Abstract
Introduction: In the context of sports practices, nutrology and the oxidation-reduction system impact the metabolism of athletes. Physical training associated with adequate nutrition is a clinically proven practice, being a cost-effective primary intervention that can delay and prevent the health burdens associated with metabolic disorders. Objective: It was to carry out a systematic review to describe the main nutritional and metabolic approaches to athlete performance, focusing on mitochondrial and oxidation-reduction activities. Methods: The PRISMA Platform systematic review rules were followed. The search was carried out from March to May 2025 in the Web of Science, Scopus, Embase, PubMed, Science Direct, Scielo, and Google Scholar databases. The quality of the studies was based on the GRADE instrument and the risk of bias was analyzed according to the Cochrane instrument. Results and Conclusion: A total of 121 articles were found, and 39 articles were evaluated in full and 28 were included in this systematic review. Considering the Cochrane tool for risk of bias, the overall assessment resulted in 10 studies with a high risk of bias and 21 studies that did not meet GRADE. Most studies showed homogeneity in their results, with X2=81.5%>50%. Redox processes are increasingly recognized as an integral part of exercise-associated metabolism and nutritional triggers. Despite the traditional perception that reactive species are exclusively harmful molecules, recent evidence suggests that exercise-induced reactive species are essential upstream signals for the activation of redox-sensitive transcription factors and the induction of exercise-associated gene expression. Redox reactions are increasingly recognized as a fundamental element of the cellular signaling mechanism, along with other well-established types of biochemical reactions that fine-tune human metabolism, for example, phosphorylation and ubiquitination. There are many other examples of responses and adaptations linked to exercise metabolism that is controlled, at least in part, by redox reactions, such as neuroprotection and cognitive function, mechanotransduction, muscle regeneration, autophagy, insulin sensitivity and glycemic control, heat shock proteins metabolism and nerve-muscle interactions.