## 4 Discussion  
This study examined the effect of acute moderate-intensity aerobic exercise, which might substantially increase in the inhalation of PM\({}_{2.5}\) particles, on the pulmonary function and lung diffusion capacity under high PM\({}_{2.5}\) conditions compared with low PM\({}_{2.5}\) conditions. To our knowledge, this is the first study to assess changes in DLCO with conventional pulmonary function parameters in response to aerobic exercise interventions in high PM\({}_{2.5}\) conditions. Our results imply that performing moderate-intensity aerobic exercise even in high PM\({}_{2.5}\) concentrations categorized as 'unhealthy for sensitive groups or unhealthy' level from AQI might not play a negative role on pulmonary function in healthy young men. Spirometry is a pulmonary function test that assesses the volume and flow rate of air during inhalation and/or exhalation. FVC and FEV\({}_{1}\), the main results from spirometry, are  
Figure 1: FVC (panel **A**) and FEV\({}_{1}\) (panel **B**) at pre- and post-exercise intervention. Data are mean \(\pm\) standard error. FVC, forced vital capacity; FEV\({}_{1}\), forced expiratory volume in 1 s; HPM, high PM\({}_{2.5}\) condition; LPM, low PM\({}_{2.5}\) condition. \(p\geq 0.50\) for time-condition interaction. Figure 2: DLCO at pre- and post-exercise intervention. Data are mean \(\pm\) standard error. DLCO, diffusing capacity of carbon monoxide; HPM, high PM\({}_{2.5}\) condition; LPM, low PM\({}_{2.5}\) condition. \(p=0.09\) for time-condition interaction. helpful in distinguishing obstructive and restrictive respiratory diseases and categorizing the severity of asthma and chronic obstructive pulmonary disease (COPD). Inhalation of PM\({}_{2.5}\) can impair the respiratory system by irritating the whole airway and inducing oxidative stress and inflammation [21; 25; 26; 27; 28; 29]. Oxidative stress and inflammation may cause mucus hypersecretion and contraction of the airway smooth muscle, increasing airway resistance [29; 30; 31]. Moreover, long-term PM\({}_{2.5}\) exposure is known to increase the risk of respiratory diseases, COPD, pneumonia, and lung cancer mortality [32]. However, even though aerobic exercise induces increased inhalation of PM\({}_{2.5}\), we could not find any changes in pulmonary function after exercise in high PM\({}_{2.5}\) conditions. Previous studies have reported inconsistent findings on the effects of exercise on pulmonary function in polluted environments [17; 18; 19; 20; 21; 33; 34]. It is speculated that the inconsistent findings resulted from studies' designs and the methodological differences among them; the source of air pollutants, exposure time, exercise type, exercise intensity, and time point of measuring pulmonary function varied. Moreover, our participants' cardiorespiratory fitness might nullify the negative effect of PM\({}_{2.5}\) on pulmonary function. They were recreationally active men with high VO\({}_{2}\)peak values, which can be defined as an excellent group according to the American College of Sports Medicine (ACSM) fitness classification [35]. VO\({}_{2}\)peak is negatively correlated with oxidative stress and inflammation, and positively related to total antioxidant capacity [36; 37]. Therefore, an increased cardiorespiratory fitness level might protect the pulmonary function against oxidation stress and inflammation caused by PM\({}_{2.5}\). We did not observe any changes in DLCO after acute moderate-intensity aerobic exercise in high PM\({}_{2.5}\) conditions. In contrast to our findings, a previous study showed a decrease in DLCO after exposure to 50 \(\mu\)g/m\({}^{3}\) of carbon ultrafine particles for two hours [38]. [PERSON] et al. suggested that pulmonary gas diffusing capacity can be reduced owing to PM-induced pulmonary vasoconstriction [38]. Pulmonary endothelial dysfunction caused by exposure to high PM\({}_{2.5}\) levels is considered a probable physiological mechanism for pulmonary vasoconstriction [39; 40].