SummaryThe 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 non-athletes. 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 40km 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 75km 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. This reaction may need to be tempered by autoimmunosuppressive manoeuvres by the immune network to prevent immunoglobulin class switching to production of potentially harmful antibodies (IgG).Cross-sectional studies suggest that resting serum immunoglobulin levels in athletes and non-athletes are similar, especially when adjusted for plasma volume. However, some elite athletes, especially during the competitive season, may experience low concentrations of serum and secretory immunoglobulins, which have been described by some researchers as important factors leading to increased risk of infection. Muscular injections of immunoglobulins have proven useful in reducing the duration but not the incidence of infections in these competitive athletes.Moderate exercise training (45 minutes brisk walking, 5 sessions per week), on the other hand, has been associated in one study with a net 20% increase in serum immunoglobulins in comparison to a control group during a 15-week period, a change which was inversely correlated with total acute upper respiratory tract symptom days. The data overall suggest that while the combined psychosocial-physiological stress of competitive exercise training may be associated with depressed serum immunoglobulin levels in some elite athletes, moderate exercise training may lead to slightly improved serum immunoglobulin levels with contrasting effects on risk of infection. The data should still be regarded as preliminary, however, until confirmed with studies using more exacting methodologies.Following acute prolonged endurance exercise or several weeks of intensive exercise training,in vivoorin vitroantibody production has not been found to be altered. The effect of hormones, T cells, and interleukins 1 (IL-1) and 2 (IL-2) on antibody production, in response to endurance exercise have also been investigated. Although IL-1, a macrophage product, tends to be elevated in response to exercise, a corresponding increase in IL-2 has not been reported, perhaps because T cell function is often reported to be suppressed. Thus, following acute and chronic exercise, B cell growth and differentiation does not appear to be enhanced by soluble factors (including IL-2) from the T helper cells.