期刊
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
卷 9, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fcell.2021.625680
关键词
physical training; muscular inflammation; neutrophil; exercise; oxidative stress
资金
- CNPq (Conselho Nacional de Desenvolvimento Cientifico e Tecnologico)
- CAPES (Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior)
- FAPEMIG (Fundacao de Amparo a Pesquisa do Estado de Minas Gerais)
- Pro-Reitoria de Pesquisa da Universidade Federal de Minas Gerais
- Pro-Reitoria de Pesquisa da Universidade do Estado de Minas Gerais
- INCT em dengue e interacao microrganismo hospedeiro
Acute high intensity exercise induces inflammation, but physical training can attenuate exercise-induced inflammation. Training enhances immune adaptations and decreases inflammatory response post-exercise.
Acute exercise increases the amount of circulating inflammatory cells and cytokines to maintain physiological homeostasis. However, it remains unclear how physical training regulates exercise-induced inflammation and performance. Here, we demonstrate that acute high intensity exercise promotes an inflammatory profile characterized by increased blood IL-6 levels, neutrophil migratory capacity, and leukocyte recruitment to skeletal muscle vessels. Moreover, we found that physical training amplified leukocyte-endothelial cell interaction induced by acute exercise in skeletal muscle vessels and diminished exercise-induced inflammation in skeletal muscle tissue. Furthermore, we verified that disruption of the gp-91 subunit of NADPH-oxidase inhibited exercise-induced leukocyte recruitment on skeletal muscle after training with enhanced exercise time until fatigue. In conclusion, the training was related to physical improvement and immune adaptations. Moreover, reactive oxygen species (ROS) could be related to mechanisms to limit aerobic performance and its absence decreases the inflammatory response elicited by exercise after training.
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