Search

Introduction: Aerobic exercise can reduce postprandial lipemia, and possibly oxidative stress, when performed prior to a lipid-rich meal., Purpose: To compare the impact of acute exercise on postprandial oxidative stress., Methods: We compared aerobic and anaerobic exercise bouts of different intensities and durations on postprandial blood triglycerides (TAG), oxidative stress biomarkers (malondialdehyde, hydrogen peroxide, advanced oxidation protein products), and antioxidant status (trolox equivalent antioxidant capacity, superoxide dismutase, catalase, glutathione peroxidase). Twelve trained men (21-35 years) underwent four conditions: (1) No exercise rest; (2) 60-min aerobic exercise at 70% heart rate reserve; (3) five 60-s sprints at 100% max capacity; and (4) ten 15-s sprints at 200% max capacity. All exercise bouts were performed on a cycle ergometer. A high-fat meal was consumed 1 h after exercise cessation. Blood samples were collected pre-meal and 2 and 4 h post-meal and analyzed for TAG, oxidative stress biomarkers, and antioxidant status., Results: No significant interaction or condition effects were noted for any variable (p > 0.05), with acute exercise having little to no effect on the magnitude of postprandial oxidative stress., Conclusion: In a sample of healthy, well-trained men, neither aerobic nor anaerobic exercise attenuates postprandial oxidative stress in response to a high-fat meal.

Two prevalent origins of oxidative stress in Western society are the ingestion of high-fat meals and the performance of strenuous exercise. The purpose of this investigation was to compare the magnitude of increase in blood oxidative stress following acute feeding and acute exercise. Twelve exercise-trained men consumed a high-fat meal or performed 1 of 3 exercise bouts (steady-state aerobic; high-intensity, moderate-duration interval sprints; maximal intensity, short-duration interval sprints) in a random order, crossover design. Blood was collected before and at times following feeding and exercise. Samples were analyzed for trigylcerides, malondialdehyde (MDA), hydrogen peroxide (H(2)O(2)), advanced oxidation protein products (AOPP), nitrate/nitrite (NOx), trolox-equivalent antioxidant capacity (TEAC), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). A significant condition effect was noted for MDA (p = 0.01), H(2)O(2) (p < 0.0001), and AOPP (p = 0.0006), with values highest for the meal condition. An increase of 88%, 247%, and 96% was noted from pre- to post-feeding for MDA, H(2)O(2), and AOPP, respectively. A condition effect was also noted for TEAC (p = 0.04) and CAT (p = 0.05), with values lowest for the meal condition (TEAC) and the meal and aerobic exercise condition (CAT). NOx, SOD, and GPx were relatively unaffected by feeding and exercise, while MDA, H(2)O(2), and AOPP experienced little change from pre- to postexercise (p > 0.05). These results illustrate that the magnitude of blood oxidative stress following a high-fat meal is significantly greater than that elicited by either aerobic or anaerobic exercise in a sample of exercise-trained men.

Unlabelled: Exercise has been noted in some, but not all, studies to elicit an oxidative stress. The discrepancy in findings may be related to differences in exercise intensity across protocols, as well as to differences in training status of participants., Purpose: We compared blood oxidative stress biomarkers in exercise-trained men after three different bouts of exercise of varying intensity and duration, as well as a nonexercise condition., Methods: On different days, men (n = 12, 21-35 yr) performed aerobic cycle exercise (60 min at 70% HR reserve) and cycle sprints (five 60-s sprints at 100% maximum wattage obtained during graded exercise testing and ten 15-s sprints at 200% maximum wattage obtained during graded exercise testing). Blood was collected before and 0, 30, and 60 min after exercise and analyzed for malondialdehyde, hydrogen peroxide (H(2)O(2)), advanced oxidation protein products, and nitrate/nitrite (NO(x)). As indicators of antioxidant status, Trolox equivalent antioxidant capacity, superoxide dismutase, catalase, and glutathione peroxidase were measured., Results: No differences were noted in malondialdehyde, H(2)O(2), advanced oxidation protein product, or NO(x) between conditions or across time (P > 0.05). Antioxidant capacity was generally highest at 30 and 60 min after exercise and lowest at 0 min after exercise., Conclusions: In trained men, and considering the limitations of the current design (e.g., inclusion of selected oxidative stress and antioxidant biomarkers measured in blood only), strenuous bouts of exercise do not result in a significant increase in blood oxidative stress during the 1-h postexercise period. These findings may be related to attenuation in reactive oxygen species production as an adaptation to chronic exercise training and/or a protective effect of the antioxidant system in response to acute strenuous exercise.

Coenzyme Q10 (CoQ10) plays an important role in bioenergetic processes and has antioxidant activity. Fifteen exercise-trained individuals (10 men and 5 women; 30-65 years) received reduced CoQ10 (Kaneka QH ubiquinol; 300 mg per day) or a placebo for four weeks in a random order, double blind, cross-over design (3 week washout). After each four-week period, a graded exercise treadmill test and a repeated cycle sprint test were performed (separated by 48 hours). Blood samples were collected before and immediately following both exercise tests and analyzed for lactate, malondialdehyde, and hydrogen peroxide. Resting blood samples were analyzed for CoQ10 (ubiquinone and ubiquinol) profile before and after each treatment period. Treatment with CoQ10 resulted in a significant increase in total blood CoQ10 (138%; P = 0.02) and reduced blood CoQ10 (168%; P = 0.02), but did not improve exercise performance (with the exception of selected individuals) or impact oxidative stress. The relationship between the percentage change in total blood CoQ10 and the cycle sprint total work (R(2) = 0.6009) was noted to be moderate to strong. We conclude that treatment with CoQ10 in healthy, exercise-trained subjects increases total and reduced blood CoQ10, but this increase does not translate into improved exercise performance or decreased oxidative stress.

Background: The purpose of this investigation was to determine the effects of a dietary supplement (Ambrotose AO®) on resting and exercise-induced blood antioxidant capacity and oxidative stress in exercise-trained and untrained men and women., Methods: 25 individuals (7 trained and 5 untrained men; 7 trained and 6 untrained women) received Ambrotose AO® (4 capsules per day = 2 grams per day) or a placebo for 3 weeks in a random order, double blind cross-over design (with a 3 week washout period). Blood samples were collected at rest, and at 0 and 30 minutes following a graded exercise treadmill test (GXT) performed to exhaustion, both before and after each 3 week supplementation period. Samples were analyzed for Trolox Equivalent Antioxidant Capacity (TEAC), Oxygen Radical Absorbance Capacity (ORAC), malondialdehyde (MDA), hydrogen peroxide (H2O2), and nitrate/nitrite (NOx). Quality of life was assessed using the SF-12 form and exercise time to exhaustion was recorded. Resting blood samples were analyzed for complete blood count (CBC), metabolic panel, and lipid panel before and after each 3 week supplementation period. Dietary intake during the week before each exercise test was recorded., Results: No condition effects were noted for SF-12 data, for GXT time to exhaustion, or for any variable within the CBC, metabolic panel, or lipid panel (p > 0.05). Treatment with Ambrotose AO® resulted in an increase in resting levels of TEAC (p = 0.02) and ORAC (p < 0.0001). No significant change was noted in resting levels of MDA, H2O2, or NOx (p > 0.05). Exercise resulted in an acute increase in TEAC, MDA, and H2O2 (p < 0.05), all which were higher at 0 minutes post exercise compared to pre exercise (p < 0.05). No condition effects were noted for exercise related data (p > 0.05), with the exception of ORAC (p = 0.0005) which was greater at 30 minutes post exercise for Ambrotose AO® compared to placebo., Conclusion: Ambrotose AO® at a daily dosage of 4 capsules per day increases resting blood antioxidant capacity and may enhance post exercise antioxidant capacity. However, no statistically detected difference is observed in resting or exercise-induced oxidative stress biomarkers, in quality of life, or in GXT time to exhaustion.

Unlabelled: We have recently noted that ingestion of dietary lipid (in the form of heavy whipping cream) leads to greater oxidative stress than dietary carbohydrate (in the form of dextrose), when consumed in isocaloric amounts., Objective: In the present investigation we attempted to replicate our work and also to determine the oxidative stress response to dextrose and lipid meals of two different kilocalorie (kcal) amounts., Design: Nine young (22 +/- 2 years), healthy men consumed in a random order, cross-over design one of four meals/drinks: dextrose at 75 g (300 kcals), dextrose at 150 g (600 kcals), lipid at 33 g (300 kcals), lipid at 66 g (600 kcals). Blood samples were collected Pre meal, and at 30 min, 60 min, 120 min, and 180 min post meal. Samples were assayed for glucose, triglycerides (TAG), malondialdehyde (MDA), and hydrogen peroxide (H2O2). Area under the curve (AUC) was calculated for each variable, and a 4 x 5 ANOVA was utilized to further analyze data., Results: A meal x time effect (p = 0.0002) and a time effect was noted for glucose (p < 0.0001; 30 min > Pre, 1 hr, 2 hr, and 3 hr). The dextrose meals primarily contributed to this time effect. No other effects were noted for glucose (p > 0.05). A meal effect was noted for TAG (p = 0.01; 66 g lipid meal > 75 g and 150 g dextrose meals). No other effects were noted for TAG (p > 0.05). An AUC effect was noted for MDA (p = 0.04; 66 g lipid meal > 75 g and 150 g dextrose meals). A meal x time effect (p = 0.02) and a meal effect was noted for MDA (p = 0.004; 66 g lipid meal > 75 g and 150 g dextrose meals). No time effect was noted for MDA (p = 0.72). An AUC effect was noted for H2O2 (p = 0.0001; 66 g lipid meal > 33 g lipid meal and 75 g and 150 g dextrose meals). A meal x time effect (p = 0.0002), a meal effect (p < 0.0001; 66 g lipid meal > 33 g lipid meal and 75 g and 150 g dextrose meals), and a time effect was noted for H2O2 (p < 0.0001; 2 hr > Pre, 30 min, and 1 hr; 3 hr > Pre). The time effect for H2O2 was primarily influenced by the 66 g lipid meal., Conclusions: These data indicate that 1) minimal oxidative stress is observed following ingestion of dextrose loads of either 75 g or 150 g, or a lipid load of 33 g and 2) lipid ingestion at 66 g leads to greater oxidative stress than lipid at 33 g or dextrose at either 75 g or 150 g. Hence, in a sample of young and healthy men, only 66 g of lipid (taken in the form of heavy whipping cream) leads to a significant increase in blood oxidative stress, as measured by MDA and H2O2.