The purpose of this study was to evaluate the effect of elevated muscle vitamin E content on skeletal muscle damage from eccentric exercise. Sixty Sprague-Dawley rats were put on a normal (40 IU vitamin E/kg food) or supplemented (10,000 IU vitamin E/kg food) diet for 5 wk. Injury in soleus muscle was determined using several criteria: reductions in maximal tetanic force and number of intact fibers per square millimeter and elevations in muscle glucose 6-phosphate dehydrogenase activity and plasma creatine kinase activity, either immediately (0 h) or 2 days (48 h) after a downhill walking protocol. Sedentary animals were also tested but did not exercise. Muscle vitamin E levels were significantly elevated (approximately 3- to 4-fold), and susceptibility of the muscles to oxidant stress was decreased, after supplementation. However, vitamin E supplementation did not attenuate injury by any of the criteria employed. Maximal tetanic force decreased approximately 20% at 0 and 48 h after exercise in both groups. The number of intact fibers per square millimeter decreased approximately 30-35% in both groups at 0 and 48 h. Glucose 6-phosphate dehydrogenase activity increased approximately 50-100% in both groups at 48 h, and plasma creatine kinase activity was elevated approximately 2- to 2.5-fold at 0 h in both groups. These findings do not support a major role for free radical damage to muscle membranes in the initiation of injury from eccentric exercise, although they do not disprove free radical involvement in the etiology.

A considerable amount of evidence now makes it clear that aerobic tissues require an elaborate enzyme system to remove the harmful reaction products of oxygen reduction. A portion of this protective system has been studied in human muscle and rat tissues. The VO2 max as well as the superoxide dismutase and catalase activity of vastus lateralis muscle of 12 healthy, male subjects was measured. The subjects with a high aerobic capacity (VO2 max greater than 60 ml . kg-1 . min-1) had significantly greater levels of both superoxide dismutase and catalase. There was also a linear relationship between both superoxide dismutase and catalase and VO2 max. The tissue oxygen consumption, and enzyme activity of the liver, heart, lung, and gastrocnemius from 24 rats was also studied. There VO2 and tissue enzyme activity of both superoxide dismutase and catalase.

Historically, exercise physiologists' interest in oxygen has primarily centered on the problem of oxygen consumption. However, the interest of the general scientific community in oxygen-centered radicals has raised awareness of the oxygen paradox and has motivated investigators to question whether exercise-stimulated "overconsumption" of oxygen might induce an oxidative stress and pose some risk to biological systems. In recent years, a considerable amount of research has demonstrated that radicals are capable of damaging a vast array of biological targets. Unfortunately, the work related to oxidative stress and antioxidants subsequent to exercise has been narrow in scope. This paper provides a brief review of the shortcomings of the present state of knowledge in this discipline and outlines topics requiring attention.Am J Clin Nutr 2000;72(suppl): 670S-4S.

Elemental and gaseous oxygen presents a conundrum in that it is simultaneously essential for and potentially destructive to human life. Traditionally the ability to consume large volumes of oxygen has been assumed to be totally beneficial to the organism. In the past 10 years it has become clear that oxygen radicals are generated even during normal resting metabolism Nevertheless, such radicals are usually of no appreciable threat since a wide array of protective biochemical systems exist. However, under certain circumstances aerobic exercise may increase free radical production to a level that overwhelms those defenses. A broad array of nutrients such as vitamin C, vitamin E, p-carotene, and so forth are known to suppress such radical events. This paper reviews the status of our knowledge relative to the potential benefits of nutritional modification in augmenting the organism's normal defense against harmful radical chemistry.

Free radicals are molecules or molecular fragments containing an unpaired electron in the valence shell. Radicals interested only a few chemists until 18 years ago when an enzyme was discovered which functioned to remove a specific oxygen-centered radical. That discovery renewed interest in radicals and has already begun to alter thinking on many clinical problems. Free radicals have been shown to be common phenomena that play a role in normal biochemistry but require an elaborate control system to be held in check. Since oxygen-centered radicals are produced in intermediate metabolism, exercise should increase their production and that has been shown to be so. There is also evidence that the consumption of large quantities of ambient oxygen during exercise induces harmful chemistry known as lipid peroxidation. Presently, there are insufficient data available to ascertain how the human body tolerates such increased production of free radicals and lipid peroxidation and how the consequences of that chemistry might relate to the overall well being of exercising humans.