Biological aging is the single greatest independent risk factor for chronic disease. Shifts in redox balance appear to underlie the onset and progression of many age-related pathologies. Aerobic organisms have evolved a vast network of antioxidant defenses, regulated predominately by the transcription factor nuclear erythroid-2 like factor-2 (Nrf2). Data from animal studies suggest exercise elicits significant increases in Nrf2 signaling, which may increase induction of phase II detoxifying enzymes, effectively restoring redox balance and resistance to oxidative stress. It is unknown whether exercise can restore resistance to oxidative challenges in humans, and to what extent exercise can directly influence Nrf2 activity in vivo. The current gaps in the literature include first and foremost a lack of translational research from animal models of exercise redox biology into humans. The purpose of the research reported in the following chapters is four-fold: 1) To determine the capacity of an exercise intervention to restore resistance to oxidative stress in older adults, 2) To determine the capacity of a single session of exercise to influence Nrf2 signaling, 3) To determine age-related differences in Nrf2 signaling, and 4) To determine the role of exercise intensity on Nrf2 activation. The data reported in the following chapters address these questions, and advance our current understanding of exercise redox biology and aging in humans.
|Commitee:||Gage, Matthew, Lindstedt, Stan, Nieto, Nathan, Nishikawa, Kiisa|
|School:||Northern Arizona University|
|School Location:||United States -- Arizona|
|Source:||DAI-B 78/01(E), Dissertation Abstracts International|
|Subjects:||Biology, Aging, Kinesiology, Physiology|
|Keywords:||Exercise, Ischemia reperfusion, Nrf2, Oxidative stress|
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