1. It is generally accepted that physical activity provokes changes in the immune system. Previous studies have demonstrated that the stress of physical activity (swimming until exhaustion) increases the phagocytic activity of peritoneal macrophages. However, the precise mechanisms remain unknown. 2. Two experiments were performed in the present study. (A) Peritoneal macrophages from control mice were incubated with plasma from three different groups of mice: (1) mice subjected to swimming until exhaustion with no previous training, (2) mice subjected to the same activity but with 1 month of training (30 min day‐1), and (3) a control (non‐exercised) group. The differences in the resulting phagocytic (attachment and ingestion) capacity were measured. (B) Changes in the concentration of plasma corticosterone after exercise were also measured, and the effect of incubation with the postexercise plasma corticosterone level on the phagocytic activity of peritoneal macrophages was then studied in vitro. 3. The results were: (A) incubation with plasma from both groups of exercised mice (with and without previous training) led to increased levels of phagocytic capacity (number of C. albicans cells ingested per 100 macrophages). (B) Incubation with a corticosterone concentration of 0.72 mumol l‐1 (similar to that observed in plasma immediately after exercise) raised the phagocytic capacity (144 +/‐ 12 after incubation with 0.72 mumol l‐1 vs. 93 +/‐ 19 after incubation with 0.24 mumol l‐1). This increase was also significantly greater than that observed with 7.2 mumol l‐1 corticosterone. 4. It is concluded that corticosterone may mediate the increased phagocytic function of peritoneal macrophages induced by exercise.

The aim of this study was to evaluate the effect of high-intensity physical activity (swimming until exhaustion) with or without previous training on the phagocytosis and destruction of inert particle capacities of macrophages, and the role of corticosterone, prolactin and thyroid hormones as possible hormonal mediators. The results indicated that high-intensity exercise provokes a stimulation of both phagocytosis and destruction of inert particles when performed in absence of previous training. However, swimming until exhaustion after a one month training program (25 min/day) induced an increase in phagocytosis but not in the destruction of latex beads. Corticosterone, prolactin and thyroid hormones can be considered as hormonal mediators of the exercise-induced stimulation of phagocytosis, since these hormones increased plasma concentration, and the in vitro incubation of macrophages with the same higher physiological plasma concentrations of each hormone, as after exercise, also induced phagocytic stimulation of these cells.

1. Exercise provokes changes in the immune system, including macrophage activity. Chemotaxis is a necessary function of macrophages if they are to reach the focus of infection and strenuous acute exercise may modulate chemotaxis. However, the precise mechanisms remain unknown. 2. Three experiments were performed in the present study. (1) The effect of strenuous acute exercise (swimming until exhaustion) on the chemotactic capacity of macrophages was evaluated. (2) Peritoneal macrophages from control mice were incubated with plasma from exercised mice or control (no exercise) mice. The differences in the resulting chemotactic capacity were measured. (3) Changes in the concentration of plasma corticosterone and prolactin after exercise were also measured, and the effect of incubation with the post‐exercise levels of plasma corticosterone and prolactin on the chemotactic capacity of the peritoneal macrophages was then studied in vitro. 3. Exercise induced an increase in the macrophage chemotaxis index (103 +/‐ 8 vs. 47 +/‐ 11 in controls). Incubation with plasma from exercised mice led to an increased level of chemotaxis (68 +/‐ 18 vs. 40 +/‐ 6 with plasma from controls). Incubation with concentrations of corticosterone and prolactin similar to those observed in plasma immediately after exercise (corticosterone, 0.72 mumol l‐1; prolactin, 88 pmol l‐1) raised the chemotactic capacity with respect to that following incubation with the basal concentrations of the hormones in control animals (90 +/‐ 9 vs. 37 +/‐ 4 for corticosterone; 72 +/‐ 9 vs. 41 +/‐ 4 for prolactin). 4. It is concluded that corticosterone and prolactin may mediate the increased chemotaxis of peritoneal macrophages induced by exercise.

No abstract

No abstract