Figure 1.

Accumulation of immune cells in the skeletal muscle after the aerobic exercise. Male C57BL/6J mice were subjected to a single bout of treadmill running exercise at a speed of 15 m/min for 1 h. Mice in the sedentary group were used as controls. A–C, at 24 h after the exercise, mice were intraperitoneally injected with insulin (1 milliunit/g of body weight). A, insulin-induced decreases in blood glucose in sedentary mice (Sed [1 h] + 24 h) and mice at 24 h after the exercise (Ex [1 h] + 24 h). B, Western blot analysis of phospho-Akt (pAkt) in the skeletal muscle. The apparent molecular weights are indicated on the right. C, quantitative analysis of pAkt. The band intensities of pAkt were normalized to total Akt and represented as the fold induction relative to the intensities of sedentary mice with no insulin injection in the bar graph. D, flow cytometric analysis of immune cells in the skeletal muscle at 24 h after the exercise. E, gene expression of M1 (iNOS and TNF-α) and M2 markers (arginase-1 [Arg1] and IL-10) in the skeletal muscle at 24 h after the exercise. F, Western blot analysis of M1 (iNOS and TNF-α) and M2 markers (arginase-1 [Arg1] and IL-10) in the skeletal muscle at 24 h after the exercise. The apparent molecular weights are indicated on the right. G, quantitative analysis of the protein expression of iNOS, TNF-α, Arg1, and IL-10. The band intensities of iNOS, TNF-α, Arg1, and IL-10 were normalized to β-tubulin and represented as the fold induction relative to the intensities of sedentary mice in the bar graph. Data are expressed as mean ± SD; n = 5 per group. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, and ∗∗∗∗p < 0.0001. Two-way ANOVA followed by Tukey’s post hoc test (A and C); Student’s t test (D, E, and G). IL, interleukin; iNOS, inducible nitric oxide synthase; TNF-α, tumor necrosis factor alpha.