Enhanced chemotaxis of macrophages by strenuous exercise in trained mice: thyroid hormones as possible mediators.

Exercise modulates the macrophage activity via 'stress hormones'. Three experiments were performed. (1) The effect of strenuous exercise performed by trained mice on macrophage chemotactic capacity was evaluated; (2) peritoneal macrophages from control mice were incubated with plasma from exercised mice or control mice and the differences in chemotaxis were measured; (3) changes in plasma T3 and T4 levels after exercise were measured, and the effect of incubation with the post-exercise levels of plasma T3 and T4 on chemotaxis was then studied in vitro. A 10(4)-fold higher concentration of each hormone was also evaluated. Exercise provoked an increase in chemotaxis (104 +/- 35 vs. 47 +/- 11 in controls). Incubation with plasma from exercised mice led to an increased level of chemotaxis. Incubation with concentrations of T3 and T4 similar to those observed in post-exercise plasma (T3, 2.3 nmol l(-1); T4, 84 nmol l(-1)) enhanced chemotaxis with respect to incubation with the basal concentrations of the hormones in control animals. A 10(4)-fold concentration of T4 reversed this effect. It is concluded that thyroid hormones stimulate macrophage chemotaxis. Also, these data support the hypothesis that thyroid hormones may be involved in exercise-induced stimulation of chemotaxis.