O papel do exercício físico na redução dos danos de DNA em linfócitos humanos: possível influência do stress oxidativo e da capacidade de reparação do DNA

Regular physical exercise induces several health benefits reducing several risk factors action that enhance the development of cardiovascular diseases, type II diabetes, hypertension, osteoporoses, cancer, mental diseases, mental, between others [1, 2]. The relevance of the relation between exercise and health increases when the age related loss of functionality is considered. Although at the organism level the results are consistent, at a cell and molecular level physical exercise benefits are inconsistent. Several methodological constrains exist namely the physical exercise control. Physical activity, exercise, and physical fitness are different concepts [3] that have been used interchangeably to establish their relation with molecular and cell changes. However, only exercise implies a planned, structured, and repetitive program that has as an objective of improvement or maintenance of physical fitness. Most of the papers that search for exercise related cell and molecular changes in humans use cross-sectional designs without the application of a controlled exercise program. Moreover, in those studies where an exercise program is used there is no daily physical activity control of both groups (control and experimental), and no control of the physical exercise program exist, which reduces de implications of the exercise load (type of physical exercise, intensity, time and frequency) used in the program. At cell and molecular level, exercise related effects may also be confounded by other lifestyle related behaviors (smoking, alcohol, diet, and mental stress) that must be controlled during the exercise program implementation. At a molecular level, acute physical exercise induces oxidative stress [4], that causes a several cell adaptations that may result in a cell functionality improvement or in cell damage. Between these adaptations, it has been described a mitochondria bioenergetics’ capacity improvement [5, 6], decrease in reactive oxygen species production (ROS) [7] and antioxidant capacity increase [8, 9] of cells from different animal tissues. Bearing in mind the aging process, these changes may reflect in a reduction of molecular damage accumulation that cause physiologic attrition and loss of functionality with increasing age. Considering cell damage, those related with DNA damage can accelerate aging [10] and are involved in several pathologies process development, whereas cancer is one [11]. Although several studies have analyzed exercise related DNA damage in animal models, only a few studies have been developed in humans, some concern physical fitness and DNA damage [22], but they didn’t control physical activity, and most of the studies analyzed acute exercise effects [4]. Coming to the point, this kind of approaches doesn’t allow a reliable relation between exercise and DNA damage accumulation, not even let us understand if they are due to oxidative stress decrease because exercise improves mitochondria bioenergetic capacity, decreases ROS production and increase antioxidant capacity, or simply because DNA repair capacity may have increased with exercise. In fact, studies about the physical exercise effect in DNA repair capacity are completely unknown, especially in humans, which enhance the importance of studying it, once it may be a valuable contribution to the comprehension of physical exercise related molecular adaptation mechanisms.