WANG Xiaoxin, YU Hongjun. The Effect of Diesel Engine Exhaust Exposure on the Lungs of Mice during Endurance and Resistance Training[J]. China Sport Science, 2024, 44(3): 51-65. DOI: 10.16469/j.css.202403006
    Citation: WANG Xiaoxin, YU Hongjun. The Effect of Diesel Engine Exhaust Exposure on the Lungs of Mice during Endurance and Resistance Training[J]. China Sport Science, 2024, 44(3): 51-65. DOI: 10.16469/j.css.202403006

    The Effect of Diesel Engine Exhaust Exposure on the Lungs of Mice during Endurance and Resistance Training

    • Objectives: To investigate the comprehensive effects of endurance training(ET) and resistance training(RT) interventions on the lungs of mice when subacute diesel engine exhaust(DEE) exposure at different doses. Methods: Sixty-nine male C57BL/6 mice were randomly divided into nine groups, they performed either ET or RT intervention except control group; at the same time,the mice were exposed to either filtered air, or low, moderate concentrations of DEE(1 h/d for 3 weeks). The lung function in mice was assessed using whole body plethysmography(WBP). Lung tissues and bronchoalveolar lavage fluid were collected to observe tissue structure, fibrosis, and apoptosis through histological staining. In addition, inflammatory and oxidative stress indicators were evaluated using assay kits and RT-qPCR. Results: The study indicated that DEE exposure led to a decline in lung function, the pathological changes were observed in lung tissue structure, the apoptosis was increased, and inflammatory and oxidative stress responses were intensified. These adverse reactions were found to escalate with the increase of pollutant concentrations. However,the ET and RT interventions during DEE exposure partially ameliorated lung function in mice, including the improvement in lung tissue damage, fibrosis, and apoptosis, accompanied by a decrease in MDA content. Remarkably, under moderate DEE exposure, RT intervention demonstrated superior effects compared with ET in alleviating lung tissue damage, which was evidenced by the reduction in LDH activity, IL-6 level, and Col3a1, Ctgf, IL-1β, NF-κB gene expression, while enhancing IL-10 level and increasing the activities of T-SOD and CAT. It is noteworthy that the exercise intervention under DEE exacerbated adverse lung reactions in mice compared with that of under filtered air. Conclusions: Exercise can mitigate DEE-induced lung injury, but it cannot completely offset all the negative effects of DEE. These findings highlight the potential benefits of exercise under DEE exposure, but the application in practice should be considered carefully.
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