Fig. 1. Exercise induced increases in endogenous GC corticosterone levels in OVA-sensitized mice. Mice were sensitized, exercised, and implanted with RU486 or placebo pellets as described under Section 2. Plasma was isolated from blood collected via cardiac puncture and then analyzed via RIA for changes in endogenous GC corticosterone levels. Results are reported as nanograms per milliliter of endogenous GC corticosterone levels (n = 10; ^†p < .05 as compared with sedentary and OVA-sensitized (SO)/placebo mice).

Fig. 2. RU486 blocked exercise-induced increases of GR nuclear translocation within the lungs of OVA-sensitized mice. Nuclear translocation of GR (denoted by arrows) was monitored in (A) SO/placebo, (B) EO/placebo, (C) SO/RU486, and (D) EO/RU486 via immunohistochemical analysis as described under Section 2. Tissue was counterstained with Hoescht to visualize nuclei (green). Representative photomicrographs of six separate experiments are shown (*, airway lumen; magnification, 25×; inset, 50×). (E) Relative changes in combined GR nuclear translocation were determined as described under Section 2 (n = 6 for each group; ^†p < .05 as compared with SO/placebo control; ^‡p < .05 as compared with EO/placebo control). (For interpretation of the references to colors in this figure legend, the reader is referred to the web version of this paper.)

Fig. 3. RU486 blocked the anti-inflammatory effects of exercise on cellular infiltration in OVA-sensitized mice. (A) Cells collected from BALF of mice were analyzed for differences in total cell count as described under Section 2. (B) Differential BALF cell counts were performed using standard hematological criteria; results for the eosinophil cell population are shown (n = 5–6 for each group; ^†p < .05 as compared with SO/placebo control; ^‡p < .05 as compared with EO/placebo control).

Fig. 4. RU486 blocked the anti-inflammatory effects of exercise on KC and sVCAM-1 levels in the BALF of OVA-sensitized mice. BALF samples were analyzed for (A) KC and (B) sVCAM-1 levels via ELISA. Results are reported as picograms per milliliter of respective protein (n = 5–6; ^†, p < .05 as compared with sedentary and OVA-sensitized (SO)/placebo control; ‡, p < .05 as compared with exercised and OVA-sensitized (EO)/placebo control).

Fig. 5. RU486 blocked exercise-induced decreases of NF-κB nuclear translocation and DNA binding within the lungs of OVA-sensitized mice. Nuclear translocation of p65 (denoted by arrows) was monitored in (A) sedentary and OVA-sensitized (SO)/placebo, (B) exercised and OVA-sensitized (EO)/placebo, and (C) EO/RU486 via immunohistochemical analysis as described under Section 2. (D) NF-κB-specific EMSA was performed as described in Materials and methods. Representative results from six independent experiments are shown (C, positive control) (TNF-α-treated AECs). (E) Densitometric analyses of NF-κB-specific DNA binding as determined via EMSAs were performed (n = 6; ^†, p < 0.05 as compared with sedentary and OVA-sensitized (SO)/placebo control; ‡, p < .05 as compared with exercised and OVA-sensitized (EO)/placebo control).