Effects of High-Intensity Swimming on Lung Inflammation and Oxidative Stress in a Murine Model of DEP-Induced Injury.

Studies have reported that exposure to diesel exhaust particles (DEPs) induces lung inflammation and increases oxidative stress, and both effects are susceptible to changes via regular aerobic exercise in rehabilitation programs. However, the effects of exercise on lungs exposed to DEP after the cessation of exercise are not clear. Therefore, the aim of this study was to evaluate the effects of high-intensity swimming on lung inflammation and oxidative stress in mice exposed to DEP concomitantly and after exercise cessation. Male Swiss mice were divided into 4 groups: Control (n = 12), Swimming (30 min/day) (n = 8), DEP (3 mg/mL-10 μL/mouse) (n = 9) and DEP+Swimming (n = 8). The high-intensity swimming was characterized by an increase in blood lactate levels greater than 1 mmoL/L between 10th and 30th minutes of exercise. Twenty-four hours after the final exposure to DEP, the anesthetized mice were euthanized, and we counted the number of total and differential inflammatory cells in the bronchoalveolar fluid (BALF), measured the lung homogenate levels of IL-1β, TNF-α, IL-6, INF-ϫ, IL-10, and IL-1ra using ELISA, and measured the levels of glutathione, non-protein thiols (GSH-t and NPSH) and the antioxidant enzymes catalase and glutathione peroxidase (GPx) in the lung. Swimming sessions decreased the number of total cells (p<0.001), neutrophils and lymphocytes (p<0.001; p<0.05) in the BALF, as well as lung levels of IL-1β (p = 0.002), TNF-α (p = 0.003), IL-6 (p = 0.0001) and IFN-ϫ (p = 0.0001). However, the levels of IL-10 (p = 0.01) and IL-1ra (p = 0.0002) increased in the swimming groups compared with the control groups, as did the CAT lung levels (p = 0.0001). Simultaneously, swimming resulted in an increase in the GSH-t and NPSH lung levels in the DEP group (p = 0.0001 and p<0.002). We concluded that in this experimental model, the high-intensity swimming sessions decreased the lung inflammation and oxidative stress status during DEP-induced lung inflammation in mice

Anti-inflammatory cytokines lung levels.

<p>Fig 4 shows the total levels of IL-10 and IL-1ra (Fig 4A and 4B, respectively) from homogenate lung tissue. Values are expressed as mean ± SD. Fig 4A, ^§p = 0.01, when compared to Control group, and Fig 4B, ^§p = 0.0002, when compared to Control group also. When compared DEP and DEP+Sw groups, there was no significant statistical difference (p>0.05) in both measurements.</p

Blood lactate concentration.

<p>* = Significantly different from the 10^th minute of the respective group (p<0.05).</p><p>Table 1 shows the values (mean ± SD) of blood lactate concentration, expressed in mmol/L. Control and DEP groups were submitted only once to exercise protocol, in order to establish lactate blood basal control.</p

Antioxidant enzymes lung levels.

<p>Fig 5 shows the pulmonary levels of CAT and GPx (Fig 5A and 5B, respectively). Values are expressed as mean ± SD. Fig 5A, ^§p = 0.0001, when compared to Control group.</p

Cells from BALF.

<p>Fig 2A shows the total number of cells from BALF. Values are expressed as mean ± SD. ^#p<0.001 when compared to all groups. Fig 2B shows the differential counting of neutrophils and lymphocytes from BALF. ^#p<0.001 for neutrophils when compared to all groups and ^§p<0.05 for lymphocytes when compared to Control group.</p