POST-EXERCISE BETA-ADRENERGIC RECEPTOR DENSITY AND cAMP IN MOUSE SPLEEN AND PERITONEAL CELLS

Abstract

112 Exercise-induced activation of the sympathoadrenal axis may alter immune responsiveness in part through catecholamine signaling of lymphocyte and macrophage β-adrenergic receptors. We studied the effects of an acute bout of prolonged exercise (3 hours) on β-adrenergic receptor density and cAMP production in unfractionated spleen and peritoneal cells from male BALB/cJ mice. Immediately post-exercise, spleen and peritoneal cells were assessed for β-adrenergic receptor expression and signaling capacity. Specific binding of [125I] cyanopindolol, a non-selective β1 and β2 adrenergic antagonist, was employed to quantify receptor affinity and density. An anti-β-3 adrenergic receptor antibody was used to assess β-3 adrenergic density by flow cytometry. The percentage of CD4+ and CD8+ T lymphocytes, sIgM+ B lymphocytes, and MAC-3+ macrophages was determined by flow cytometery. Intracellular cAMP in response to isoproterenol and PGE1 was analyzed by ELISA. Prolonged exercise did not alter splenic β-adrenergic receptor density or T and B cell populations. Isoproterenol-induced cAMP production in spleen cells and peritoneal cells was not altered following exercise. Exercise decreased β-3 adrenergic receptor density in MAC3+, sIgM+, and MAC3-/sIgM- peritoneal exudate cells. It is possible that elevated levels of catecholamines associated with exercise downregulate β-3 adrenergic receptor density in specific cell populations. Catecholamines may mediate exercise-induced alterations in immune reactivity in a cell subset-specific and β-adrenergic receptor subtype-specific manner.