Particulate matter (PM) has deleterious consequences not only on the respiratory system but also on essential human organs, such as the heart, blood vessels, kidneys, and liver. However, the effects of PM inhalation on skeletal muscles have yet to be sufficiently elucidated. Female C57BL/6 or mt-Keima transgenic mice were randomly assigned to one of the following four groups: control (CON), PM exposure alone (PM), treadmill exercise (EX), or PM exposure and exercise (PME). Mice in the three-treatment group were subjected to treadmill running (20 m/min, 90 min/day for 1 week) and/or exposure to PM (100 μg/m³). The PM was found to exacerbate oxidative stress and inflammation, both at rest and during exercise, as assessed by the levels of proinflammatory cytokines, manganese-superoxide dismutase activity, and the glutathione/oxidized glutathione ratio. Furthermore, we detected significant increases in the levels of in vivo mitophagy, particularly in the PM group. Compared with the EX group, a significant reduction in the level of mitochondrial DNA was recorded in the PME group. Moreover, PM resulted in a reduction in cytochrome c oxidase activity and an increase in hydrogen peroxide generation. However, exposure to PM had no significant effect on mitochondrial respiration. Collectively, our findings in this study indicate that PM has adverse effects concerning both oxidative stress and inflammatory responses in skeletal muscle and mitochondria, both at rest and during exercise.

PURPOSE: The purpose of this study was to investigate the effects of hyperventilation in the presence of fine particulate matter (PM2.5) on inflammatory and apoptotic responses in the lungs of mice during a single bout of aerobic exercise.METHODS: The FVB/N mice were housed in a controlled SPF room and randomly divided into four groups: control (CON, n=7), fine particulate matter exposure (PM, n=7), PM and exercise (PME, n=7), and exercise only (EX, n=7). Acute PM exposure and/or aerobic treadmill exercise were undertaken according to the groups using a specially designed PM treadmill chamber.RESULTS: Protein expression and phosphorylation of p65 NF-kB in mouse lungs were significantly increased by acute exercise, but not by PM exposure. Basal protein levels and phosphorylation of MAPKs (p38, ERK, and JNK) were significantly increased in the PME group, but were lower in the PM and EX groups. Although the percentage of collagen fibers in lung tissue was not affected by PM exposure, the expression of pro- and antiapoptotic factors BAX, BID, and Bcl-2 was significantly elevated by inhalation of PM during exercise.CONCLUSIONS: In this study, the MAPKs family was activated by excessive PM inhalation during exercise and similar changes in apoptosis-related signaling were observed. This suggests that even a single bout of inhalation of fine particulate matter during exercise can affect factors associated with inflammation and cell death.