Day to Day Variability and Reliability of Blood Oxidative Stress Markers within a Four-Week Period in Healthy Young Men.

The present study aimed to determine the day to day variability and reliability of several blood oxidative stress markers at rest in a healthy young cohort over a four-week period. Twelve apparently healthy resistance trained males (24.6 ± 3.0 yrs) were tested over 7 visits within 4 weeks with at least 72 hrs between visits at the same time of day. Subjects rested 30 minutes prior to blood being obtained by vacutainer. Results. The highest IntraClass correlations (ICC's) were obtained for protein carbonyls (PC) and oxygen radical absorbance capacity (ORAC) (PC = 0.785 and ORAC = 0.780). Cronbach's α reliability score for PC was 0.967 and for ORAC was 0.961. The ICC's for GSH, GSSG, and the GSSG/TGH ratio ICC were 0.600, 0.573, and 0.570, respectively, with Cronbach's α being 0.913, 0.904, and 0.903, respectively. Xanthine oxidase ICC was 0.163 and Cronbach's α was 0.538. Conclusions. PC and ORAC demonstrated good to excellent reliability while glutathione factors had poor to excellent reliability. Xanthine oxidase showed poor reliability and high variability. These results suggest that the PC and ORAC markers were the most stable and reliable oxidative stress markers in blood and that daily changes across visits should be considered when interpreting resting blood oxidative stress markers.

Resistance exercise effects on blood glutathione status and plasma protein carbonyls: influence of partial vascular occlusion.

Seven weight-trained males performed both light resistance with partial occlusion (LRO: 30% 1 RM) and moderate resistance (MR: 70% 1 RM) to failure to ascertain whether blood protein carbonyls (PC) and glutathione status was altered compared to partial occlusion (PO) in a counterbalanced fashion. PO was identical in duration to the LRO session and all sessions were on separate days. PC did not differ for the three conditions at PRE (0.05 nM mg protein(-1)). PC significantly increased for PO and MR over time and was greater than the LRO treatment at POST (0.13 nM mg protein(-1)). The GSSG/TGSH ratio at PRE did not differ across treatments (8%) whereas the ratio at POST was significantly elevated for PO and MR treatments (17%). In contrast, no change occurred for the LRO session at any time. These results indicate that MR to failure and PO can significantly increase blood oxidative stress but LRO did not elicit oxidative stress.

Effect of high dose vitamin C supplementation on muscle soreness, damage, function, and oxidative stress to eccentric exercise.

This study investigated if vitamin C supplementation before and after eccentric exercise could reduce muscle soreness (MS), oxidative stress, and muscle function. Eighteen healthy men randomly assigned to either a placebo (P) or vitamin C (VC) (3 g/d) treatment group took pills for 2 wk prior and 4 d after performing 70 eccentric elbow extensions with their non-dominant arm. MS increased in both groups with significantly reduced MS for the first 24 h with VC. Range of motion was reduced equally in both groups after the exercise (P > or = 0.05). Muscle force declined equally and was unaffected by treatment. VC attenuated the creatine kinase (CK) increase at 48 h after exercise with similar CK after this time. Glutathione ratio (oxidized glutathione/total glutathione) was significantly increased at 4 and 24 h with P but VC prevented this change. These data suggest that vitamin C pretreatment can reduce MS, delay CK increase, and prevent blood glutathione oxidation with little influence on muscle function loss.

Clotting and fibrinolytic activity change during the 1 h after a submaximal run.

PURPOSE: To determine the changes in clotting and fibrinolytic activity during the 1-h period after an acute submaximal exercise at a specific relative exercise intensity to ascertain whether during this time there is a greater risk for developing a clot formation or thrombus. METHODS: Ten healthy men reported between 0700 and 1000 h and ran at 70-75% VO2max or walked at 1.2 mph for 30 min in a random counter-balanced order. Venous blood was obtained at rest, immediately after, and every 20 min during the 1-h recovery. RESULTS: There were no differences in the resting parameters for each treatment. Walking did not alter the activity of any of the measures analyzed compared with rest. Clotting indicators activated partial thromboplastin time (APTT) was significantly decreased by approximately 2 s and remained at this level during the 1-h recovery, and factor VIII activity was elevated 66% immediately after the run and remained elevated at this level during the 1-h recovery period. Fibrinolytic indicators, t-PA, and D-dimers were significantly increased immediately after the run. However, t-PA demonstrated a quadratic negative slope during the 1-h recovery time. D-dimers remained elevated during the 1-h recovery time. CONCLUSIONS: These results suggest that running at 70-75% VO2max resulted in elevated clotting and fibrinolytic activity. However, the clotting activity was sustained during a time when fibrinolytic activity declined, which suggests a more favorable situation for clot formation during this time after exercise.

Beta-endorphin infusion during exercise in rats does not alter hepatic or muscle glycogen.

The aim of this study was to determine whether beta-endorphin infusion influences liver or muscle glycogen concentration during exercise. Thirty-two rats (Harlan Co., IN, USA) with a body mass of 265-290 g were assigned at random to four groups, each of eight rats: (1) beta-endorphin infusion for 90 min at rest; (2) beta-endorphin infusion for 90 min while running on a rodent treadmill at 22 m x min(-1) and 0% grade; (3) saline infusion (0.9% NaCl) for 90 min at rest; and (4) saline infusion for 90 min while running on a rodent treadmill at 22 m x min(-1) and 0% grade. Beta-endorphin infusion elevated plasma beta-endorphin concentration by 2.5-fold at rest compared with saline infusion at rest, and by two-fold after exercise compared with saline infusion after exercise. Beta-endorphin infusion attenuated exercise-induced glucose concentration but did not alter the fasting hepatic glycogen concentration at rest or after exercise compared with saline infusion. Fasting hepatic glycogen decreased significantly as a result of 90 min of exercise independent of treatment. Deep intermedius muscle glycogen concentration at rest was similar after 90 min of both beta-endorphin and saline infusion and decreased significantly as a result of 90 min of exercise independent of treatment. Our results suggest that liver and muscle glycogenolysis is not responsible for the differences in plasma glucose with beta-endorphin infusion during exercise.

Beta-endorphin infusion during exercise in rats: blood metabolic effects.

UNLABELLED: Beta-endorphin (betaE) bolus (0.05 mg x kg(-1)) infusion (0.05 mg x kg(-1) x h(-1)) was previously shown in rats to attenuate the decline in plasma glucose during exercise. PURPOSE: The present investigation compared betaE and saline infusion in rats without a bolus of betaE to determine whether 1) the attenuation in the glucose decline was attributable to the type of administration (bolus betaE + continuous betaE infusion vs continuous betaE infusion), and 2) whether circulating catecholamines or FFAs were in part involved in the glucose decline. METHODS: Forty untrained Sprague-Dawley rats were randomly assigned to one of four treatments: 1) betaE infusion at rest (betaR), 2) betaE infusion during exercise (betaX), 3) saline infusion at rest (SR), and 4) saline infusion during exercise (SX). Infusions (betaE or saline) with running (22 m x min(-1), 0% grade) lasted 90 min. RESULTS: A 2 x 2 ANOVA indicated betaE infusion significantly attenuated the decline in plasma glucose due to exercise at 90 min (SX = 4.16 +/- 0.1 vs betaX = 4.61 +/- 0.1 mM). BetaE infusion elevated plasma betaE about 2.5-fold at rest compared with SR and two-fold after exercise (betaX) compared with SX. BetaE infusion had no effect at rest on any of the other variables measured. Exercise significantly increased catecholamines, FFAs and glucagon compared with resting levels. BetaE infusion enhanced the glucagon response to exercise (SX = 577 +/- 67.5 vs betaX = 913 +/- 153 ng x L(-1), P < 0.02). Epinephrine and norepinephrine and FFAs were similar with betaE infusion either at rest or during exercise compared with saline infusion. CONCLUSION: These results suggest that betaE infusion independent of the betaE bolus can attenuate the decline in glucose during exercise by enhancing glucagon levels and the betaE infusion did not influence circulating catecholamines or FFA's response to exercise.

Nutritional antioxidants as therapeutic and preventive modalities in exercise-induced muscle damage.

Several mechanisms have been forwarded to explain the etiology of exercise-induced muscle damage. Free-radical mediated processes appear to be an important component of the inflammatory mediated response. Free radicals have also been demonstrated to be a contributing factor in the loss of calcium homeostasis within the cell. Therefore, one of the proposed treatments for preventing or reducing the extent of this damage is the intervention of free-radical mediated processes. Antioxidants are agents that typically work to prevent free-radical mediated alterations within cells by quenching free radicals. The traditional dietary antioxidants most commonly investigated to inhibit free-radical damage are vitamin E, vitamin C, and beta carotene. Other nutritional agents have also been noted to contain antioxidant properties. Isofavonoids and some phytochemicals have been proposed to contain antioxidant properties. This paper briefly reviews some aspects of these agents and the! ! ir role, either proven or proposed, in the prevention of oxidative stress and muscle damage.

Effect of exercise during the follicular and luteal phases on indices of oxidative stress in healthy women.

PURPOSE: Eleven healthy nonsmoking women (24+/-1.1 yr) exercised for 30 min at 75-80% VO2max during the follicular (F) and luteal (L) phases of their menstrual cycle to determine whether menstrual phase influenced indices of oxidative stress. METHODS: Subjects completed the exercise in a randomized order. Subjects reported between 0800 and 0900 in a postabsorptive state, rested for 15-30 min, and had a venous blood sample obtained by Vacutainer before and after exercise. RESULTS: Resting estradiol was 54.4+/-12.0 pg.mL(-1) for F phase and was significantly higher in L phase (147.2+/-25.5 pg.mL(-1)). Plasma malondialdehyde and thiobarbituric acid substances were no different before and after exercise independent of menstrual cycle phase. No differences in resting blood total glutathione (TGSH), oxidized glutathione (GSSG), and reduced glutathione (GSH) were evident comparing the F and L phases. After exercise, TGSH decreased (P = 0.03) but reached significance only in the F phase = 8.1 %(P = 0.04), L phase = 2.5% (P = 0. 15). Exercise increased GSSG 10.5% in F (P = 0.15) and 27.8% in L phases(P = 0.01). GSH decreased after exercise independent of menstrual phase (F = 17%, L = 16%, P = 0.01). CONCLUSION: These data suggest that 30 min of moderate-intensity exercise in female subjects can result in mild oxidative stress as indicated by blood glutathione status and that menstrual cycle phase has minimal influences on these exercise responses.

Gender effect on beta-endorphin response to exercise.

PURPOSE: Twelve healthy men (26.4 yr) and women (26.8 yr) were compared at rest and after cycling for 25 min at 60 and 80% VO2max to determine whether gender and menstrual cycle influenced circulating beta-endorphin concentration (BE). METHODS: VO2max was determined on a cycle ergometer, and subjects completed the exercise in a randomized order. Women were tested in both the luteal (L) and follicular (F) phases of their menstrual cycle, which was confirmed by their blood estrogen levels. All tests were conducted in the morning after a 30-min rest (12-h postabsorptive). An indwelling venous catheter placed in a forearm vein enabled blood sampling at rest, 25 min of cycling, and 25 min of recovery. RESULTS: Resting BE was similar for men before both 60 and 80% intensities of exercise, 5.27 +/- 0.43 and 5.30 +/- 0.33 pmol.mL-1, respectively. BE was not significantly changed at 60% VO2max (6.54 +/- 0.33 pmol.mL-1) but significantly increased at 80% VO2max (11.90 +/- 1.98 pmol.mL-1). Women tended to have slightly lower BE during the L compared with F, but this did not reach significance (L = 4.40 +/- 0.22, F = 4.73 +/- 0.30 pmol.mL-1). Cycling at 60% VO2max did not significantly increase BE in the L (5.41 +/- 0.42 pmol.mL-1) nor the F (5.35 +/- 0.40 pmol.mL-1). Cycling at 80% VO2max increased BE to a similar extent in both the L and F phase, respectively (10.44 and 10.96). Although the BE concentrations tended to be slightly lower in women compared with men at 80% VO2max, this did not reach statistical significance. CONCLUSIONS: These data suggest that women cycling at 80% VO2max will have a similar BE response to men independent of their menstrual cycle. BE in women at rest and who exercise at lower exercise intensities may have slightly lower BE levels then men independent of the time of the women's menstrual cycle.

Beta-endorphin response to exercise. An update.

beta-Endorphin, a 31-amino-acid peptide, is primarily synthesised in the anterior pituitary gland and cleaved from pro-opiomelanocortin, its larger precursor molecule. beta-Endorphin can be released into the circulation from the pituitary gland or can project into areas of the brain through nerve fibres. Exercise of sufficient intensity and duration has been demonstrated to increase circulating beta-endorphin levels. Previous reviews have presented the background of opioids and exercise and discussed the changes in beta-endorphin levels in response to aerobic and anaerobic exercise. The present review is to update the response of beta-endorphin to exercise. This review suggests that exercise-induced beta-endorphin alterations are related to type of exercise and special populations tested, and may differ in individuals with health problems. Additionally, some of the possible mechanisms which may induce beta-endorphin changes in the circulation include analgesia, lactate or base excess, and metabolic factors. Based on the type of exercise, different mechanisms may be involved in the regulation of beta-endorphin release during exercise.

Comparison of methods for evaluating exercise-induced changes in thromboxane B2 and beta-thromboglobulin.

This study compared the effects of exercise or TXB2 and beta-TG when evaluated by four methods: 1) not adjusted; 2) adjusted for plasma volume changes (PV); 3) standardized per 10(5) platelets (PC); 4) or both PC and PV (PC-PV). Blood was collected from 16 men (41.3 +/- 8.1 yr) at rest after 30 min of exercise (IPE) and after 30 min recovery. Resting TXB2 and beta-TG concentrations were 62.0 +/- 6.2 pg.mL-1 and 129.8 +/- 12.5 ng.mL-1, respectively. When expressed on a per 10(5) platelet basis, resting PCTXB2 was 23.8 +/- 2.8 pg.mL-1.10(5-1) platelets and PC beta-TG was 50.77 +/- 6.0 ng.mL-1. 10(5-1) platelets. At IPE, TXB2 decreased 20.5% and beta-TG increased 13.6%. Thirty minutes after exercise TXB2 was 4.2% lower than resting values, whereas beta-TG was 26% higher. TXB2, beta-TG, PVTXB2, and PV beta-TG were not significantly altered by exercise. The only significant changes in TXB2 occurred at IPE when values were adjusted for changes in platelet count. At IPE, PCTXB2, and PC-PVTXB2 decreased 32.8% and 33.6%, respectively (P < 0.05). Similarly, beta-TG were not altered significantly by exercise except when the samples taken after 30 min of recovery were adjusted for changes in platelet count. At 30 min post-exercise PC beta-TG and PC-PV beta-TG were 21.2% and 28.4% greater (P < 0.05) than the resting beta-TG values. These data suggest that methods used to adjust concentrations of platelet derived substances for changes owing to exercise may influence conclusions about the effect of exercise on platelet function. Thus, it is imperative that researchers consider the purpose for which they are collecting TXB2 and beta-TG, as well as other constituents derived from blood cells, before they determine which methods of analysis to use.

Exercise-induced oxidative stress before and after vitamin C supplementation.

Vitamin C (ascorbic acid) was supplemented (1 g/day) for 1 day and 2 weeks in the same subjects. Plasma thiobarbituric acid reacting substances (TBARS) and oxygen radical absorbance capacity (ORAC) before and after 30 min submaximal exercise were measured. Different vitamin C supplementations did not affect resting TBARS or ORAC. Following 30 min exercise, values for TBARS were 12.6 and 33% above rest with 1 day and 2 weeks of vitamin C supplementation, respectively, compared to 46% higher with placebo. ORAC did not significantly change (11%) after exercise with a placebo, nor when subjects were given vitamin C supplements for 1 day or 2 days (4.9% and 5.73%, respectively). TBARS:ORAC, a ratio representing oxidative stress, increased 32% (p < .05) with placebo compared to 5.8 and 25.8% with vitamin C supplements for 1 day and 2 weeks, respectively. It was concluded that exercise-induced oxidative stress was highest when subjects did not supplement with vitamin C compared to either 1 day or 2 weeks of vitamin C supplementation.

Beta-endorphin infusion alters pancreatic hormone and glucose levels during exercise in rats.

beta-Endorphin (BE) infusion at rest can influence insulin and glucagon levels and thus may affect glucose availability during exercise. To clarify the effect of BE on levels of insulin, glucagon and glucose during exercise, 72 untrained male Sprague-Dawley rats were infused i.v. with either: (1) BE (bolus 0.05 mg.kg-1 + 0.05 mg.kg-1.h-1, n = 24); (2) naloxone (N, bolus 0.8 mg.kg-1 + 0.4 mg.kg-1, n = 24); or (3) volume-matched saline (S, n = 24). Six rats from each group were killed after 0, 60, 90 or 120 min of running at 22 m.min-1, at 0% gradient. BE infusion resulted in higher plasma glucose levels at 60 min [5.93 (0.32) mM] and 90 min [4,16 (0.29) mM] of exercise compared to S [4.62 (0.27) and 3.41 (0.26 mM] and N [4.97 (0.38) and 3.44 (0.25) mM]. Insulin levels decreased to a greater extent with BE [21.5 (0.9) and 18.3 (0.6) uIU.ml-1] at 60 and 90 min compared to S [24.5 (0.5) and 20.6 (0.6) uIU.ml-1] and N [24.5 (0.4) and 21.6 (0.7) uIU.ml-1] groups. Plasma C-peptide declined to a greater extent at 60 and 90 min of exercise with BE infusion compared to both S and N. BE infusion increased glucagon at all times during exercise compared to S and N. These data suggest that BE infusion during exercise influences plasma glucose by augmenting glucagon levels and attenuating insulin release.

Vitamin E attenuates myocardial oxidative stress induced by DHEA in rested and exercised rats.

Sixty-four male Sprague-Dawley rats were randomly assigned to one of eight treatment groups to determine whether vitamin E (VitE) could help protect the heart from oxidative stress induced by either dehydroepiandrosterone (DHEA) or exercise. Oxidative stress was indicated by lipid peroxidation [i.e., thiobarbituric acid-reactive substances (TBARS)] and two scavenger enzymes. VitE supplementation (250 IU VitE/kg of diet) was given to one-half of the rats. DHEA acetate (0.35 mol/kg body wt) was injected intraperitoneally to one-half of the animals while the others were injected with corn oil vehicle. All treatments lasted for 5 wk. Next, 32 rats were randomly assigned to run for 1 h on a motorized rodent treadmill at 21 m/min up a 12% grade and then were killed. The remaining rats were killed at rest. Exercise increased TBARS in heart independent of treatment (1.94 +/- 0.12 vs. 2.43 +/- 0.11 nmol/mg protein). VitE attenuated the amount of TBARS in heart when DHEA was given. DHEA significantly increased TBARS in heart. Total and selenium-dependent glutathione peroxidase activities in heart were unaffected by any treatment. DHEA increased catalase activity at rest. Exercise increased catalase activity (71.5 +/- 7.9 vs. 97.4 +/- 9.5 mu mol x min-1 x mg protein-1); however, when VitE was given, the response to exercise was attenuated (74.1 +/- 8.4 vs. 80.9 +/- 9.9 mu mol center dot min-1 x mg protein-1). These results suggest that aerobic exercise and DHEA are mild oxidative stressors on the heart and that VitE supplementation can be beneficial in attenuating these combined stressors on the heart.

Combined effects of age and exercise on thromboxane B2 and platelet activation.

Nine healthy young (27.8 +/- 0.8 yr old, YM) and nine healthy older men (55.4 +/- 1.3 yr old, OM) ran on a treadmill at 70-75% of maximal O2 consumption for 30 min to determine the combined effects of age and acute exercise on plasma thromboxane B2 (TxB2) and beta-thromboglobulin (beta-TG). Blood samples (10 ml) were collected in tubes containing 0.5 ml of 4.5 mM EDTA, 30 mM acetylsalicylic acid, and 1 microM prostaglandin E1 after 15 min of rest, immediately after exercise, and at 30 min of recovery. Concentrations of TxB2 and beta-TG were determined by radioimmunoassay. Samples were adjusted for hemoconcentration and changes in platelet count not accounted for by plasma volume shifts. Data were analyzed with repeated-measures analysis of variance and Tukey's post hoc technique. Resting TxB2 was 53.3 +/- 9.6 and 79.0 +/- 18.2 pg/ml for the YM and OM, respectively. beta-TG at rest was 152.5 +/- 13.9 and 114.0 +/- 10.9 ng/ml for the YM and OM, respectively. No significant age group or exercise-induced differences for TxB2 or beta-TG were found immediately after exercise. TxB2 in the OM (101.7 +/- 16.4 pg/ml) 30 min after exercise was significantly (P = 0.05) higher than that in the YM (54.4 +/- 6.2 pg/ml). beta-TG values 30 min after exercise were not significantly different: 183.3 +/- 26.9 and 169.9 +/- 17.0 ng/ml in the OM and YM, respectively. These data suggest that OM may experience greater increases in TxB2 than YM 30 min after exercise and may be more predisposed to platelet activation.

Vitamin E effects on indexes of lipid peroxidation in muscle from DHEA-treated and exercised rats.

Sixty-four male Sprague-Dawley rats were randomly assigned to one of eight treatment groups to determine the effects of vitamin E (VitE), dehydroepiandrosterone (DHEA), and exercise on antioxidant status in plasma and skeletal muscle. Indexes of oxidative stress were determined by measuring two markers of lipid peroxidation and the activity of two free radical scavenging enzymes. One-half of the rats had their diets supplemented with 250 IU VitE/kg of diet. One-half of the rats were injected with 0.35 mol/kg body wt ip of DHEA-acetate, whereas the others were injected with vehicle. All treatments lasted 5 wk. Before being killed, one-half of each treatments group of rats was randomly assigned to run for 1 h on a motorized rodent treadmill at 21 m/min up a 12% grade. The other rats remained rested before being killed. Exercise increased thiobarbituric acid-reactive substances (TBARS) and lipid hydroperoxides in plasma and TBARS in red slow-twitch and white fast-twitch muscles. VitE reduced the amount of lipid hydroperoxides and TBARS in plasma and TBARS in all three muscle fiber types. VitE also reduced glutathione peroxidase (GPX) activity in plasma and red fast-twitch muscle. DHEA increased indexes of oxidative stress in plasma and white fast-twitch muscle. DHEA reduced GPX activity in plasma but increased GPX activity in all three muscle fiber types. These results indicate that aerobic exercise is a mild oxidative stressor with DHEA exacerbating this response and that VitE helps diminish this effect in certain muscle fiber types.

Differences in the effects of carbohydrate food form on endurance performance to exhaustion.

This investigation examined the metabolic and performance effects of ingesting solid compared to slurried carbohydrate food (bananas) between two prolonged exhaustive exercise bouts. Eight highly trained male triathletes performed four exhaustive endurance tests (ET), each separated by at least 2 weeks. Each ET consisted of a 90-min run followed by 90 min of cycling, both at 70% VO2max. Workloads were then gradually increased on the cycle, and subjects continued to cycle until exhausted. They then rested for 20 min and ingested one of the following: an artificially sweetened placebo drink (P), slurried bananas (SL), or solid bananas (SO). Bananas were given in equal portions relative to each subject's body weight. Subjects cycled to exhaustion a second time at 70% of their VO2max, at which point the mean blood glucose concentration for the combined carbohydrate treatments was significantly higher than that from the P treatment. The mean glucose concentration from the SL treatment did not differ significantly from the SO treatment. These data demonstrate that solid bananas are as effective as slurried bananas in maintaining plasma glucose and in enhancing endurance exercise performance.

Vitamin E alters hepatic antioxidant enzymes in rats treated with dehydroepiandrosterone (DHEA).

The effects of vitamin E on hepatic antioxidant enzymes and plasma indicators of tissue damage were studied in rats treated with dehydroepiandrosterone (DHEA). Thirty-two male Sprague-Dawley rats were randomly allotted to one of four groups of eight rats each. Rats were treated with DHEA [100 mg/(kg body wt.d), i.p.], vitamin E (1 g/kg diet), or DHEA+vitamin E, or were untreated (controls) for 5 wk. Treatment with DHEA reduced (P < 0.05) weight gain, fat pad weight and carcass lipid concentration and increased carcass protein and ash concentration compared with control rats. The DHEA-treated rats had significantly lower concentrations of serum triglycerides and total cholesterol, yet greater amounts of liver lipid, than did control rats. Supplementation of DHEA-treated rats with vitamin E had no significant effect on weight gain, carcass composition or plasma metabolites compared with rats treated with DHEA alone. The rate of hepatic peroxisomal fatty acid oxidation in DHEA-treated rats was approximately 240% of that in control or vitamin E-supplemented rats. The specific activities of enzymes that defend against oxidative stress (e.g., glutathione reductase, glutathione transferase, catalase) or are indicators of tissue damage (e.g., alanine and aspartate aminotransferases) were all significantly higher in DHEA-treated rats compared with control rats. Supplementation of DHEA-treated rats with vitamin E generally reduced these indices of oxidative stress compared with rats treated with DHEA alone, suggesting that vitamin E may have a protective effect against potential oxidative damage associated with DHEA treatment.

Antioxidants: role of supplementation to prevent exercise-induced oxidative stress.

Exercise of a sufficient intensity and duration has been shown to increase indicators of oxidative stress. Oxidative stress has been indicated in skeletal muscle, liver, blood, and in expired air samples as indicated by the by-products of lipid peroxidation. Antioxidants are known to reduce oxidative-radical-induced reactions. This paper presents information concerning the effects of exercise on vitamin E and C concentrations in several tissues. This paper also discusses the effects of supplementation of vitamin E and vitamin C on their ability to alter exercise-induced lipid peroxidation. This paper indicates that limited information is available concerning the effects of both vitamins on exercise-induced oxidative stress. The viability of antioxidants alone and in conjunction with each other in preventing exercise-induced lipid peroxidation requires further investigation.

Effect of exercise intensity on 6-keto-PGF1 alpha, TXB2, and 6-keto-PGF1 alpha/TXB2 ratios.

Six men (X = 27.3 yr) ran at 60%, 70% and 80% of maximal oxygen consumption on separate days for 30 minutes to determine exercise intensity effects on 6-keto-PGF1 alpha, TXB2, and 6-keto-PGF1 alpha/TXB2 ratios. At rest, 6-keto-PGF1 alpha was 384 +/- 68.3 pg/ml; TXB2 was 147 +/- 55.6 pg/ml; and the 6-keto-PGF1 alpha/TXB2 ratio was 4.63 +/- 1.3. After exercise at 60%, 70%, and 80% TXB2 increased to 523.2 +/- 117.5, 611.7 +/- 155.4*, and 643.8 +/- 121.7* pg/ml, respectively (*p less than .05). Post-exercise ratios tended to be inversely related to exercise intensity; however, no statistically significant differences were found between these values. These data suggest that exercise-induced increases in TXB2 may be related to intensity.