Artículos de revistas
Prolonged Physical Training Decreases mRNA Levels of Glucocorticoid Receptor and Inflammatory Genes
Fecha
2010Registro en:
HORMONE RESEARCH IN PAEDIATRICS, v.74, n.1, p.6-14, 2010
1663-2818
10.1159/000313586
Autor
SILVA, Tatiane Sousa e
LONGUI, Carlos Alberto
ROCHA, Mylene Neves
FARIA, Claudia Dutra Costantin
MELO, Murilo Rezende
FARIA, Thelma Gomes
SOUZA, Julio Antonio de
RIZZO, Luiz Vicente
Institución
Resumen
Background/Aims: Prolonged physical exercise induces adaptive alterations in the hypothalamic-pituitary axis, increasing cortisol metabolism, and reducing cortisol synthesis and glucocorticoid sensitivity. The mechanisms responsible for this relative glucocorticoid resistance remain unknown but may involve expression of genes encoding glucocorticoid receptor (GR) and/or inflammatory molecules of nuclear factor kappa B1 (NFkB1) signaling pathway and cytokines. This study aimed to determine the impact of prolonged physical training on the expression of genes involved in glucocorticoid action and inflammatory response. Methods: Normal sedentary male cadets of the Brazilian Air Force Academy were submitted to 6 weeks of standardized physical training. Eighteen of 29 initially selected cadets were able to fully complete the training program. Fasting glucose, insulin and cortisol levels, cytokine concentration and the expression of genes encoding GR, NFkB1, inhibitor of NFkB1 and IkB kinase A were determined before and after the training period. Results: Prolonged physical exercise reduced the basal cortisol levels and the percent cortisol reduction after dexamethasone. These findings were associated with a significant reduction in the mRNA levels of GR (6.3%), NFkB1 (63%), inhibitor of NFkB1 (25%) and IkB kinase A (46%) with concomitant reduction in cytokine concentrations (ELISA). Conclusions: Prolonged physical training decreases the glucocorticoid sensitivity and the mRNA levels of the GR gene combined with decreased mRNA of genes related to the NFkB pathway. Copyright (C) 2010 S. Karger AG, Basel