Free Radicals and Antioxidants
Research: Is exercise the best antioxidant supplement?
As an unexpected consequence of the metabolic steps that convert food into energy, the body produces molecules commonly called “free radicals.” When not produced in too much abundance, free radicals are harmless to the body’s life process and in fact are known to be helpful.
However, when cells overproduce free radicals, they can become dangerous cellular adversaries to numerous life-sustaining processes. To combat the potentially harmful effects, cells in turn produce free-radical scavengers, referred to as antioxidants. In essence, antioxidants help to neutralize the destructive characteristics of free radicals. Personal trainers and exercise professionals are regularly asked whether exercise contributes to or helps buffer the effect of free radicals and whether it is advisable to supplement with antioxidants. This article will offer insight into this complex mystery.
Free radicals, also referred to as reactive oxygen species (ROS), are molecules that contain one or more unpaired electrons in their outer orbit, rather than having matched pairs of electrons. Thus, these molecules have an odd number of electrons. Molecules in this unpaired-electron state are unstable and become highly reactive with other molecules in the quest to attain molecular stability.
During mitochondrial respiration—the sequence of chemical reactions that manufacture energy for our cells—ROS are naturally produced as byproducts of this essential metabolic process (see Figure 1). There are several different types of ROS (e.g., the hydroxyl radical, the superoxide radical, the nitric oxide radical and the lipid peroxyl radical), which also come from cigarette smoke, environmental pollutants, radiation, ultraviolet light, certain drugs, pesticides and industrial solvents (Bagchi & Puri 1998).
In their effort to become more stable, free radicals attach themselves to other molecular structures, robbing those molecules of one or more electron(s). Each attachment spontaneously generates another free radical, starting a chain reaction that can damage cell membranes, DNA and protein breakdown (Clarkson & Thompson 2000). It should be noted that not all ROS are harmful. Some free radicals help wipe out invading pathogenic (disease-causing) microbes as part of the body’s defense mechanism (Bagchi & Puri 1998).
Antioxidants defend against the harmful effect of free radicals, which are associated with heart disease, cancer, arthritis, many other diseases and aging (Bonnefoy, Drai & Kostka 2002). Antioxidants are very stable molecules capable of neutralizing free radicals by donating an electron to them. Some antioxidants (e.g., glutathione, ubiquinol and uric acid) are produced during metabolism, while many others are obtained from foods in the diet. In children, it appears that the body’s arsenal of antioxidants is a most satisfactory defense process. However, Bonnefoy and colleagues explain that this stockpile of defense mechanisms appears to weaken considerably with aging. The best-known antioxidants are vitamin E, vitamin C and carotenoids. Vitamin E is an important fat-soluble antioxidant in cell membranes; vitamin C is a water-soluble antioxidant; and beta-carotene, the major carotenoid precursor of vitamin A, is also a very specialized antioxidant. Essentially the body attempts to maintain a balance between the production of free radicals and the antioxidants that combat them. Production of too many ROS leads to a condition referred to as oxidative stress, which is a precursor to cell, tissue and organ damage.
During cardiovascular exercise, oxygen consumption increases dramatically. This leads to a corresponding increase in free-radical production. So, does free-radical production during regular exercise exceed the protective capacity of the body’s antioxidant defense system? According to Gomez-Cabrera et al. (2005), it appears that ROS will cause damage only when the aerobic exercise is consistently too exhaustive. (Note: this finding was based on animal model research in which “exhaustion” was defined as “progressively increasing running speed to the point of not being able to continue.”) More intriguing, new research suggests that exercise-induced free-radical production actually promotes insulin sensitivity in humans (Ristow et al. 2009) and thus is a catalyst in the prevention of type 2 diabetes.
Insulin, which is released from the pancreas, triggers muscle and liver tissues in the body to consume glucose from the blood and store the glucose for fuel (the liver and muscle tissues store glucose in the form of glycogen). This process lowers blood sugar to stable levels. Thus, in someone with improved insulin sensitivity (as a result of exercise), the liver and muscles respond very effectively in absorbing blood glucose, keeping it at preferred levels and potentially managing or preventing insulin resistance and type 2 diabetes.
Ristow and colleagues (2009) state that antioxidant supplementation may actually block the many beneficial effects that exercise has on insulin sensitivity. The authors add that as an adaptive response to moderate-intensity exercise, muscle antioxidant defense systems are “up-regulated” (a process in the regulation of gene expression in which the number or activity of gene receptors increases in order to increase the sensitivity of a response). This stimulates specialized signaling message pathways to activate a number of enzymes and proteins that play important roles in the maintenance of intracellular oxidant-antioxidant homeostasis (see Figure 2).
The supplement industry is booming with manufacturers proclaiming that athletes can perform better, recover more quickly and exercise more rigorously with antioxidant supplements. However, Clarkson and Thompson (2000) caution that further long-term research is needed to assess the efficacy and safety of long-term antioxidant supplementation. These authors conclude that there is insufficient data suggesting that athletes and regular exercisers benefit from antioxidant supplementation. Indeed, Ristow and colleagues claim from their research that the supplemental doses of antioxidants some people are taking are more harmful than beneficial.
While the controversy about the benefits and/or harmful effects of antioxidant supplementation continues, most recent research supports the importance of regular, moderate-intensity cardiovascular exercise in conjunction with a diet rich in foods high in antioxidants. Food choices such as fruits (cranberries, blueberries, blackberries), vegetables (beans, artichokes, Russet potatoes), nuts (pecans, walnuts, hazelnuts) and spices (ground cloves, ground cinnamon, oregano) are high in natural antioxidants.
Be sure the cardiovascular exercise isn’t consistently too exhaustive (i.e., pushing the aerobic bout faster and faster to the point where the client can’t continue), as it seems there may be a threshold for the body in building and developing its optimal antioxidant defenses (Gomez-Cabrera et al. 2005). Encourage clients to be creative with their antioxidant food choices and stay committed to their exercise programs—their long-term health may depend on it.
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In mitochondrion A, a minimal number of free radicals are produced during mitochondrial respiration (the chemical sequence that produces ATP, the energy molecule of all cells). In mitochondrion B, many more free radicals are produced, which impairs DNA function and harms ATP-synthesizing proteins, resulting in less production of ATP.
Bonnefoy, M., Drai, J., & Kostka, T. 2002. Antioxidants to slow aging; facts and perspectives. Presse Medicine, 31 (25), 1174–84. Clarkson, P.M., &
Thompson, H.S. 2000. Antioxidants: What role do they play in physical activity and health? American Journal of Clinical Nutrition, 72 (Suppl.), 637S–46S.
Gomez-Cabrera, M.-C., et al. 2005. Decreasing xanthine oxidase-mediated oxidative stress prevents useful cellular adaptations to exercise in rats. Journal of Physiology, 567 (Pt. 1), 113–20.
Ristow, M., et al. 2009. Antioxidants prevent health-promoting effects of physical exercise in humans. PNAS, 106 (21), 8665–70.
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