Impact of life style factors on oxidative stress

There are convincing epidemiologic data to support the role of increased physical activity and exercise with reduced risks of various chronic diseases, including cardiovascular disease, certain cancers, type 2 diabetes mellitus (T2DM), and osteoporosis. Reversing global population trends in physical inactivity is therefore a major public health priority. Better understandings of the biologic mechanisms that link sedentary lifestyle to poor health are needed to refine and support physical activity guidelines. Traditionally, the underlying mechanisms that have been proposed to link physical inactivity to various disease outcomes have been disease specific. For example, reduced circulating estrogens are often cited as one mechanism that links physical activity to reduced risk of breast cancer; in parallel, reduced insulin and insulin like growth factors are regularly offered to explain the link between physical activity and colon cancer. More recently, data are emerging to suggest that persistent physical activity may decrease resting levels of oxidative stress. At first, this connection may seem paradoxical since acute exercise transiently increases local and systemic oxidative stress levels. This paradox is resolved by the concept of hormesis: low-to-moderate level of reactant species that form during non-exhaustive exercise may lead to adaptations in the antioxidant defense system. Whether reduced resting levels of oxidative stress further translate to reduced risks of chronic disease is another emerging research question. While some studies support a connection between oxidative stress and chronic disease, prospective and well-powered studies are still relatively rare.