Aging leads to a diminution of resting immune function, increasing the risk of infection, tumor development, and autoimmune diseases (Shephard and Shek, 1995). The production of IL-2 is decreased, sometimes with a decrease of total T-cell count, and often with changes in T-cell subsets and proliferative responses to mitogens. However, NK cell activity remains unchanged. In theory, moderate exercise training should help to reverse the adverse effects of aging upon the immune system. However, there have been relatively few studies comparing the immune responses of young and older individuals to acute exercise and to training. A single bout of moderate exercise seems to be well tolerated by the elderly. The NK cell response is as much as in younger individuals, but perhaps because of a low initial proliferative capacity, older subjects show less stimulation of lymphocyte proliferation by moderate activity and less suppression with exhausting exercise. Perhaps because resting immune function is less than in the young, moderate training programs seem to stimulate immune function to a greater extent in the elderly than in young subjects (Shephard et al., 1994). The proliferative response of the T-cells is enhanced in aging rodents, whereas in young animals, it is suppressed. Moreover, the resting NK cell activity of elderly human subjects seems to be increased by training. Nevertheless, the therapeutic use of exercise must be cautious in the elderly, because aging also enhances susceptibility to overtraining.
Aging affects the muscle precursor cells (satellite cells or myobloasts) and their regeneration after exercise (Grounds 1998). Aging may also affect proliferation and fusion of myoblasts in response to injury; signaling molecules that stimulate satellite cells with aging; host environment, inflammatory cells, growth factors and their receptors, and the extracellular matrix. There is a reduction in growth hormone, total and free testosterone, and cortisol, both at baseline and after exercise. The decreased anabolic effects on muscles may explain the loss of muscle mass and strength with aging (Hakkinen et al., 1998). The more primitive components of immune defense, including natural killer cells, phagocytes, acute-phase proteins, and regulatory cytokines, may be altered in elderly. Several investigators have found that the proportion of neutrophils will be increased in the circulation following physical exercise. An increase in neutrophils has been correlated with an increase in plasma cortisol. The number of circulating monocytes and NK cells change as a result of exercise. Nonspecific immunity may be further stressed by maximal physical exertion that may contribute to an increased susceptibility of the elite sports person to infection.
At rest, the total number of lymphocytes and CD4+ and CD8+ T-cell subset populations was lower in the elderly than the young (Mazzeo et al., 1998). There is significant exercise-induced leukocytosis, primarily lymphocytosis and neutrophilia, in both young and elderly; however, the magnitude in the elderly is reduced (Ceddia et al., 1999). The elderly have higher memory and lower CD4 and CD8 T-cells than the young. Acute maximal exercise increases CD8+ and CD4+ in the elderly and young. The aged recruited fewer numbers of CD4+naive and transitional cells than the young (Ceddia et al., 1999). Proliferative responses are lower in the elderly than the young. Proliferative response does not increase above rest in elderly subjects as it does in young subjects. Middle-aged subjects had a blunted growth hormone response to exercise than the young subjects, and this was not altered by training (Zaccaria et al., 1999) and which could not be explained by augmentation of somatostatin tone and/or diminished GH-release hormone (Marcell et al., 1999).
The immune system is loosely linked to the neuroendorcine system, which responds to stress. Increased cortisol, catecholamines, glucocorticoids, adrenaline, ^-endorphin, growth hormones, other stress hormones, and insulin are decreased during aging. There is an increase in soluble IL-2 receptors (sIL-2R), soluble intercellular adhesion molecule-1 (sICAM-1), soluble TNF-P receptors (sTNF-R), and neopterin with exercise. These insoluble matter increases suggest that immune activation may be involved in the patho-genesis of impaired immune function after exercise. The natural-killer cell response to a single bout of exercise is normal in older individuals, but immediately after exercise, the elderly subjects manifest less suppression of phytohemagglutinin (PHA)-induced lymphocyte proliferation than younger individuals (Shinkai et al 1998). Strenuous exercise seems to induce a more sustained post-exercise suppression of cellular immunity in the elderly than in the young. The magnitude of the increase in cortisol is substantially lower in trained subjects who exercise at the same level or intensity as untrained subjects. Habitual physical activity enhances NK cell activity through mitogenesis and reduced cytokine production (Shinkai et al., 1998).
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