Abstract
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.
Highlights
It is commonly accepted that physical activity stimulates inflammation [1,2,3,4,5,6], which triggers muscle repair and regeneration [7,8,9]
The expression ratio of the studied genes calculated between the start time and the Lactic acid (LA)-recovery time point revealed that the expression of all genes except CXCL11 was significantly higher in the repeated speed ability (RSA) group than in the Beep group (Table 4)
The intense efforts induced by the progressive endurance test protocol and anaerobic speed test caused an increase in the expression of genes encoding chemokines involved in the invasion and migration of immune cells
Summary
It is commonly accepted that physical activity stimulates inflammation [1,2,3,4,5,6], which triggers muscle repair and regeneration [7,8,9]. Cellular and psychological stressors initiate the release of endogenous factors known as danger- or damage-associated molecular patterns (DAMPs) to promote sterile inflammation via the activation of inflammation processes in the absence of exogenous factors such as pathogens [10,11,12,13]. In the context of the sterile inflammation theory [14,15], this mediation can help to better understand the impact of intense stimulating factors on the modulation of the immune system. Intracellular signal transduction results in the activation of transcription factors that regulate gene expression proteins whose autocrine or paracrine secretion develops a cascade of cellular response within a given tissue. The role of cytokine secretion in the cell death pathway is well known [18,19,20]
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