We studied the effects of ingesting an antioxidant vitamin mixture for 6 wk on breath pentane and serum malondialdehyde (MDA) levels before and after exercise. Twenty young (mean age 25.0 +/- 2.9 yr) healthy males were randomly assigned to either an antioxidant vitamin group (daily doses of 592 mg of alpha-tocopherol equivalents, 1,000 mg of ascorbic acid, and 30 mg of beta-carotene) or a placebo group. Exercise consisted of 30 min of treadmill running at 60% of maximal O2 consumption (VO2max) followed by 5 min of running at a pace that elicited approximately 90% of VO2max. Blood and breath samples were collected immediately after the two exercise bouts. The antioxidant supplement did not prevent the exercise-induced increase in lipid peroxidation, as reflected by the rate of pentane production and the increase in serum MDA concentration. However, ingestion of the antioxidant vitamins did result in significantly lower resting and postexercise levels of expired pentane and serum MDA. We conclude that taking ascorbate, alpha-tocopherol, and beta-carotene in the amounts used in this study serves to lower markers of lipid peroxidation at rest and after exercise but does not prevent the exercise-induced increase in oxidative stress.

Free radicals have been implicated in the development of diverse diseases such as cancer, diabetes, and cataracts, and recent epidemic-logical data suggest an inverse relationship between antioxidant intake and cardiovascular disease risk. Data also suggest that antioxidants may delay aging, Research has indicated that free radical production and subsequent lipid peroxidation are normal sequelae to the rise in oxygen consumption with exercise. Consequently, antioxidant supplementation may detoxify the peroxides produced during exercise and diminish muscle damage and soreness. Vitamin E, beta carotene, and vitamin C have shown promise as protective antioxidants. Other ingestible products with antioxidant properties include selenium and coenzyme. The role (if any) that free radicals play in the development of exercise-induced tissue damage, or the protective role that antioxidants may play, remains to be elucidated. Current methods used to assess exercise-induced lipid peroxidation are not extremely specific or sensitive; research that utilizes more sophisticated methodologies should help to answer many questions regarding dietary antioxidants.

The purpose of this study was to correlate the exercise-induced changes of oxidant stress enzymes with possible modification of the response to the putative oxidant stressor doxorubicin. Enzymatic and histological changes were studied in mice placed on a 21-wk swim training program (1 h/day, 5 days/wk) with and without anthracycline administration. Doxorubicin (4 mg/kg) was administered intravenously through a tail vein on 10 separate days over a 7-wk period (twice weekly during weeks 10, 11, 14, 15, and 16). Blood, liver, and heart levels of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GP) were measured following the 9th and 21st wk. Myocardial histomorphological observations were made by light microscopy after 21 wk. Following 9 wk of training swim-trained animals had significantly elevated levels of CAT, SOD, and GP in blood, as well as elevated GP in liver. After 21 wk, trained animals, regardless of drug status, had elevated blood CAT and SOD activity and increased liver CAT and GP. Training also produced increases in blood GP, liver SOD, and heart CAT; however, in conjunction with doxorubicin these changes were not seen. The degree of cardiotoxicity was significantly greater in the sedentary drug-treated animals than in the swim-trained drug-treated animals. The results suggest a correlation between antioxidant enzyme levels in blood and liver and the degree of damage caused by an anthracycline drug. It was concluded that exercise ameliorates severe toxic damage caused by doxorubicin administration, possibly by increasing enzymes that combat free radical damage.

Pre and post race serum malondialdehyde (MDA), creatine kinase (CK) and lactate dehydrogenase (LDH) levels were studied in runners following an 80 km (50 mile) race. MDA is an indicator of lipid peroxidation. Subjects averaged 47.4 years (range 35-60), had a mean maximal oxygen uptake (VO2max) of 48.2 ml/kg, and averaged 121 km (75 miles) per week in training. Throughout the race, runners maintained a pace approximating 72% of VO2max. Previous data from our laboratory indicated a high correlation between resting MDA and total CK and CK-MB. Present resting data confirms prior results (r = 0.84 and 0.69 respectively). In addition, the relationship established at rest persisted following exercise (r = 0.62 and 0.85 respectively). Post race CK, CK-MB, LDH and MDA values for all subjects were significantly greater than resting values (p less than 0.01). Mean post CK and CK-MB levels were nearly 10 and 4 times lower, respectively, than prior values from our laboratory in subjects following a 100 km (62 mile) race. It was concluded that post exercise serum enzyme elevations, universally accepted as a marker of tissue damage, correlate well and may be related to an exercise induced lipid peroxidation.