The cause-effect relationship between lactic acid, acidosis, and muscle fatigue has been established in the literature. However, current experiments contradict this premise. Here, we describe an experiment developed by first-year university students planned to answer the following questions: 1) Which metabolic pathways of energy metabolism are responsible for meeting the high ATP demand during high-intensity intermittent exercise? 2) Which metabolic pathways are active during the pause, and how do they influence phosphocreatine synthesis? and 3) Is lactate production related to muscular fatigue? Along with these questions, students received a list of materials available for the experiment. In the classroom, they proposed two protocols of eight 30–m sprints at maximum speed, one protocol with pauses of 120 s and the other protocol with pauses of 20 s between sprints. Their performances were analyzed through the velocity registered by photocells. Blood lactate was analyzed before the first sprint and after the eighth sprint. Blood uric acid was analyzed before exercise and 15 and 60 min after exercises. When discussing the data, students concluded that phosphocreatine restoration is time dependent, and this fact influenced the steady level of performance in the protocol with pauses of 120 s compared with the performance decrease noted in the protocol with pauses of 20 s. As the blood lactate levels showed similar absolute increases after both exercises, the students concluded that lactate production is not related to the performance decrement. This activity allows students to integrate the understanding of muscular energy pathways and to reconsider a controversial concept with facts that challenge the universality of the hypothesis relating lactate production to muscular fatigue.