Acute, strenuous physical exertion requiring high levels of energy production induces the production of reactive oxygen species and metabolic disturbances that can damage the mitochondria. Thus, selective autophagic elimination of defective mitochondria may improve resistance to oxidative stress and potentially to inflammation. The main goal of this study was to evaluate the impacts of intense effort on changes in the expression of select genes related to post-effort inflammation and autophagy. Thirty-five men aged 16-21 years were recruited to the study. The impacts of both aerobic (endurance) and anaerobic (speed) efforts on selected genes encoding chemokines (CXCL5, 8-12) were analyzed. Significant increases in the expression of all studied genes excluding CXCL12 were observed. Moreover, both types of effort induced an increase in the expression of genes encoding IL-2, -4, -6, -10, IFN-γ and TNF-α, excluding IL-17A. Generally, these efforts caused a significant increase in the relative expression of apoptosis- (BCL2 and BAX) and autophagy- (BNIP3, BECN1, MAP1LC3B, ATG5, ATG7, ATG12, ATG16L1 and SQSTM1) related genes. It seems that the duration of physical activity and its bioenergetic cost has an important impact on the degree of increase in expression of this panel of autophagy-related genes. Anaerobic effort is more strenuous than aerobic effort and requires a higher bioenergetic investment. This may explain the stronger impact of anaerobic effort on the expression of the studied genes. This observation seems to support the protective role of autophagy proposed in prior studies.
Keywords: cell death; chemokines; cytokines; effort; gene expression; inflammation; leukocytes.