EFFECTS OF EXHAUSTIVE EXERCISE AND VITAMIN-B-6 DEFICIENCY ON FREE-RADICAL OXIDATIVE PROCESS IN MALE TRAINED RATS

There is growing evidence that oxygen free radical production and subs equent lipid peroxidation are normal sequelae to the rise in oxygen co nsumption concomitant with exercise. In addition, increased lipid pero xidation has also been shown in vitamin B-6-deficient rat plasma, live r, and kidney. To investigate the potential for a role of vitamin B-6 in exercise-induced oxidative stress, 36 male Sprague-Dawley rats rece ived 0 (n = 12), 2 (n = 12), and 8 mg pyridoxine (PN)-HCl/kg diet (n = 12) and were trained by a 9-week swimming program. After 9-weeks of t raining, six rats (exhausted: E rats) of each vitamin group were exerc ised to exhaustion by swimming while the other six rats rested (nonexh austed: NE rats). Ascorbate, ascorbate free radical and antilipoperoxi dant capability (AC) were evaluated in plasma. These parameters were h igher in E rats than in NE rats. Free radical-mediated lipid peroxidat ion was measured in tissue and plasma by evaluation of thiobarbituric acid reactive substances (TEARS) content. This index of peroxidation w as significantly increased in liver of E rats but not in plasma, heart , and gastrocnemius muscle. Concentration of TEARS in liver was the hi ghest in vitamin B-6-deficient rats (consuming 8 mg PN-HCl/kg diet) an d the lowest in vitamin B-6-sufficient rats (consuming 8 mg PN-HCl/kg diet). Vitamin E (alpha-tocopherol) levels in liver and heart were neg atively related to vitamin B-6 levels in the diet. Independently of vi tamin B-6 liver and muscle alpha-tocopherol levels were significantly higher in E animals than in NE animals. There is good evidence accordi ng to our results that exercise induced an oxidative stress, as indica ted by a significant increase of ascorbyl radical levels in the plasma . The effects of vitamin B-6 deficiency on the free radical metabolism are low in trained rats. On the contrary, exhaustive exercise induced modifications in the metabolism pathways of vitamin C and E objectiva ted by variations of levels of vitamin C in the plasma and vitamin fin liver.