Transcriptomics and metabolomics revealed the pulmonary protective mechanism of aerobic exercise in COPD

<bold>Background:</bold> Current studies indicates that regular aerobic exercise can alleviate lung damage induced by cigarette smoke in COPD, however, the specific mechanisms remain elusive. <bold>Objectives:</bold> The present study aims to identify the mechanisms by which aerobic exercise attenuates smoke-induced lung injury in COPD mice through the integration of transcriptomics and metabolomics. <bold>Methods:</bold> Male C57BL/6 mice were divided into three groups: control, smoke, and smoke+exercise. The study investigated the effects of aerobic exercise and its underlying mechanism in a smoke-induced mouse model of COPD by employing metabolomics and transcriptomics analyses. Additionally, pulmonary function tests, assessment of inflammatory factors in serum and bronchoalveolar lavage fluid, and histological examination using hematoxylin and eosin staining were conducted to elucidate the protective effects of aerobic exercise on COPD. <bold>Results:</bold> Aerobic exercise aids in diminishing inflammation, oxidative stress, and emphysema formation following smoke exposure. Moreover, omics analysis revealed significant regulation of numerous genes and metabolites post smoking and exercise intervention. Differential genes primarily align with immune response, cytochrome P450, and glutathione metabolism, while differential metabolites predominantly correlate with sphingolipid metabolism, along with metabolism of glycine, serine, and threonine. <bold>Conclusions:</bold> Aerobic exercise has been shown to confer beneficial effects against COPD, possibly by modulating inflammation and oxidative stress via the regulation of Glutathione S-transferase.