Role of PGC-1α in Athletes' Response to Air Pollution and Hypoxia: Implications for Respiratory Health and Performance

Abstract

The role of peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α) in mediating the cellular response to environmental stressors like particulate matter (PM2.5) and hypoxia, which are common in urban and high-altitude athletic environments, remains poorly understood. This study investigates the expressions of PGC-1α, peroxisome proliferator-activated receptor gamma (PPAR-γ), and nuclear factor-kappa B (NF-κB) p65 at the transcriptional and protein levels in human bronchial epithelial cells exposed to these conditions. We measured intracellular malondialdehyde (MDA) content and superoxide dismutase (SOD) activity to evaluate oxidative damage, a critical concern for athletes’ respiratory health and performance. Additionally, the antioxidant N-acetyl-L-cysteine (NAC) was used to assess the protective role of PGC-1α signaling in this context. Our findings reveal that NAC (5 μg/ml) significantly mitigates the simultaneous alterations induced by PM2.5 and hypoxia in PGC-1α, PPARγ, and NF-κB p65 expression, alongside changes in MDA content and SOD activity. The protective effects of NAC were notably reduced by the knockdown of PGC-1α, highlighting its essential role in shielding against oxidative stress under these conditions. These results suggest that PGC-1α may be crucial in managing oxidative damage in athletes exposed to pollution and low-oxygen environments, offering novel insights for enhancing athletic performance and designing interventions to protect respiratory health against environmental stressors.