In recent years there has been considerable interest in how exercise and training may affect the immune system. There is now substantial cross-sectional and epidemiological evidence that exercise causes significant changes in the distribution and function of a number of cellular and humoral immune parameters. Neutrophils represent one of the key nonspecific host defence cell populations responsible for the phagocytosis of many microbial, bacterial and viral pathogens. The neutrophil is also known to be involved in the synthesis and release of immunomodulatory cytokines that influence both T cell and B cell activities. Therefore, it plays an important role in both the efferent (phagocytosis and degranulation) and afferent (release of immunomodulatory molecules) limbs of the immune response. Neutrophils and macrophages respond both to phagocytosable particles (e.g. bacteria, viruses and cell debris) and to a number of soluble factors. There is an increase in the number of circulating neutrophils with exercise as a result of demargination of cells from endothelial tissues (mediated by catecholamines) and bone marrow (mediated by Cortisol), or as part of the phagocytic and inflammatory response to exercise-induced tissue damage. Following exercise-induced mobilisation into the circulation and migration into tissues, neutrophils undergo adherence, phagocytosis (engulfment) of bacteria or tissue fragments, degranulation of cytoplasmic granules and, ultimately, activation of the respiratory burst. The capacity of the respiratory burst largely determines the cytotoxic potential of the neutrophil. The respiratory burst involves a sudden increase in nonmitochondrial oxidative metabolism, resulting in the production of the superoxide anion (O2 −) and other reactive oxygen species by the nicotinamide adenine dinucleotide phospahate (NADPH) oxidase enzyme complex located at the plasma membrane. Although the biochemistry of the respiratory burst has been well studied, the mechanisms by which exercise and training may influence its activity are not well characterised or understood. Studies on the acute effects of exercise show that exercise generally elicits an initial activation of neutrophils — evidenced by release of cytoplasmic enzymes (degranulation) with secondary changes in key effector functions such as the phagocytic and respiratory burst activity. The nature of the functional changes is still unclear, as some studies show a transient suppression of the respiratory burst and/or phagocytic capacity immediately after exercise, while others report that moderate intensity exercise elicits an enhanced response. The variability in findings may be attributable to differences in the age, gender and initial fitness levels of the people studied, the intensity and duration of the exercise protocols used, and the different methodological procedures employed. Elucidation of the mechanisms involved in the exercise-related modulation of neutrophil distribution and function would permit more specific monitoring of the immune system in individuals exposed to a high level of physical stress. Further studies are required to determine definitively whether the chronic effects of long term training can influence illness patterns in both recreational and elite athletes.
|Number of pages||14|
|Journal||Sports Medicine: An International Journal of Applied Medicine and Science in Sport and Exercise|
|Publication status||Published - 1 Jan 1994|