Blood metabolic response to a long-term wheelchair rugby training.

STUDY DESIGN: A cross-sectional study with comparison group. OBJECTIVES: To evaluate the effects of long-term wheelchair rugby (WR) training on lipid profile, blood antioxidant status and the brain-derived neurotrophic factor (BDNF) level. SETTING: Academy of Physical Education, Katowice, Poland. METHODS: Thirty-two males with chronic cervical spinal cord injury (SCI) assigned into the physically active 'low-point' (LP, n=15) or 'high-point' (HP, n=8) WR players groups and the sedentary manual wheelchair users (SED, n=9) participated in this study. Fasting blood samples were collected at rest for assessment of activities of antioxidant enzymes, concentrations of reduced glutathione, uric acid, malondialdehyde (MDA), lipid profile measures and BDNF. RESULTS: No significant differences were found in anthropometric measures and serum lipid profile indices, although a slight tendency toward higher high-density lipoprotein cholesterol level was evidenced in WR players. Significantly lower serum malondialdehyde (MDA) and significantly higher levels of the overall enzymatic antioxidant potential index (EAP) in WR players, compared with SED, may reflect some WR training-induced increase in the blood's antioxidant capacity. There was also a slight tendency toward higher serum BDNF level in WR players compared with the SED group and a significant positive association between years of WR training and the BDNF level. CONCLUSION: A voluntary participation in a long-term WR training program has several health promoting outcomes for individuals with chronic SCI. Among the most important are enhancement of the blood antioxidant defense capacity evidenced by lower MDA and higher EAP levels, as well as WR training-induced activation of BDNF signaling.

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.

Effects of supplementation with acai (Euterpe oleracea Mart.) berry-based juice blend on the blood antioxidant defence capacity and lipid profile in junior hurdlers. A pilot study.

The purpose of this pilot study was to examine whether regular consumption of an acai berry-based juice blend would affect sprint performance and improve blood antioxidant status and lipid profile in junior athletes. Seven junior hurdlers (17.5±1.2 years) taking part in a pre-season conditioning camp were supplemented once a day, for six weeks, with 100 ml of the juice blend. At the start and the end of the camp the athletes performed a 300-m sprint running test on an outdoor track. Blood samples were taken before and immediately after the test and after 1 h of recovery. Blood antioxidant status was evaluated based on activities of antioxidant enzymes (superoxide dismutase [SOD], catalase [CAT], glutathione peroxidase [GSH-Px], glutathione reductase [GR]), concentrations of non-enzymatic antioxidants (reduced glutathione [GSH], uric acid), total plasma polyphenols, ferric reducing ability of plasma (FRAP), thiobarbituric acid reactive substances (TBARS) and activities of creatine kinase (CK) and lactate dehydrogenase (LDH) as muscle damage markers. In order to evaluate potential health benefits of the acai berry, the post-treatment changes in lipid profile parameters (triglycerides, cholesterol and its fractions) were analysed. Six weeks' consumption of acai berry-based juice blend had no effect on sprint performance, but it led to a marked increase in the total antioxidant capacity of plasma, attenuation of the exercise-induced muscle damage, and a substantial improvement of serum lipid profile. These findings strongly support the view of the health benefits of supplementation with the acai berry-based juice blend, mainly attributed to its high total polyphenol content and the related high in vivo antioxidant and hypocholesterolaemic activities of this supplement.

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.

The effects of sprint (300 m) running on plasma lactate, uric acid, creatine kinase and lactate dehydrogenase in competitive hurdlers and untrained men.

BACKGROUND: High intensity exercise may induce muscle damage especially in individuals unaccustomed to regular physical efforts. Our aim was to compare the impact of 300 m sprint running on muscle enzymes release into blood in competitive hurdlers and untrained but physically fit adults. EXPERIMENTAL DESIGN: Comparative study. SETTING: General community. PARTICIPANTS: Nine competitive hurdlers (CH; 21.3 yrs+/-3.1) and six matched moderately active untrained men (UT). INTERVENTIONS: Subjects performed a single 300 m sprint running test. MEASURES: Plasma creatine kinase (CK) and lactate dehydrogenase (LD) activities, and concentrations of lactate (LA) and uric acid (UA) measured before the warm-up and 5 min, 2 and 20 hrs postrun. RESULTS: Mean runner performance achieved by CH was significantly better (35.53-s+/-0.64) and LA concentrations significantly higher (14.95 mM+/-0.59) than those recorded in UT (41.52-s+/-2.22; 10.13 mM+/-0.59). Pre- and postrun CK activities until the 2nd hour of recovery were found to be significantly higher (p<0.05) in CH than in UT, whereas LD activities were similar in both groups pretest, but significantly higher in UT immediately postrun. In CH, the highest CK activity (32 percent increase) was recorded immediately post-test, whereas in UT the peak CK (135 percent increase) was attained in the 20th hour of recovery. In both groups UA reached the peak level in the 2nd hour of recovery. CONCLUSIONS: More pronounced and delayed postrun increase in CK, as recorded in UT, may provide evidence of a larger exercise-induced muscle injury in the untrained adults. Higher postexercise UA levels as recorded in CH might account for a more marked involvement of adenylate kinase reaction in ATP resynthesis.

Antioxidant defense in centenarians (a preliminary study).

The study was designed to assess the antioxidant defense mechanisms, either enzymatic or non-enzymatic, in a group of sixteen centenarians (one male and fifteen female subjects aged 101 to 105 years) living in the Upper Silesia district (Poland) in order to evaluate the potential role of antioxidant defenses in human longevity. The results of our preliminary study showed that in comparison with young healthy female adults the centenarians had significantly higher red blood cell glutathione reductase and catalase activities and higher, although insignificantly, serum vitamin E level.

Bioaccumulation of Germanium by Pseudomonas putida in the Presence of Two Selected Substrates.

The uptake of germanium by Pseudomonas putida ATCC 33015 was studied in the presence of catechol or acetate or both as representative substrates differing in their ability to form complexes with this element. The bacteria were taken from a batch culture grown on acetate as the sole carbon source. Cells introduced into a medium containing germanium and either catechol or a mixture of catechol and acetate accumulated germanium in a biphasic way. After a lower level of accumulation that corresponded to the value obtained in the presence of acetate was reached, a further increase in the germanium content up to a higher saturation level was observed. The appearance of the second step of accumulation, which corresponded to the linear degradation of catechol, proved that catechol facilitated the transport of germanium into the cells through the nonspecific uptake of the germanium-catechol complex by an inducible catechol transport system.

Binding of Germanium to Pseudomonas putida Cells.

The binding of germanium to Pseudomonas putida ATCC 33015 was investigated by using whole intact cells grown in a medium supplemented with GeO(2) and catechol or acetate. Electron-microscopic examination of the control and metal-loaded samples revealed that germanium was bound within the cell envelope. A certain number of small electron-dense deposits of the bound element were found in the cytoplasm when the cells were grown in the presence of GeO(2) and catechol. The study of germanium distribution in cellular fractions revealed that catechol facilitated the intracellular accumulation of this element.