During efforts with low muscle glycogen (B-Glic), fatigue is classically related to peripheral factors, such as energy unavailability. However, the B-Glic situation also induces systemic changes, which can decrease the muscle activation by the nervous system (i.e., central fatigue).Considering these two strands of thought, this thesis aimed to investigate the possible influences of muscle glycogen on the origin of fatigue in different domains of intensity. To test the different origins of fatigue, we used techniques such as twitch interpolation (TI) and transcranial magnetic stimulation (TMS). In addition, we tested whether the B-Glic situation may be responsible for the decrease in the activation of the motoneurons (i.e., central fatigue), mainly by the action of circulating tryptophan (TrP). Basically, we tried to evaluate the origin of fatigue in efforts with B-Glic, induced by previous exercise, and after the recovery of this substrate (R-Glic), through a diet with high carbohydrate levels. In the first experiment, 11 participants underwent depletion effort, 24-hour with solution application containing (10% Maltodextrin; R-Glic) or not (placebo, B-Glic) carbohydrates, and a high-intensity intermittent effort (6x1min to 120% of VO2PICO, separated by 3 min of passive recovery). In this experiment, the glycogen content was estimated by ultrasound. The main results demonstrate that i) glycogen is preserved in efforts with B-Glic and ii) the fatigue has peripheral origin regardless of the previous glycogen content. In another experiment we investigated the origin of fatigue in prolonged exertion and its relationships with the blood concentrations of TrP, this time we performed a 5day period for glycogen depletion (exercises and diet with low amounts of carbohydrates (0.3 ± 0, 2 g.kg -1 . Day -1 )). The R-Glic situation was induced by three days of rest and diet with high amounts of carbohydrate (4.5 ± 1.7 g.Kg -1 .day -1 ). In this experiment, glycogen levels were determined by muscle biopsy (B-