THE ROLE OF STRESS HORMONES IN EXERCISE-INDUCED SUPPRESSION OF ALVEOLAR MACROPHAGE ANTIVIRAL FUNCTION

We hypothesized that a previously observed exercise-induced suppressio n of alveolar macrophage antiviral resistance results from increases i n corticosterone and/or epinephrine. Mice (CD-1) were run to fatigue o n a treadmill (exercise), or placed in Plexiglas lanes above the tread mill (control). The role of corticosterone was assessed by further div iding mice into groups receiving one of the following treatments; sham surgery, adrenalectomy, or adrenalectomy plus corticosterone replacem ent. Macrophage antiviral function was suppressed in the exercised mic e compared to the control mice. However, macrophage antiviral function was not suppressed in the exercised mice that underwent adrenalectomy or adrenalectomy plus corticosterone replacement. We tested whether a nother adrenal factor (epinephrine) may be involved by dividing mice i nto exercise and control groups treated with either saline or proprano lol. Macrophage antiviral function was again suppressed in the saline- treated exercised mice compared to saline-treated control mice, but no differences were found between the exercised mice receiving propranol ol, control mice receiving propranolol, or saline-treated control mice . Isoproterenol, when added to alveolar macrophages in culture, also s uppressed antiviral resistance. These findings suggest that decreased macrophage antiviral function following exercise may be due to increas ed release of adrenal catecholamines. (C) 1998 Elsevier Science B.V.