Generation of reactive oxygen species after exhaustive aerobic and isometric exercise

• Published in: Medicine and science in sports and exercise 2000-09, Vol.32 (9), p.1576-1581
• Main Authors: ALESSIO, Helaine M, HAGERMAN, Ann E, FULKERSON, Bethany K, AMBROSE, Jessica, RICE, Robyn E, WILEY, Ronald L
• Format: Article
• Language: English
• Subjects: Adult; Biological and medical sciences; Exercise - physiology; Female; Fundamental and applied biological sciences. Psychology; Hand Strength; Humans; Lipid Peroxidation; Male; Oxidative Stress; Oxygen Consumption - physiology; Reactive Oxygen Species; Space life sciences; Vertebrates: body movement. Posture. Locomotion. Flight. Swimming. Physical exercise. Rest. Sports
• ISSN: 0195-9131; 1530-0315
• DOI: 10.1097/00005768-200009000-00008

Many studies have implicated elevated oxygen consumption (VO2) associated with aerobic exercise as contributing to oxidative stress. Only a few studies have investigated nonaerobic exercise and its relation to pro-oxidant and antioxidant activities. The purpose of this study was to compare biomarkers of oxidative stress: lipid peroxidation, protein oxidation, and total antioxidants in blood after exhaustive aerobic (AE) and nonaerobic isometric exercise (IE). Blood samples were collected from 12 subjects who performed a maximum AE and IE test and were analyzed for thiobarbituric acid (TBARS), carbonyls, lipid hydroperoxides (LH), and oxygen radical absorbance capacity (ORAC). VO2 increased 14-fold with AE compared with 2-fold with IE. Protein carbonyls increased 67% (P < 0.05) pre- to immediately and 1 h post-AE, and 12% pre- to immediately post-IE and returned to baseline 1 h post-IE. TBARS did not increase significantly with either treatment. LH increased 36% above rest during IE compared with 24% during AE (P < 0.05). ORAC increased 25% (P < 0.05) pre- to post-AE, compared with 9% (P < 0.05) pre- to post-IE. There was evidence of oxidative stress after both exhaustive aerobic and isometric exercise. Lipid hydroperoxides, protein carbonyls, and total antioxidants increased after both IE and AE. Due to the different metabolic demands of aerobic and isometric exercise, we can rule out a mass action effect of VO2 as the sole mechanism for exercise-induced oxidative stress.