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Search Results: 1 - 10 of 1907 matches for " Kelsey Fisher-Wellman "
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Systemic Oxidative Stress Is Increased to a Greater Degree in Young, Obese Women Following Consumption of a High Fat Meal
Richard J. Bloomer,Kelsey H. Fisher-Wellman
Oxidative Medicine and Cellular Longevity , 2009, DOI: 10.4161/oxim.2.1.7860
Abstract: High fat meals induce oxidative stress, which is associated with the pathogenesis of disease. Obese individuals have elevated resting biomarkers of oxidative stress compared to non-obese. We compared blood oxidative stress biomarkers in obese (n = 14; 30 ± 2 years; BMI 35 ± 1 kg•m−2) and non-obese (n = 16; 24 ± 2 years; BMI 23 ± 1 kg•m−2) women, in response to a high fat meal. Blood samples were collected pre-meal (fasted), and at 1, 2, 4 and 6 hours post meal, and assayed for trolox equivalent antioxidant capacity (TEAC), xanthine oxidase activity (XO), hydrogen peroxide (H2O2), malondialdehyde (MDA), triglycerides (TAG), and glucose. An obesity status effect was noted for all variables (p < 0.001; MDA p = 0.05), with obese women having higher values than non-obese, except for TEAC, for which values were lower. Time main effects were noted for all variables (p ≤ 0.01) except for TEAC and glucose, with XO, H2O2, MDA and TAG increasing following feeding with a peak response at the four or six hour post feeding time point. While values tended to decline by six hours post feeding in the non-obese women (agreeing with previous studies), they were maintained (MDA) or continued to increase (XO, H2O2 and TAG) in the obese women. While no interaction effects were noted (p > 0.05), contrasts revealed greater values in obese compared to non-obese women for XO, H2O2, MDA, TAG and glucose, and lower values for TEAC at times from 1–6 hours post feeding (p ≤ 0.03). We conclude that young, obese women experience a similar pattern of increase in blood oxidative stress biomarkers in response to a high fat meal, as compared to non-obese women. However, the overall oxidative stress is greater in obese women, and values appear to remain elevated for longer periods of time post feeding. These data provide insight into another potential mechanism related to obesity-mediated morbidity.
Oxidative Stress and Antioxidant Defense Mechanisms Linked to Exercise During Cardiopulmonary and Metabolic Disorders
Kelsey Fisher-Wellman,Heather K. Bell,Richard J. Bloomer
Oxidative Medicine and Cellular Longevity , 2009, DOI: 10.4161/oxim.2.1.7732
Abstract: 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.
Postprandial Oxidative Stress in Exercise Trained and Sedentary Cigarette Smokers
Richard J. Bloomer,Kelsey H. Fisher-Wellman
International Journal of Environmental Research and Public Health , 2009, DOI: 10.3390/ijerph6020579
Abstract: Cigarette smokers experience an exaggerated triglyceride (TAG) and oxidative stress response to high fat feeding. Exercise training may serve to attenuate the rise in these variables, by improving TAG clearance and antioxidant defense. We compared blood TAG, antioxidant capacity, and oxidative stress biomarkers in exercise trained (>2 hrs per wk) and untrained smokers matched for age, in response to a high fat test meal. We report here that low volume exercise training can attenuate postprandial lipid peroxidation, but has little impact on blood TAG and other markers of oxidative stress. Higher volumes of exercise may be needed to allow for clinically meaningful adaptations in postprandial lipemia and oxidative stress.
Effect of Ambrotose AO? on resting and exercise-induced antioxidant capacity and oxidative stress in healthy adults
Richard J Bloomer, Robert E Canale, Megan M Blankenship, Kelsey H Fisher-Wellman
Nutrition Journal , 2010, DOI: 10.1186/1475-2891-9-49
Abstract: 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.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.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.Oxidative stress may
Glycine propionyl-L-carnitine increases plasma nitrate/nitrite in resistance trained men
Richard J Bloomer, Webb A Smith, Kelsey H Fisher-Wellman
Journal of the International Society of Sports Nutrition , 2007, DOI: 10.1186/1550-2783-4-22
Abstract: In the present study, we sought to determine the impact of oral GPLC on plasma NOx at rest and in response to a period of reactive hyperemia in resistance trained men.Using a double blind, crossover design, 15 healthy men (24 ± 4 years) were assigned to GPLC (3 g/d PLC + 1044 mg glycine) and a placebo in random order, for a four-week period, with a two-week washout between condition assignment. Blood samples were taken from subjects at rest and at 0, 3, and 10 minutes following an ischemia-reperfusion protocol (six minutes of upper arm cuff occlusion at 200 mmHg followed by rapid reperfusion with cuff removal). Blood samples were taken from a forearm vein from the same arm used for the protocol and analyzed for total nitrate/nitrite. Data are presented as mean ± SEM.A condition main effect (p = 0.0008) was noted for NOx, with higher values in subjects when using GPLC (45.6 ± 2.8 μmol·L-1) compared to placebo (34.9 ± 1.2 μmol·L-1). No time main effect was noted (p = 0.7099), although values increased approximately 12% from rest (37.7 ± 2.7 μmol·L-1) to a peak at 10 minutes post protocol (42.3 ± 3.3 μmol·L-1). The interaction effect was not significant (p = 0.8809), although paired time contrasts revealed higher values for GPLC compared to placebo at 3 (48.2 ± 6.7 vs. 34.9 ± 2.4 μmol·L-1; p = 0.033) and 10 (48.8 ± 5.9 vs. 35.7 ± 2.1 μmol·L-1; p = 0.036) minutes post protocol, with non-statistically significant differences noted at rest (41.8 ± 4.5 vs. 33.6 ± 2.5 μmol·L-1; p = 0.189) and at 0 minutes (43.6 ± 5.1 vs. 35.4 ± 2.7 μmol·L-1; p = 0.187) post protocol. An analysis by subject (collapsed across time) indicated that 11 of the 15 subjects experienced an increase in NOx with GPLC treatment.These findings indicate that short-term oral GPLC supplementation can increase NOx in resistance trained men. However, as with many dietary supplements, there exist both "responders" and "non-responders" to treatment. Future work may focus on the mechanisms for the discrepancy i
Effect of oral acetyl L-carnitine arginate on resting and postprandial blood biomarkers in pre-diabetics
Richard J Bloomer, Kelsey H Fisher-Wellman, Patrick S Tucker
Nutrition & Metabolism , 2009, DOI: 10.1186/1743-7075-6-25
Abstract: Twenty-nine pre-diabetic men and women were randomly assigned to either 3 g·day-1 of ALCA (n = 14; 31 ± 3 yrs) or placebo (n = 15; 35 ± 3 yrs) in a double-blind design, to consume for eight weeks. Fasting blood samples were taken from subjects both pre and post intervention. After each fasting sample was obtained, subjects consumed a high fat, high carbohydrate meal and additional blood samples were taken at 1, 2, 4, and 6 hours post meal. Samples were analyzed for a variety of metabolic variables (e.g., glucose, HbA1c, lipid panel, C-reactive protein, nitrate/nitrite, and several markers of oxidative stress). Area under the curve (AUC) was calculated for each variable measured post meal, both pre and post intervention.ALCA, but not placebo, resulted in an increase in nitrate/nitrite (25.4 ± 1.9 to 30.1 ± 2.8 μmol·L-1) from pre to post intervention, with post intervention values greater compared to placebo (p = 0.01). No other changes of statistical significance were noted (p > 0.05), although ALCA resulted in slight improvements in glucose (109 ± 5 to 103 ± 5 mg·dL-1), HbA1c (6.6 ± 1.1 to 6.2 ± 1.2%), and HOMA-IR (3.3 ± 1.3 to 2.9 ± 1.2). AUC postprandial data were not statistically different between ALCA and placebo for any variable (p > 0.05). However, nitrate/nitrite demonstrated a moderate effect size (r = 0.35) for increase from pre (139.50 ± 18.35 μmol·L-1·6 hr-1) to post (172.40 ± 21.75 μmol·L-1·6 hr-1) intervention with ALCA, and the magnitude of decrease following feeding was not as pronounced as with placebo.Supplementation with ALCA results in an increase in resting nitrate/nitrite in pre-diabetics, without any statistically significant change in other metabolic or oxidative stress variables measured at rest or post meal.More than 70 million individuals within the United States alone currently live with cardiovascular disease [1], while nearly 21 million people have diabetes and 54 million are diagnosed with pre-diabetes [2]. Oxidative stress is suggeste
Dietary supplement increases plasma norepinephrine, lipolysis, and metabolic rate in resistance trained men
Richard J Bloomer, Kelsey H Fisher-Wellman, Kelley G Hammond, Brian K Schilling, Adrianna A Weber, Bradford J Cole
Journal of the International Society of Sports Nutrition , 2009, DOI: 10.1186/1550-2783-6-10
Abstract: Following publication of our recent article [1], we noticed an error in Figure 2 A. The units of measure on the y-axis should range from 0 to 100 pg ml-1 rather than 100–240 pg ml-1 as stated in the original article.The corrected Figure 2 is presented here (Figure 1). The results and conclusions of this article remain unchanged.
Dietary supplement increases plasma norepinephrine, lipolysis, and metabolic rate in resistance trained men
Richard J Bloomer, Kelsey H Fisher-Wellman, Kelley G Hammond, Brian K Schilling, Adrianna A Weber, Bradford J Cole
Journal of the International Society of Sports Nutrition , 2009, DOI: 10.1186/1550-2783-6-4
Abstract: 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.AUC was greater for the dietary supplement compared to the placebo for NE (1332 ± 128 pg·mL-1·90 min-1 vs. 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 < 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 > 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 > 0.05).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.The prevalence of obesity has grown to epidemic proportions within the United States in recent years, with an estimated 400 million peo
Effect of eicosapentaenoic and docosahexaenoic acid on resting and exercise-induced inflammatory and oxidative stress biomarkers: a randomized, placebo controlled, cross-over study
Richard J Bloomer, Douglas E Larson, Kelsey H Fisher-Wellman, Andrew J Galpin, Brian K Schilling
Lipids in Health and Disease , 2009, DOI: 10.1186/1476-511x-8-36
Abstract: Treatment with EPA/DHA resulted in a significant increase in blood levels of both EPA (18 ± 2 μmol·L-1 vs. 143 ± 23 μmol·L-1; p < 0.0001) and DHA (67 ± 4 μmol·L-1 vs. 157 ± 13 μmol·L-1; 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 H2O2) (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.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.Oxidative stress is a condition in which the production of reactive oxygen and nitrogen species (RONS) overwhelms the body's available antioxidant defenses, possibly resulting in oxidation within susceptible tissues [1]. This has been reported in response to both aerobic [2] and anaerobic [3] exercise, with over 300 original investigations published over the past 30 years [2]. While a low level of RONS production is necessary to maintain normal physiological function [4], as well as to allow for exercise-induced adaptations to the endogenous antioxidant defense system [5,6], excessive production of RONS can lead to the oxidation of lipids, proteins, and nucleic acids, potentially altering normal cellular function [7]. For example, acute and significant elevations in RONS may impair muscle force production [8], while more prolonged RONS production (possibly resulting from exercise overtraining) may impede exercis
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
Richard J Bloomer, Robert E Canale, Megan M Blankenship, Kelley G Hammond, Kelsey H Fisher-Wellman, Brian K Schilling
Lipids in Health and Disease , 2009, DOI: 10.1186/1476-511x-8-32
Abstract: Ten men (24 ± 4 yrs) and 10 women (22 ± 2 yrs) ingested Meltdown? 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 post hoc testing.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? compared to placebo for EPI (367 ± 58 pg·mL-1·6 hr-1 vs. 183 ± 27 pg·mL-1·6 hr-1; p = 0.01), NE (2345 ± 205 pg·mL-1·6 hr-1 vs. 1659 ± 184 pg·mL-1·6 hr-1; p = 0.02), glycerol (79 ± 8 μg·mL-1·6 hr-1 vs. 59 ± 6 μg·mL-1·6 hr-1; p = 0.03), FFA (2.46 ± 0.64 mmol·L-1·6 hr-1 vs. 1.57 ± 0.42 mmol·L-1·6 hr-1; p = 0.05), and kilocalorie expenditure (439 ± 26 kcal·6 hrs-1 vs. 380 ± 14 kcal·6 hrs-1; 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?. No sex × condition × time interactions were noted for any variable (p > 0.05).Ingestion of Meltdown? results in an increase in catecholamine secretion, lipolysis, and metabolic rate in young men and women, with a similar response for both sexes. Meltdown? 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.The prevalence of obesity has increased to epidemic proportions in rec
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