Aging is characterized by a gradual decline in numerous physiological processes, including changes in the immune system, which are collectively called immunosenescence and the circadian rhythm that show significant changes related to age. The relationships between clock genes, aging and immunosenescence are not well understood. The role of clock genes in innate immunity is evident, but few studies have demonstrated the role of these genes in adaptive immunity. Monocytes and macrophages show great rhythmicity with a high expression range of clock genes. Consequently, different functions of macrophages and monocytes exhibit circadian rhythms, such as the response of pattern recognition receptors (PRRs), the expression of cytokines in response to an endotoxin challenge, recruitment to tissues and phagocytosis. The elucidation of the process by which immunosenescence impairs the activity of innate immunity favoring the installation of chronic low-grade inflammation, in addition to the decreased response against invaders, mainly viruses, in addition to the greater susceptibility to septic shock can help in the development of new approaches delay and decrease the amplitude of immunosenescence. Regular practice of physical exercise throughout life slows down the aging processes, providing better quality and prolonging life. Given the anti-inflammatory nature of aerobic physical training, the hypothesis of the present study is that the differentiation mechanisms of monocytes may be related to the genes that control the circadian rhythm in immunosenescence, which are regulated positively by physical training. Thus, the objective of the study will be to evaluate the role of physical training during life in immunosenescence and the relationship of this protective effect with the modulation of clock genes.
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