The concept of L-carnitine supplementation to improve muscular performance is based on the role of L-carnitine in the rate limiting step of β-oxidation of fatty acids (1). L-carnitine attenuates free radical induced oxidative stress during recovery after exercise stress (2) and in pathological conditions (3). Thus it was hypothesized that L-carnitine may reduce intermittent hypoxia induced oxidative stress and thereby delays muscle fatigue. Thirty-six adult male Sprague Dawley rats were divided in two batches and each comprising three groups (n=6/group)- unexposed control; intermittent hypoxia exposed (6 hrs/day for continuous 7 days), intermittent hypoxia exposed (6 hrs/day for continuous 7 days) with L-carnitine supplementation (100mg/kg body weight/ day for 7 days). After the completions of exposure in batch I, rats were anaesthetized with ketamine (50 mg/kg bw, i.p.) and xylazine (10mg/kg bw, i.p.) and sacrificed. The thiobarbituric acid reactive substances, protein carbonyl and lipid hydroperoxides were estimated in the muscle tissue to investigate the efficacy of carnitine in attenuating oxidative stress. In batch II experiment, rats were anaesthetized with intramuscular dose of ketamine (50mg/kg bw). The gastrocnemius muscle of right hind limb with intact sciatic nerve was dissected with the Achilles tendon and connected to a force transducer. The gastrocnemius muscle was set at a length which produced an optimal force during each tetanic contraction. Electrical stimulation was used to induce six tetanic muscular contractions in gastrocnemius muscle after completion of exposure. Percentages of mean performed work, time of decay to 50% of peak force of contraction, and peak force of contraction were measured during tetanic contractions using high-speed data acquisition system. Mean frequency during recovery between tetanic contractions was measured from electromyography. Muscle damage was indirectly measured from plasma creatine kinase and lipid hydroperoxides. Significant reduction in thiobarbituric acid reactive substances, protein carbonyl, lipid hydroperoxides, and creatine kinase activity in L-carnitine supplemented-intermittent hypoxia exposed group when compared with placebo treated-intermittent hypoxia exposed group suggests that L-carnitine reduces oxidative damage and thereby delays muscular fatigue, which was further evident from improvement in maximum force of tetanic contraction, time of decay to 50% of peak force of tetanic contraction and mean frequency of contraction during muscle recovery between tetanic stimulation in L-carnitine supplemented-intermittent hypoxia exposed group as compared to unsupplemented and exposed group of rats. From these results it is concluded that L-carnitine delays skeletal muscle fatigue in rats by reducing free radical induced oxidative damage in intermittent hypoxic exposure.