Essay: Immunity, Exercise, and Chronic Disease

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Immunity, Exercise, And Chronic Disease

Susceptibility to the development of chronic diseases has been shown to depend on at least two processes, a reduced capacity to manage oxidative stress and chronic inflammation (reviewed by Lee, Park, Zuidema, Hannink, and Zhang, 2011, p. 18-19). Diseases that have been linked to these conditions are some of the more debilitating and life-threatening diseases found in developed countries and include type-2 diabetes, atherosclerosis, coronary artery disease, myocardial infarction, stroke, Alzheimer's disease, depression, Parkinson's disease, and cancer (Lee, Park, Zuidema, Hannink, and Zhang, 2011, p. 18-19; Walsh et al., p. 34). This essay will review how oxidative stress and chronic inflammation levels can be modified through exercise and antioxidant-focused nutrition to reduce the risk of disease and premature death.

Oxidative Stress, Exercise, and Nutrition

Above normal levels of oxygen radicals (oxidants) in healthy cells activates of a host of genes that encode a large number of enzymes that have antioxidant activity (reviewed by Lee, Park, Zuidema, Hannink, and Zhang, 2011, p. 19). A failure of this protective process to function normally has disease implications. For example, when the vascular tissue in aging rats was examined antioxidant activity was found to be lower than normal (reviewed by Lee, Park, Zuidema, Hannink, and Zhang, 2011, p. 19). Heart tissue in mice lacking a master antioxidant control gene was unable to contract normally, similar to what would be expected of an aged heart. There was also evidence of oxidative stress and cell death in these hearts. When the blood flow to rat hearts was restricted artificially and then resumed, to mimic what occurs during a heart attack, levels of the master antioxidant control gene was found to be below normal (reviewed by Lee, Park, Zuidema, Hannink, and Zhang, 2011, p. 19). These studies reveal how the heart muscle and vascular tissue become susceptible to oxidative damage when burdened with cardiovascular disease and/or the effects of aging.

The above findings encouraged researchers to examine whether antioxidant supplementation could compensate for disease- or aging-compromised endogenous antioxidant activity and thus provide protection against oxidative damage. Phytochemicals found in fruits, vegetables, and whole grains have been shown to have antioxidant activity and experiments in laboratory rodents suggest these naturally-occurring compounds induce endogenous antioxidant activity (reviewed by Lee, Park, Zuidema, Hannink, and Zhang, 2011, p. 19-20). For example, in the heart attack model daily consumption of broccoli increased the expression levels of an antioxidant gene and provided protection against heart attack-induced oxidative damage.

A large number of epidemiological studies have found a link between regular exercise and a reduced prevalence of diabetes and cardiovascular disease (reviewed by Lee, Park, Zuidema, Hannink, and Zhang, 2011, p. 19-20). Although further studies need to be performed, experiments have revealed the antioxidant enzyme expression levels are increased in the vascular system in laboratory mice and pigs that were exercised on a regular basis. However, endurance athletes have reduced levels of at least one antioxidant gene and may therefore experience increased susceptibility to oxidative damage. The existence of a 'sweet spot' for how… [END OF PREVIEW]

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