Diversity of endurance training effects on antioxidant defenses and oxidative damage in different brain regions of adolescent male rats.

Studies on the effect of physical activity on brain oxidative stress, performed mostly in adult rats, have shown that moderate aerobic activity increases resistance to oxidative stress and reduces cellular damage. These effects can greatly differ between various brain regions. The postnatal period of the highest brain sensitivity to various stimuli is adolescence. We hypothesized that endurance training will modify brain antioxidant barrier differently in various regions, depending on their role in locomotion. Therefore, we studied the effect of moderate intensity endurance training on the activities of selected antioxidant enzymes (superoxide dismutase, gluthathione peroxidase and catalase and the contents of thiobarbituric acid-reactive substances (the key index of lipid peroxidation) and glutathione in several brain regions with dissimilar relationship to locomotion, as well as in circulating blood. Additionally, we investigated the effect of the training on nitric oxide synthase activity that may be a major player in exercise-related oxidative stress in brain regions that are directly involved in the locomotion control and execution (the striatum, midbrain and cerebellum). The training significantly enhanced nitric oxide synthase activity only in the latter three regions. Surprisingly, it elevated the activities of all studied antioxidant enzymes (excepting gluthathione peroxidase) in the neocortex, while no appreciable change in these activities was found in either the cerebellum (except for elevated catalase activity), or the striatum, or the midbrain. The training also elevated total glutathione content (a key protector of brain proteins under the conditions of enhanced nitric oxide production) in the cerebellum and striatum, but not in the other regions. The observed brain changes greatly differed from those in circulating blood and did not prevent the training-related increases in oxidative damage as evidenced by elevations in cerebellar and striatal thiobarbituric acid-reactive substances. These data suggest an increased susceptibility of adolescent brain to enhanced physical activity-related oxidative stress.

Blood antioxidant status in road cyclists during progressive (VO2max) and constant cyclist intensity test (MLSS).

AIM: The aim of the study was to evaluate the effect of two different cycling intensities on the blood antioxidant status in seven road cyclists male (M) (age 25.6±4.9 years; height 1.8±0.0 m; body mass 72.4±3.4 kg, and VO2max 66.8±8.9 mL*kg-1*min-1) and six road cyclists females (F) (age 26.5±2.5 years; height 1.67 ±0.01 m; body mass 56.5±5.3 kg; and VO2max 57.2±4.1 mL*kg-1*min-1). METHODS: The experiment was carried out with two tests: a progressive test (VO2max) (TP), and a 30-minute submaximal steady state test (TMLSS). The activity of superoxide dismutase, catalase (CAT), glutathione peroxidase, glutathione reductase, and creatine kinase, and the concentration of uric acid, reduced glutathione, malondialdehyde (MDA), blood lactate as well as total antioxidant potential, were assayed. RESULTS: Exercise significantly differentiated the activity and level of antioxidants. In both tests, after exercise a significant increase of CAT (P≤0.05) and CK (P≤0.05) activity was observed, as well as MDA (P≤0.05) level. CONCLUSION: It was demonstrated that neither the type of test (TP, TMLSS) nor the sex of the subjects exerted significant influence upon the activity of antioxidant enzymes and the level of low molecular weight antioxidants. Due to the workload in road cycling, where an average race or stage lasts a few hours, the 30-minute test was probably too weak a stimulus for the organism to disturb the pro- and antioxidative homeostasis.

Diverging oxidative damage and heat shock protein 72 responses to endurance training and chronic testosterone propionate treatment in three striated muscle types of adolescent male rats.

The aim of the study was to assess the effects of a combination of anabolic-androgenic steroid abuse and endurance training during adolescence on selected aspects of oxidative stress and antioxidant defenses in various striated muscle types. The effects were studied of testosterone propionate (TP) treatment (8 and 80 mg/kg/week, for 6 weeks), given alone or in combination with moderate-intensity endurance training, starting at adolescence, on thiobarbituric acid-reactive substances and heat shock protein 72 (Hsp72) contents, and androgen receptorm(AR) mRNA level in the heart left ventricle, soleus and extensor digitorum longus of male Wistar rats. TP treatment alone markedly elevated thiobarbituric acid-reactive substances only in the left ventricle and soleus; this effect was but marginally enhanced by endurance training. The training alone markedly elevated Hsp72 content in all muscles studied. TP treatment alone dose-dependently upregulated Hsp72, while the lower TP dose slightly curtailed the effect of the training. Low-dose TP treatment alone elevated, whereas high-dose TP treatment alone lowered androgen receptor mRNA level in the soleus and extensor digitorum longus. Endurance training alone elevated AR mRNA in all muscles studied, whereas TP treatment dose-dependently counteracted this effect. Exercise-associated rise in body temperature was significantly less in the TP-treated rats. We came to the conclusion that chronic suprapharmacological TP treatment might exert a protective effect on muscle cell proteins in adolescent sedentary rats, but it markedly enhanced lipid peroxidation. These effects were unlikely to result from an androgen receptor-mediated genomic action of testosterone. Exercise-related heat stress, and not oxidative stress, was mainly responsible for Hsp72 upregulation in striated muscles of chronic TP-treated endurance-trained adolescent male rats.

Effects of castration and testosterone replacement on the antioxidant defense system in rat left ventricle.

There is strong evidence that oxidative stress plays a key role in the pathophysiology of several cardiovascular diseases. On the other hand, the presence of specific receptors for androgens and estrogens in the myocardium implies that sex hormones play a physiological role in cardiac function, myocardial injury, and the regulation of the redox state in the heart. The present study was designed to determine whether castration and androgen replacement result in changes in the capacity of the antioxidant defense system in the left ventricle (LV) of adult male rats. To assess this, the activities of antioxidant enzymes (superoxide dismutase [SOD], glutathione peroxidase [GPX], catalase [CAT], and glutathione reductase [GR]), concentrations of nonenzymatic antioxidants (reduced glutathione [GSH] and alpha- and gamma-tocopherols), and oxidative stress biomarkers (tissue sulfhydryl groups, protein nitrotyrosine levels, and lipid peroxidation) were measured in castrated animals (CAS), castrates replaced with testosterone (CAS+T), and sham-operated controls (Sham). Testosterone was not detectable in serum from gonadectomized rats. The results indicate that castration significantly and negatively affected the antioxidant status of rat LV, as evidenced by a significant decline in activities of all antioxidant enzymes, by a tendency toward lower levels of GSH and protein thiol groups, and by enhanced lipid peroxidation and higher nitrotyrosine concentrations in left ventricular tissue. Increases in LV tissue concentrations of alpha- and gamma-tocopherols seem to be a compensatory response to enhanced oxidative stress induced by gonadectomy. The reestablishment of physiological serum testosterone level by androgen replacement resulted in a tendency toward a further decrease in the antioxidant defense status in the LV tissue.

Evaluation of autoantibodies against oxidized LDL (oLAB) and blood antioxidant status in professional soccer players.

Low-density lipoproteins (LDL) are very sensitive to oxidative processes initiated by oxygen free radicals, known to be produced in large quantities during intense physical exercise. Oxidatively modified lipoprotein particles (oxLDL) are strongly atherogenic and immunogenic, as a consequence specific autoantibodies (oLAB) against oxLDL are produced by the immune system. This study was designed to evaluate the oLAB titres in professional soccer players and to find out whether the immune response to oxidative modification of LDL correlates with the antioxidant status of individual players. Eleven players volunteered to participate in an incremental treadmill running exercise to volitional fatigue twice (in October and January) during the competitive season. Venous blood samples were withdrawn before and 3 min after the cessation of the test. Serum levels of oLAB were measured by ELISA (Biomedica). Blood samples were analyzed for glutathione peroxidase, reduced glutathione, superoxide dismutase, catalase and glutathione reductase. The activity of creatine kinase (CK) and concentrations of malondialdehyde (MDA), vitamin E and retinol were determined in plasma. From 11 subjects only in 4 players, in both graded running tests, the oLAB titres were low (< 200 mU.ml(-1)). The remaining athletes presented elevated oLAB (800-1400 mU.ml(-1)). Significantly lower activities of catalase and glutathione reductase and lower concentration of alpha-tocopherol were recorded in the 2nd trial. When the data were arranged according to the oLAB titres no significant between-group differences were found in either pre- and post-test activities of antioxidant enzymes or in concentrations of antioxidants. However, significantly higher CK activities and a tendency towards more elevated plasma MDA concentrations were observed in subjects with higher oLAB levels. It seems justified to presume that high titres of antibodies against oxLDL, as evidenced in most of the players, could be accounted for by their higher in vivo susceptibility of LDL to structural modification under conditions of intensive training-induced oxidative stress, despite their apparently normal antioxidant status.