Acute exercise increases the amount of circulating inflammatory cells and cytokines tomaintain physiological homeostasis. However, it remains unclear how physical trainingregulates exercise-induced inflammation and performance. Here, we demonstratethat acute high intensity exercise promotes an inflammatory profile characterized byincreased blood IL-6 levels, neutrophil migratory capacity, and leukocyte recruitment toskeletal muscle vessels. Moreover, we found that physical training amplified leukocyte–endothelial cell interaction induced by acute exercise in skeletal muscle vessels anddiminished exercise-induced inflammation in skeletal muscle tissue. Furthermore, weverified that disruption of the gp-91 subunit of NADPH-oxidase inhibited exercise-induced leukocyte recruitment on skeletal muscle after training with enhanced exercisetime until fatigue. In conclusion, the training was related to physical improvement andimmune adaptations. Moreover, reactive oxygen species (ROS) could be related tomechanisms to limit aerobic performance and its absence decreases the inflammatoryresponse elicited by exercise after training.