The subject of antioxidants and oxidative stress, as they pertain to endurance sports, is a particular passion and (healthy) obsession for me, so I though I'd share some meta-analysis on the subject. Sorry it is so long. Think of it as a comprehensive look inside the cell of the endurance athlete.
[..] Much research in the last decade has been done on how exercise, at high intensities or long duration, can overload the above defenses, thereby allowing elevated OS. Free Radical Biology and Medicine, 36(8): 966-975, 2004, reveals that intense exercise increases OS in humans due to a 10 to 20-fold increase in whole body oxygen consumption and up to a 200 fold increase in exercising-muscle oxygen consumption. While the majority of the oxygen used in the metabolic process is transformed to water, 2-5% is converted to superoxide anion, a ROS, which in turn is transformed into hydrogen peroxide and then hydroxyl radicals, the most destructive of ROS. This process of ROS production is known “Electron Leakage.†( Journal of Cerebral Blood Flow & Metabolism /v18/n2).
Another mechanism by with ROS are generated during physical exertion is by way of ischemia-reperfusion, systemically and locally. High-intensity exercise leads to local muscle ischemia, as contracting muscles force out blood. When the muscle relaxes, oxygenated blood flows back in, the re-oxygenation which takes place when exercise stops results in a burst of ROS. (Pflugers Arch. 2006 Apr;452(1):109-16. Epub 2006 Jan 10.) Systemically, redistribution of blood to the working muscles results in hypoxia within the kidneys and in the region of the liver and spleen. Again, when intensity lowers or cessation of activity occurs, the reperfusion results in ROS production. (Biomedical and Life Sciences Volume 20, Number 2 / April, 1997).
Another mechanism by which ROS production may be increased during exercise is by way of auto-oxidation of catecholamines (adrenaline, noradrenalin) which generates a superoxide anion radical (Life Sci 1999;65:915–24) (Braz J Med Biol Res, June 1998, Volume 31(6) 827-833).
[..] An external manifestation to the increased OS (Oxidative stress) and subsequent cellular degradation and glycosylation is particularly evident in the appearances of Ironman level triathletes, Tour de France level cyclists and marathoners et al. Leanness and muscularity notwithstanding, as a group these athletes appear many years older than they are, as a result of increased and prolonged OS surpassing the bodies natural antioxidant defenses. Excessive exposure to sunlight is also a contributing factor to said aged appearance (photoaging). Ironically or not, photoaging itself is a result of UV induced dermal oxidative stress.
From an athletic standpoint, OS plays a part in limits to ultimate strength and endurance capacity and serial repeatability of activity. As far back as 1982 (Davies et al.
1) we have known that a bout of exercise can increase free radical concentration with damage to mitochondria in muscle. Sjodin B, et al.
2, while investigating sources of muscle soreness and damage associated with exercise, concluded that during exercise semiquinone in the mitochondria and xanthine oxidase in the capillary endothelial cells are generated at a greatly increased rate, which may exceed the capacity of the cellular defense system, may lead to a loss of cell viability and to cell necrosis and could initiate the skeletal muscle damage and inflammation caused by exhaustive exercise.
A step further, Marzatico
3, et al., found that both strenuous long distance exercise and exhaustive sprint training overwhelm our capacity to detoxify ROS and concluded that an adequate supply of antioxidants could be appropriate.
Ji
4 demonstrated that in the skeletal muscle, an isolated load of exhaustive work produced an increase on the lipoperoxidation and a significant increase in activity of the antioxidant enzymes glutathione reductase, GPx, SOD and CAT was significantly increased. A few years later Ji and Leeuwenburgh
5 conclude that GSH homeostasis is essential for the prooxidant-antioxidant balance during prolonged physical exercise. In a later study
6, Ji concluded that exercise induced ROS pose a serious threat to the cellular antioxidant defense system, such as diminished reserves of antioxidant vitamins and glutathione, and increased tissue susceptibility to oxidative damage. Thus, the balance between pro-oxidants and antioxidants suggests that supplementation of antioxidants can be desirable for physically active individuals under certain physiological conditions by providing a larger protective margin.
Palazzetti et al.
7 submitted triathletes to increased training loads, which caused significant elevation of urinary adrenaline and CK plasmatic activity in rest. From Mehta, et al.,
8 we know that adrenaline is one instigator of the superoxide anion generation. However, Palazzetti showed through various markers, that that overload impairs the antioxidant defense mechanisms related to exercise-induced response. Runners seem particularly susceptible to OS. Briviba et al.
9 found among half-marathon and marathon runners, a decrease in antioxidant capacity and a statistically significant increase in the levels of oxidative DNA damage in lymphocytes. Manchefer et al.
10 studied extreme distance runners at The Marathon of Sands, and concluded the run induced a significant alteration of the blood antioxidant defense capacity. In studying underwater rugby players, Cavas
11 concluded that underwater rugby can stimulate over-production of ROS and antioxidant systems and affect oestradiol (estrogen) levels in male players, and that complex antioxidant supplementation including co-factors of antioxidant enzymes such as Cu, Zn, Fe, Se and antioxidant vitamins such as vitamin C and E may be recommended to players before the UWR game.
1. Davies KJA, Quintanilha AT, Brooks GA, Packer L. Free radicals and tissue damage produced by exercise. Biochem Biophys Res Commun 1982;vol.107, pp. 1198-205. 2. Sjodin B, Hellsten Westing Y, Apple FS., “Biochemical mechanisms for oxygen free radical formation during exercise.†Sports Med. 1990 Oct; 10(4):236-54. 3 Marzatico et al., “Blood free radical antioxidant enzymes and lipid peroxides following long-diatance and lactademic performances in highly trained aerobic and sprint athletes.†J Sports Med Phys Fitness, vol. 37, No. 4, pp.235-9 1997 Dec. 4 Ji LL, Fu R. Responses of glutathione system and antioxidant enzymes to exhaustive exercise and hydroperoxide. J Appl Physiol, vol.72, pp. 549-54 1992 5 Leeuwenburgh C, Ji LL, “Glutathione depletion in rested and exercised mice: biochemical consequence and adaptation.†Arch Biochem Biophys, 1;316(2):941-9,1995 Feb. 6 J LL, “Antioxidants and oxidative stress in exercise.†Proc Soc Exp Biol Med. 1999 Dec;222(3):283-92. 7 Palazzetti S, Richard M-J, Favier A, Margaritis I, “Overloaded training increases exercise-induced oxidative stress and damage.†Can J Appl Physiol, vol.28, pp. 588-604, 2003 8 Mehta JL, Li D, “Epinephrine upregulates superoxide dismutase in human coronary artery endothelial cells.†Free Radic Biol Med. Vol 30, No. 2, pp. 148-53 Jan 15 9 Briviba et al., “A half-marathon and a marathon run induce oxidative DNA damage, reduce antioxidant capacity to protect DNA against damage and modify immune function in hobby runners.†Redox Rep., vol. 10 No. 6, pp. 325-31, 2005 10 Machefer et al., “Extreme running competition decreases blood antioxidant defense capacity.†J Am Coll Nutr. Vol. 23, No. 4, pp. 358-64, 2004 Aug 11 Cavas L, “Does underwater rugby stimulate the over-production of reactive oxygen species?†Cell Biochem Funct., Vo. 23, No.1 pp. 59-63, 2005 Jan-Feb
Ted Zuhlsdorf
www.redoxhealth.com The Science of Making Cells Happy