The effects of acute exercise (both graded-maximal and submaximal) and exercise training on resting immunoglobulin levels and immunoglobulin production are reviewed. Brief graded-maximal or intensive short term submaximal exercise tends to be associated with increases in serum immunoglobulins, the pattern of which does not vary between athletes and nonathletes. Plasma volume changes appear to largely explain these acute increases. Acute moderate exercise, such as a 45-minute bout of walking, on the other hand, has been associated with a transient rise in serum immunoglobulin levels despite no change in plasma volume. This increase is probably the result of contributions from extravascular protein pools and an increased lymph flow. Total serum immunoglobulin changes following less than 40 km of running are minor and/or statistically insignificant, although the concentration of IgG is observed to be at its lowest by 1.5 hours after exercise. The greatest effect of acute submaximal exercise appears to be on serum IgM levels which tend to increase, although results are somewhat inconsistent. Various mechanisms of stimulation have been proposed to explain the exercise-induced effect on IgM, which is the first antibody class produced in an immune response. These mechanisms include nonspecific noradrenergic sympathetic neural interactions with the immune system and the possibility of antigen stimulation through greater-than-normal quantities of microorganisms entering the body through both increased ventilation rates and breakdown of natural mucosal immunity by drying of airway secretions. When athletes run 45 to 75 km at high intensities, serum immunoglobulin levels have been reported to be depressed for up to 2 days. Thus intense ultramarathon running may lead to greater and longer lasting decreases in serum immunoglobulin levels than following exercise of shorter duration. IgA and IgG, immunoglobulins commonly found in airway and alveolar space secretions, may have diffused from the serum during recovery from prolonged endurance exercise nonspecifically and/or in response to microbial agents and antigens introduced into the airways during the exercise bout. It has been well established that prolonged endurance exercise is associated with muscle cell damage and local inflammation. It has been hypothesised that natural (IgM) autoantibodies may be used to assist macrophages in disposal of muscle cell breakdown products. This could occur either by IgM binding to breakdown products present in the blood, followed by their clearance from the circulation, or it is possible that these antibodies may leave the circulation to carry out this same function in tissues.(ABSTRACT TRUNCATED AT 400 WORDS)