Oxidative stress is an imbalance that leads to some pathophysiological disorders in the body. Oxidative stress is demonstrated by fatigue, decrease eyesight, memory loss, headaches and sensitivity to sounds, muscle and joint pain and susceptibility to diseases. Some of the pathophysiological conditions include neurodegenerative disorders such as Alzheimer's disease, gene mutations, Parkinson's disease, cancers, cardiovascular disorders, inflammatory diseases, and chronic fatigue syndrome. Body cells continuously produce reactive oxygen species and free radicals during the metabolic processes. Increased aerobic metabolism during physical exercise leads to oxidative stress (Bloomer, & Smith, 2009). Oxidative stress and anaerobic physical activity are related since the intense anaerobic activity causes damage to proteins, nucleic acids, and lipids in blood and muscle cells.
Transformations confirm the majority of the research into physical activity and inactivity and their impact on oxidative stress in particular biomarkers that indicate for proteins modification and lipid peroxidation. Oxidative stress is assessed by measuring the free radicals using the spectroscopic method, the activity of enzymatic antioxidants and looking at the harm to protein, lipids and DNA molecules caused by the impacts of formation of free radicals. It is essential to investigate oxidative stress as it becomes clearly understood. Research indicates it is an underlying cause of cancer, therefore, understanding it is an important strategy for individual's wellness. Physically inactive people are more susceptible to significant changes in the body from oxidative stress than those involved in regular exercises. According to Goldfarb, McKenzie, & Bloomer, (2007), there is no distinction in oxidative stress in the bases of gender during physical activity.
Physical activity induces a change in the metabolic process in organisms leading to the activation of the adaptive mechanism that is used in establishing a new dynamic equilibrium. One of the essential changes happens in the muscular tissue since the energy demand from exercise generates an increased utilization of oxygen by the mitochondria (Stankovic, & Radovanovic, 2012). Physical activity especially exercises training is associated with increased antioxidant capacity and reduced oxidative stress (Powers, & Jackson, 2008). Physical training enhances exercising activity, improves endothelial function and collateralization in individuals with the disease of the coronary artery. Nevertheless, highly intensive exercise has been seen to increase oxidative stress since increased aerobic metabolism is a source of oxidative stress. More research is required on the existing uncertainties regarding the effect of physical exercise on reactive oxygen species. Long-term moderate physical activity decreases levels of oxidative stress prompted by the antioxidant enzymes.
Physical inactivity is prevalent among a considerable number of people both young and old in the world. Physical activity has been named as an independent factor that leads to increased risk of cardiovascular disorders. The underlying, molecular mechanisms that result from physical inactivity are not clearly defined. Inactivity increases vascular oxidative stress as it increases production of free radicals potentially harming cells. Research shows that vigorous or moderate exercises are linked to reductions in the occurrence of cardiovascular disorders. In a study by Laufs, et al. (2005), they observed wild mice in a state of physical inactivity and the outcome was increased levels of lipid peroxidation which acts as a global indicator of oxidative stress. Reactive oxygen species lead to atherosclerosis and endothelial dysfunction. Laufs et al. (2005), suggests that physical inactivity increases activity and expression of NADPH oxidase that contributes to cardiovascular diseases in sedentary living compared to a physically active life.
Bloomer, R. J., & Smith, W, A. (2009). Oxidative stress in response to aerobic and anaerobic power testing: Influence of exercise training and carnitine supplementation. Res Sports Med, 17(1), 1-16.Goldfarb, A. H., McKenzie, M. J., & Bloomer, R. J. (2007). Gender comparisons of exercise-induced oxidative stress: influence of antioxidant supplementation. Applied Physiology, Nutrition, and Metabolism, 32(6), 11241131.
Laufs, U., Wassmann, S., Czech, T., Munzel, T., Eisenhauer, M., Michael B., & Nickenig, G. (2005). Physical Inactivity Increases Oxidative Stress, Endothelial Dysfunction, and Atherosclerosis. American Heart Association.
Powers, S. K., & Jackson, M. J. (2008). Exercise-Induced Oxidative Stress: Cellular Mechanisms and Impact on Muscle Force Production. Physiological Reviews, 88, 1243-1276.
Stankovic, M. & Radovanovic, D. (2012). Oxidative Stress and Physical Activity. Faculty of Sport and Physical Education, University of Nis, Serbia.
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