Theses and Dissertations from UMD
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Item REGULATORY EFFECTS OF ACUTE AND CHRONIC ENDURANCE EXERCISE ON NITRIC OXIDE AND REACTIVE OXYGEN SPECIES IN HUMAN CIRCULATING ANGIOGENIC CELLS(2011) Jenkins, Nathan Thomas; Hagberg, James M; Kinesiology; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)This dissertation research comprised three studies examining the effects of acute and chronic endurance exercise on circulating angiogenic cells (CACs). Because the balance between nitric oxide (NO) and reactive oxygen species (ROS) is a critical aspect of the physiological function/dysfunction of CACs, each study determined the effects of exercise on NO-ROS balance within a variety of CAC types. Study #1 demonstrated that regular endurance exercise is associated with greater basal intracellular NO levels in cultured CACs, and that one mechanism underlying this association was increased NADPH oxidase enzyme activity in the sedentary state. Study #2 suggested an association between a sedentary lifestyle and increased nitro-oxidative stress in freshly-isolated CD34+ progenitor cells. Study #3 demonstrated that prior exercise attenuates high-fat meal induced-increases in mitochondrial-derived intracellular ROS in CD31+ CACs. Overall, it is concluded that acute and chronic endurance exercise enhance intracellular NO and ROS dynamics in CACs.Item Circulating biomarkers of nitro-oxidative stress in young and older active and inactive men(2010) Bjork, Lori; Hagberg, James M; Kinesiology; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)Oxidative stress markers may be novel factors contributing to cardiovascular (CVD) risk. The purpose of this study was to examine the effects of long-term exercise, age, and their interaction on the plasma levels of the oxidative stress markers oxidized LDL (ox-LDL), nitrotyrosine, and myeloperoxidase (MPO), and to investigate whether these levels correlated with plasma NOx levels. Older (62 ± 2 yr) active (n=12) men who had exercised regularly for over 30 years and young (25 ± 4 yr) active (n=7) men who had exercised regularly for over 3 years were matched to older (n=11) and young (n=8) inactive males. Young subjects showed lower plasma nitrotyrosine levels than older subjects (P = 0.047). Young inactive subjects had higher ox-LDL levels than either the young active (P = 0.042) or the older active (P = 0.041) subjects. In addition, plasma oxidative stress levels, particularly ox-LDL, were correlated with various conventional CVD risk factors, and in older subjects were associated with Framingham risk score (r = 0.49, P = 0.015). The study found no relationships between plasma markers of oxidative stress and plasma NOx levels. The findings suggest that a sedentary lifestyle may be associated with higher ox-LDL levels and that the levels of oxidative stress markers may contribute to CVD risk.Item Effect of long-term exercise on endothelial progenitor cells in healthy humans(2008-04-24) Witkowski, Sarah; Hagberg, James M; Kinesiology; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)Endothelial progenitor cells (EPCs) are derived from the bone marrow and have been found to play a role in postnatal neovascularization and re-endothelialization. Reduced EPC number and function have been associated with death from cardiovascular diseases, CVD risk factors, and endothelial dysfunction. Oxidative stress, specifically, oxidized LDL (OxLDL) has been shown to decrease EPC number and function, and increase EPC senescence in vitro. Regular physical activity is related to lower rates of CVD; however the mechanisms underlying the benefits of exercise in the prevention of CVD are not fully clear. Exercise may improve the number, and function of EPCs while improving oxidative stress status. The primary purpose of this study was to compare CD34+/KDR+ EPC number, EPC clonogenic capacity, and senescence, in healthy men that have participated in greater than 20 years of moderate- to high-intensity exercise with low-active control subjects. To assess the effect of physical inactivity on these markers, a subset of exercisers (n=10) stopped exercising for 10 days after which, measures of EPC number, colony forming units, and senescence, endothelial function and oxidative stress were re-evaluated. Results showed that, CD34+/KDR+ cell number, CFU-Hill colonies, and EPC senescence were not statistically different between athlete and control groups. CD34+/KDR+ cell number was closely related to endothelial function. Specifically, the forearm blood flow response to reactive hyperemia was correlated with CD34+/KDR+ number in sedentary participants. Additionally, 5 athletes significantly decreased their CD34+/KDR+ number, which was related to a significant decline in endothelial function, indicating that regular physical activity is important for some athletes to maintain healthy endothelial function, perhaps through the maintenance of elevated number of circulating CD34+/KDR+ cells. CFU-Hill colony number was strongly correlated with hyperemic blood flow response in control participants and related to oxLDL independent of physical activity status. Athletes who participated in 10-days of exercise detraining demonstrated a significant decrease in EPC senescence, which was related to improved total antioxidant capacity. Overall, these results show that CD34+/KDR+ number is closely related to endothelial function. Moreover, the function of EPCs appears to be affected by oxidative stress and antioxidant availability.Item Influence of AT1R polymorphisms and aerobic exercise training on angiotensin II, oxidative stress and urinary nitric oxide(2007-04-26) Fenty, Nicola Melissa; Hagberg, James M; Kinesiology; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)Oxidative stress is implicated in the pathogenesis of cardiovascular disease (CVD) and angiotensin II (AngII), via the type 1 receptor (AT1R), is a major factor contributing to oxidative stress. Protection against oxidative injury is provided by several antioxidants, including superoxide dismutase (SOD). Aerobic exercise training (AEX) is a non-pharmacological intervention that reduces the risk of CVD, partly through reducing levels of oxidative stress. We investigated whether the AT1R A1166C and -825 T/A polymorphisms and AEX influence oxidative stress, urinary NOx and plasma AngII. One hundred sedentary, hypertensive individuals underwent 6 months of standardized AEX. Plasma levels of AngII and SOD, and urinary excretion of NOx and 8-iso-PGF2α were measured before and after AEX. Subject characteristics and baseline values of outcome variables were similar among all genotype groups. Overall, there was a significant increase in 8-iso-PGF2α (p = 0.002) and a significant decrease in NOx excretion (p = 0.0001) however, there were no significant changes in SOD activity or AngII levels with AEX. Neither oxidative stress markers nor urinary NOx were significantly different between genotype groups with AEX. There was a significant difference in AngII levels with AEX between A1166C genotype groups (p = 0.04) resulting in a significant interactive effect of the A1166C polymorphism and AEX on the change in AngII (p < 0.05). The TT genotype group of the -825 T/A polymorphism had a significant reduction (p = 0.02) in plasma AngII, while there was no change in carriers of the A allele. Risk allele analysis revealed that there was a significant reduction in plasma AngII (p = 0.04), a significant increase in 8-iso-PGF2α (p = 0.01) and a significant decrease in urinary NOx (p = 0.0001) with AEX in individuals with 2 risk alleles. Our findings suggest that variation in the AT1R gene is associated with differential changes in plasma AngII but not with oxidative stress. Furthermore, our results may have clinical implications for the prescription of AEX in a population at risk for CVD as exercise intensities that surpass moderate intensity, may attenuate some of the beneficial effects of regular exercise by leading to increased oxidative stress.Item Evaluating the Effects of Weight Loss on Exercise-Induced Oxidative Stress in Obese/Overweight Soliders(2006-08-03) Andrews, Anne; Kantor, Mark A; Nutrition; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)Exercise is known to increase reactive oxygen species, a condition recognized as oxidative stress. Obese individuals may experience even greater amounts of oxidative stress after exercise compared to normal weight people. It is not clear how weight loss affects exercise-induced oxidative stress in overweight subjects. The objectives of this study were to 1) evaluate the effect of the Army Physical Fitness Test (APFT) on biomarkers of oxidative stress in overweight/obese soldiers 2) determine the effects of dietary antioxidants, fitness level, body composition on exercise-induced oxidative stress, and 3) determine the effect of weight loss on changes in biomarkers of oxidative stress as a result of the APFT. A total of 60 subjects (35 M, 25 F) were recruited. After completing the 1st APFT (n=47), subjects followed a 3-month weight loss program and then completed the 2nd APFT (n=29). Blood measurements of the oxidative stress biomarkers creatine kinase (CK), C-reactive protein (CRP), glutathione peroxidase (GPX), and superoxide dismutase (SOD) were taken pre, immediately after and 24hrs after each exercise test. Dietary antioxidant intake, fitness level and body composition were also assessed at each APFT. After completing the 1st APFT, subjects showed a significant increase in CK and CRP levels immediately post-exercise and in CK at 24hrs post-exercise. There was a significant decrease in GPX immediately post-exercise but no significant change in SOD following exercise. Each of the oxidative stress biomarkers were found to be influenced by the antioxidant vitamins A, C and E, fitness level, total fat mass and total fat percentage. There were also significant interactions between fitness level and vitamins A, C, and E, and between fitness level and total fat mass and total fat percentage. There was no significant effect of attempted weight loss on the exercise-induced changes in the biomarkers, but there were significant changes in BMI, fat mass and fat percentage after the weight loss period. In conclusion, the APFT produced oxidative stress in overweight subjects which was not affected by attempted weight loss. Changes in oxidative stress biomarkers at the different time points were significantly affected by dietary antioxidants, fitness level, and body composition.Item LOX-1 genotype, dietary fat intake, and aerobic exercise training: Influence on endothelial function, oxidative stress, lipoprotein-lipids, and soluble LOX-1(2006-07-25) Ellis, Tina Janelle; Hagberg, James M.; Kinesiology; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)The lectin-like oxidized LDL receptor (LOX-1) is the major receptor for oxidized LDL (ox-LDL) in endothelial cells and plays a major role in the initiation and progression of atherosclerosis. Ox-LDL via LOX-1 causes endothelial activation and injury, induces lipid peroxidation, and alters inflammatory gene expression, and variation in the LOX-1 gene has been associated with cardiovascular disease risk. In addition, a soluble form of LOX-1 has been identified in plasma and may predict atherosclerotic disease progression. Thus, the purpose of this study was to investigate the effect of the LOX-1 3'UTR C/T and G501C polymorphisms on endothelial function, oxidative stress, plasma lipoprotein-lipids, and soluble LOX-1. The effect of these polymorphisms on the responses to dietary fat intake and aerobic exercise training was also examined. Forearm blood flow was measured using venous occlusion plethysmography at rest and during reactive hyperemia, and plasma levels of nitrates/nitrites, nitrotyrosine, ox-LDL, total antioxidant capacity, lipoprotein-lipids, and soluble LOX-1 were measured before and after six months of aerobic exercise training. The dietary ratio of polyunsaturated fat to saturated fat (P:S ratio) was determined using 7-day food records. The 3'UTR/CC and 501GC+CC groups had significantly higher baseline soluble LOX-1 levels than the CT/TT and GG groups, respectively. The G501C polymorphism was a significant predictor of baseline soluble LOX-1 levels, even after accounting for age, gender, race, BMI, and the 3'UTR polymorphism (p=0.024). There was a significant interaction between the 3'UTR polymorphism and dietary fat intake for plasma ox-LDL levels (p=0.011). At a high P:S ratio, the 3'UTR/CC group had significantly higher ox-LDL levels than the TT group (p=0.025). The opposite relationship was found at a low P:S ratio (p=0.044). The 3'UTR polymorphism also influenced changes in plasma TG levels with exercise training (p=0.036), while the G501C polymorphism influenced changes in soluble LOX-1 levels (p=0.012). In conclusion, variation in the LOX-1 gene does not appear to be associated with endothelial function, oxidative stress, or plasma lipid levels, but may influence changes in these variables in response to dietary fat intake and exercise training. Moreover, polymorphisms in LOX-1, especially the G501C polymorphism, may regulate circulating levels of soluble LOX-1.