glutathione peroxidase, superoxide dismutase) and nonenzymatic antioxidants (vitamins E, A, and C; glutathione; uric acid) can attenuate exercise- induced oxidative stress. Antioxidants are present in all body luids and tissues, and they protect against endogenously formed free radicals, usually produced by leakage of the electron transport system (Halliwell, 1991). Antioxidant enzymes like glutathione peroxidase (GPx) provide protection within cells. Two forms of GPx are known: classical cellular GPx and extracellular GPx, which serves an important antioxidant role in many extracellular surfaces and spaces (Sies, Sharov, Klotz, & Briviba, 1997). Polyunsaturated fatty acids (PUFAs) are highly susceptible to ROS attacks. As a result of ROS interac- tion with PUFAs in cell membranes or lipoproteins, the process of uncontrolled lipid peroxidation occurs. Malondialdehyde (MDA) is an indicator of lipid peroxi- dation and one of its inal decomposition products that has numerous deleterious effects on biological systems (Matés, Pérez-Gómez, & Núñez de Castro, 1999). Filaire, Massart, Portier, and Rouveix are with the Unité de Formation en Sciences et Techniques des Activités Physiques et Sportives, Orleans, France. Rosado is with the Center of Investigation of Sport and Physical Activity, Coimbra, Portugal. Bage, Gobert, and Durand are with the Centre de Clermont- Ferrand/Theix, St.-Genès-Champanelle, France.