Purpose: Regular physical activity induces oxidative stress but also causes adaptations in antioxidant defences including the nuclear factor κB (NF-κB) pathway, which activates target genes related to antioxidant defences such as uncoupling proteins (UCPs), and mitochondrial biogenesis mediated by peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α). The aim of the study was to determine the effect of long-term training and acute exercise on oxidant/antioxidant status and the expression of mitochondrial biogenesis genes in peripheral blood mononuclear cells (PBMCs).
Methods: Twelve professional football players performed an 8-week exercise programme comprising a daily 2-h football training session. Blood samples were taken before and after the training season.
Results: The results reported a significant increase in antioxidant protein levels and in mitochondrial proteins in resting conditions after the 8-week training period. PGC1α, UCP-2 and mitofusin 2 protein levels also increased after acute exercise compared to pre-exercise levels. After the training, the expression of PGC1α, cytochrome c oxidase subunit IV and mitochondrial NADH dehydrogenase subunit 5 messenger RNA (mRNA) significantly augmented after the acute physical activity compared to pre-exercise levels; while no changes occurred in these mRNA in basal conditions. NF-κB activation and ROS production reported a significant increase after acute exercise.
Conclusions: Training increases the levels of proteins related to mitochondrial biogenesis and improves the antioxidant capabilities of mitochondria in PBMCs among well-trained football players. Acute exercise may act as an inducer of mitochondrial biogenesis through NF-κB activation and PGC1α gene expression.
Keywords: Biogenesis; Fission; Fusion; Mitochondria; PBMCs; Training.