183 research outputs found

    Oxidative stress and antioxidant defense mechanisms linked to exercise during cardiopulmonary and metabolic disorders

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    Oxidative stress has been implicated in the pathophysiology of multiple human diseases, in addition to the aging process. Although various stimuli exist, acute exercise is known to induce a transient increase in reactive oxygen and nitrogen species (RONS), evident by several reports of increased oxidative damage following acute bouts of aerobic and anaerobic exercise. Although the results are somewhat mixed and appear disease dependent, individuals with chronic disease experience an exacerbation in oxidative stress following acute exercise when compared to healthy individuals. However, this increased oxidant stress may serve as a necessary “signal” for the upregulation in antioxidant defenses, thereby providing protection against subsequent exposure to prooxidant environments within susceptible individuals. Here we present studies related to both acute exercise-induced oxidative stress in those with disease, in addition to studies focused on adaptations resulting from increased RONS exposure associated with chronic exercise training in persons with disease

    Effect of eicosapentaenoic and docosahexaenoic acid on resting and exercise-induced inflammatory and oxidative stress biomarkers: a randomized, placebo controlled, cross-over study

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    <p>Abstract</p> <p>Background</p> <p>The purpose of the present investigation was to determine the effects of EPA/DHA supplementation on resting and exercise-induced inflammation and oxidative stress in exercise-trained men. Fourteen men supplemented with 2224 mg EPA+2208 mg DHA and a placebo for 6 weeks in a random order, double blind cross-over design (with an 8 week washout) prior to performing a 60 minute treadmill climb using a weighted pack. Blood was collected pre and post exercise and analyzed for a variety of oxidative stress and inflammatory biomarkers. Blood lactate, muscle soreness, and creatine kinase activity were also measured.</p> <p>Results</p> <p>Treatment with EPA/DHA resulted in a significant increase in blood levels of both EPA (18 ± 2 μmol·L<sup>-1 </sup>vs. 143 ± 23 μmol·L<sup>-1</sup>; p < 0.0001) and DHA (67 ± 4 μmol·L<sup>-1 </sup>vs. 157 ± 13 μmol·L<sup>-1</sup>; p < 0.0001), while no differences were noted for placebo. Resting levels of CRP and TNF-α were lower with EPA/DHA compared to placebo (p < 0.05). Resting oxidative stress markers were not different (p > 0.05). There was a mild increase in oxidative stress in response to exercise (XO and H<sub>2</sub>O<sub>2</sub>) (p < 0.05). No interaction effects were noted. However, a condition effect was noted for CRP and TNF-α, with lower values with the EPA/DHA condition.</p> <p>Conclusion</p> <p>EPA/DHA supplementation increases blood levels of these fatty acids and results in decreased resting levels of inflammatory biomarkers in exercise-trained men, but does not appear necessary for exercise-induced attenuation in either inflammation or oxidative stress. This may be due to the finding that trained men exhibit a minimal increase in both inflammation and oxidative stress in response to moderate duration (60 minute) aerobic exercise.</p

    Effect of the dietary supplement Meltdown on catecholamine secretion, markers of lipolysis, and metabolic rate in men and women: a randomized, placebo controlled, cross-over study

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    <p>Abstract</p> <p>Background</p> <p>We have recently reported that the dietary supplement Meltdown<sup>® </sup>increases plasma norepinephrine (NE), epinephrine (EPI), glycerol, free fatty acids (FFA), and metabolic rate in men. However, in that investigation measurements ceased at 90 minutes post ingestion, with values for blood borne variables peaking at this time. It was the purpose of the present investigation to extend the time course of measurement to 6 hours, and to include women within the design to determine if sex differences to treatment exist.</p> <p>Methods</p> <p>Ten men (24 ± 4 yrs) and 10 women (22 ± 2 yrs) ingested Meltdown<sup>® </sup>or a placebo, using a randomized, cross-over design with one week separating conditions. Blood samples were collected immediately before supplementation and at one hour intervals through 6 hours post ingestion. A standard meal was provided after the hour 3 collection. Samples were assayed for EPI, NE, glycerol, and FFA. Five minute breath samples were collected at each time for measurement of metabolic rate and substrate utilization. Area under the curve (AUC) was calculated. Heart rate and blood pressure were recorded at all times. Data were also analyzed using a 2 (sex) × 2 (condition) × 7 (time) repeated measures analysis of variance, with Tukey <it>post hoc </it>testing.</p> <p>Results</p> <p>No sex × condition interactions were noted for AUC for any variable (p > 0.05). Hence, AUC data are collapsed across men and women. AUC was greater for Meltdown<sup>® </sup>compared to placebo for EPI (367 ± 58 pg·mL<sup>-1</sup>·6 hr<sup>-1 </sup>vs. 183 ± 27 pg·mL<sup>-1</sup>·6 hr<sup>-1</sup>; p = 0.01), NE (2345 ± 205 pg·mL<sup>-1</sup>·6 hr<sup>-1 </sup>vs. 1659 ± 184 pg·mL<sup>-1</sup>·6 hr<sup>-1</sup>; p = 0.02), glycerol (79 ± 8 μg·mL<sup>-1</sup>·6 hr<sup>-1 </sup>vs. 59 ± 6 μg·mL<sup>-1</sup>·6 hr<sup>-1</sup>; p = 0.03), FFA (2.46 ± 0.64 mmol·L<sup>-1</sup>·6 hr<sup>-1 </sup>vs. 1.57 ± 0.42 mmol·L<sup>-1</sup>·6 hr<sup>-1</sup>; p = 0.05), and kilocalorie expenditure (439 ± 26 kcal·6 hrs<sup>-1 </sup>vs. 380 ± 14 kcal·6 hrs<sup>-1</sup>; p = 0.02). No effect was noted for substrate utilization (p = 0.39). Both systolic and diastolic blood pressure (p < 0.0001; 1–16 mmHg), as well as heart rate (p = 0.01; 1–9 bpm) were higher for Meltdown<sup>®</sup>. No sex × condition × time interactions were noted for any variable (p > 0.05).</p> <p>Conclusion</p> <p>Ingestion of Meltdown<sup>® </sup>results in an increase in catecholamine secretion, lipolysis, and metabolic rate in young men and women, with a similar response for both sexes. Meltdown<sup>® </sup>may prove to be an effective intervention strategy for fat loss, assuming individuals are normotensive and their treatment is monitored by a qualified health care professional.</p

    Dietary Supplement Increases Plasma Norepinephrine, Lipolysis, and Metabolic Rate in Resistance Trained Men

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    Background Dietary supplements targeting fat loss and increased thermogenesis are prevalent within the sport nutrition/weight loss market. While some isolated ingredients have been reported to be efficacious when used at high dosages, in particular in animal models and/or via intravenous delivery, little objective evidence is available pertaining to the efficacy of a finished product taken by human subjects in oral form. Moreover, many ingredients function as stimulants, leading to increased hemodynamic responses. The purpose of this investigation was to determine the effects of a finished dietary supplement on plasma catecholamine concentration, markers of lipolysis, metabolic rate, and hemodynamics. Methods Ten resistance trained men (age = 27 ± 4 yrs; BMI = 25 ± 3 kg· m-2; body fat = 9 ± 3%; mean ± SD) ingested a dietary supplement (Meltdown®, Vital Pharmaceuticals) or a placebo, in a random order, double blind cross-over design, with one week separating conditions. Fasting blood samples were collected before, and at 30, 60, and 90 minutes post ingestion and were assayed for epinephrine (EPI), norepinephrine (NE), glycerol, and free fatty acids (FFA). Area under the curve (AUC) was calculated for all variables. Gas samples were collected from 30–60 minutes post ingestion for measurement of metabolic rate. Heart rate and blood pressure were recorded at all blood collection times. Results AUC was greater for the dietary supplement compared to the placebo for NE (1332 ± 128 pg·mL-1·90 min-1vs. 1003 ± 133 pg·mL-1·90 min-1; p = 0.03), glycerol (44 ± 3 μg·mL-1·90 min-1 vs. 26 ± 2 μg·mL-1·90 min-1; p \u3c 0.0001), and FFA (1.24 ± 0.17 mmol·L-1·90 min-1 vs. 0.88 ± 0.12 mmol·L-1·90 min-1; p = 0.0003). No difference between conditions was noted for EPI AUC (p \u3e 0.05). For all variables, values were highest at 90 minutes post ingestion. Total kilocalorie expenditure during the 30 minute collection period was 29.6% greater (p = 0.02) for the dietary supplement (35 ± 3 kcal) compared to placebo (27 ± 2 kcal). A condition main effect was noted for systolic blood pressure (p = 0.04), with values increasing from 117 ± 2 mmHg to 123 ± 2 mmHg with the dietary supplement, while remaining unchanged for placebo. No other hemodynamic changes were noted (p \u3e 0.05). Conclusion The dietary supplement results in an acute increase in plasma NE and markers of lipolysis, as well as metabolic rate. This occurs without altering hemodynamic variables in a clinically significant manner. Intervention studies to determine the impact of this dietary supplement on weight/fat loss are warranted. Backgroun

    Language and theory of mind in autism spectrum disorder : the relationship between complement syntax and false belief task performance.

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    This study aimed to test the hypothesis that children with autism spectrum disorder (ASD) use their knowledge of complement syntax as a means of “hacking out” solutions to false belief tasks, despite lacking a representational theory of mind (ToM). Participants completed a “memory for complements” task, a measure of receptive vocabulary, and traditional location change and unexpected contents false belief tasks. Consistent with predictions, the correlation between complement syntax score and location change task performance was significantly stronger within the ASD group than within the comparison group. However, contrary to predictions, complement syntax score was not significantly correlated with unexpected contents task performance within either group. Possible explanations for this pattern of results are considered

    Effect of Ambrotose AO® on resting and exercise-induced antioxidant capacity and oxidative stress in healthy adults

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    <p>Abstract</p> <p>Background</p> <p>The purpose of this investigation was to determine the effects of a dietary supplement (Ambrotose AO<sup>®</sup>) on resting and exercise-induced blood antioxidant capacity and oxidative stress in exercise-trained and untrained men and women.</p> <p>Methods</p> <p>25 individuals (7 trained and 5 untrained men; 7 trained and 6 untrained women) received Ambrotose AO<sup>® </sup>(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 (H<sub>2</sub>O<sub>2</sub>), 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.</p> <p>Results</p> <p>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<sup>® </sup>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, H<sub>2</sub>O<sub>2</sub>, or NOx (p > 0.05). Exercise resulted in an acute increase in TEAC, MDA, and H<sub>2</sub>O<sub>2 </sub>(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<sup>® </sup>compared to placebo.</p> <p>Conclusion</p> <p>Ambrotose AO<sup>® </sup>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.</p

    Multi-layered Ruthenium-modified Bond Coats for Thermal Barrier Coatings

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    Diffusional approaches for fabrication of multi-layered Ru-modified bond coats for thermal barrier coatings have been developed via low activity chemical vapor deposition and high activity pack aluminization. Both processes yield bond coats comprising two distinct B2 layers, based on NiAl and RuAl, however, the position of these layers relative to the bond coat surface is reversed when switching processes. The structural evolution of each coating at various stages of the fabrication process has been and subsequent cyclic oxidation is presented, and the relevant interdiffusion and phase equilibria issues in are discussed. Evaluation of the oxidation behavior of these Ru-modified bond coat structures reveals that each B2 interlayer arrangement leads to the formation of α-Al 2 O 3 TGO at 1100°C, but the durability of the TGO is somewhat different and in need of further improvement in both cases

    Global redox proteome and phosphoproteome analysis reveals redox switch in Akt.

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    Protein oxidation sits at the intersection of multiple signalling pathways, yet the magnitude and extent of crosstalk between oxidation and other post-translational modifications remains unclear. Here, we delineate global changes in adipocyte signalling networks following acute oxidative stress and reveal considerable crosstalk between cysteine oxidation and phosphorylation-based signalling. Oxidation of key regulatory kinases, including Akt, mTOR and AMPK influences the fidelity rather than their absolute activation state, highlighting an unappreciated interplay between these modifications. Mechanistic analysis of the redox regulation of Akt identified two cysteine residues in the pleckstrin homology domain (C60 and C77) to be reversibly oxidized. Oxidation at these sites affected Akt recruitment to the plasma membrane by stabilizing the PIP3 binding pocket. Our data provide insights into the interplay between oxidative stress-derived redox signalling and protein phosphorylation networks and serve as a resource for understanding the contribution of cellular oxidation to a range of diseases
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