Resumen de A lifelong competitive training practice attenuates age-related lipid peroxidation
Yaira Barranco Ruiz, Antonio Martínez-Amat, Cristina Casals Vázquez, Jerónimo Aragón Vela, Silvia Rosillo, Silvana N. Gomes, Ana Rivas García, Rafael Guisado Barrilao, Jesús Rodríguez Huertas
The effect of exercise-induced oxidative stress on health and aging is not clearly explained. This study examined the effects of habitual sport practice, age, and submaximal exercise on the blood markers of oxidative stress, muscle damage, and antioxidant response. Seventy-two healthy men were grouped by their habitual sport practice: inactive (<1.5 h/week), recreational (3–8 h/week), and trained athletes (>8 h/week), and further divided by age: young (18–25 years), adult (40–55 years), and senior (>55 years). Blood samples were collected at rest and after submaximal effort. Hydroperoxides and superoxide dismutase, glutathione peroxidase, and catalase activities were measured by spectrophotometry. Nuclear DNA damage was analyzed by comet assay. The alpha-actin release was analyzed by Western blot. Alpha-tocopherol, retinol, and coenzyme-Q10 were quantified by high-performance liquid chromatography analysis. Data was analyzed through a factorial ANOVA and the Bonferroni post hoc test. Lipid peroxidation increased significantly with age and submaximal effort (p < 0.05). However, the trained athlete group presented lower lipid peroxidation compared with the recreational group (MD = 2.079, SED = 0.58, p = 0.002) and inactive group (MD = 1.979, SED = 0.61, p = 0.005). Trained athletes showed significant higher alpha-actin levels (p < 0.001) than the other groups. Recreational group showed lower nuclear DNA damage than trained athletes (MD = 3.681, SED = 1.28, p = 0.015). Nevertheless, the inactive group presented significantly higher superoxide dismutase and catalase (p < 0.05) than the other groups. Data suggested that habitual competitive training practice could prevent age-related increases of plasma lipid peroxidation, which, according with our results, cannot be entirely attributed to blood antioxidant defense systems.
