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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.

The objective of this study is to test the hypothesis that increased muscle mass has positive effects on cardiovascular function. Specifically, we tested the hypothesis that increases in lean body mass caused by deletion of myostatin improves cardiac performance and vascular function. Echocardiography was used to quantify left ventricular function at baseline and after acute administration of propranolol and isoproterenol to assess β-adrenergic reactivity. Additionally, resistance vessels in several beds were removed, cannulated, pressurized to 60 mmHg and reactivity to vasoactive stimuli was assessed. Hemodynamics were measured using in vivo radiotelemetry. Myostatin deletion results in increased fractional shortening at baseline. Additionally, arterioles in the coronary and muscular microcirculations are more sensitive to endothelial-dependent dilation while nonmuscular beds or the aorta were unaffected. β-adrenergic dilation was increased in both coronary and conduit arteries, suggesting a systemic effect of increased muscle mass on vascular function. Overall hemodynamics and physical characteristics (heart weight and size) remained unchanged. Myostatin deletion mimics in part the effects of exercise on cardiovascular function. It significantly increases lean muscle mass and results in muscle-specific increases in endothelium-dependent vasodilation. This suggests that increases in muscle mass may serve as a buffer against pathological states that specifically target cardiac function (heart failure), the β-adrenergic system (age), and nitric oxide bio-availability (atherosclerosis). Taken together, pharmacological inhibition of the myostatin pathway could prove an excellent mechanism by which the benefits of exercise can be conferred in patients that are unable to exercise. [ABSTRACT FROM AUTHOR]