The project has just begun as protocol 08-H-0108.
The aims of the study are to address and answer these scientific and public health questions: 1) Are the determinants of endothelial function different when weight loss is achieved in conjunction with improved fitness versus improved fitness alone? For example, does improved insulin sensitivity or reduced levels of C-reactive protein, anticipated with weight loss, add anything to multivariate modeling for endothelial predictors beyond improved fitness alone? Are predictors different for obese versus overweight women? Post-menopausal versus premenopausal? Caucasian versus African-American? 2) Does increased nitric oxide bioavailability (manifest as improved endothelial function) have any role in reducing arterial stiffness, independent of changes in exercise fitness, adiposity, insulin sensitivity, lipid levels, C-reactive protein, adiponectin? Or can arterial compliance improve with improved exercise fitness alone in the absence of improvement in endothelial function? Are there important age interactions? 3) Is there a difference in the relationship of body size to exercise fitness at study entry or after exercise training--with or without weight loss--between Caucasian and African-American women? 4) Does improved fitness with weight loss (versus improved fitness alone) change atheroprotective HDL subparticle composition (HDL2, pre--HDL) and function (resistance to oxidation, protection from inflammation, cholesterol efflux) and if so, are these independent of changes in HDL cholesterol levels, reduction in fat mass, improvement in insulin sensitivity or treatment with hormone therapies (oral contraceptives, hormone replacement therapy)? 5) What magnitude of fat mass reduction is required for increased insulin sensitivity? Any differences between obese versus overweight women? Post-menopausal versus premenopausal? Caucasian versus African-American? 6) Do levels of C-reactive protein in overweight or obese women correlate with other markers of inflammation? Do improved fitness and weight loss reduce levels of C-reactive protein greater than improved fitness alone, and are there correlations with changes in fat mass? With changes in adiponectin? 7) Do the structured exercises change other daily physical activities? Since the exercises typically represent only small amount of time and energy spent during the day, even small compensatory reduction in spontaneous physical activity accumulated over time can significantly alter the effectiveness of the weight loss intervention. Similarly, do the exercises modify the amount or patterns of food intake, enhance or impede continued dietary interventions? How do these components of energy balance interact in different individuals and regulate weight loss? 8) Do nutrition education sessions in combination with physical activity (versus physical activity alone) in the worksite setting result in greater weight loss? 9) Do nutrition education sessions (versus physical activity alone) in the worksite setting result in changes in dietary intake choices (energy, macronutrients, fatty acids, fiber)? The primary endpoint will be measure of endothelial function at baseline and following 6 months of program participation, with comparison of change between subjects randomized to exercise coupled with weight-loss intervention versus those randomized to exercise alone. Secondary endpoints will include comparisons of changes in dietary intake, adiposity, arterial stiffness, lipoprotein metabolites/functionality, insulin sensitivity and markers of inflammation. Secondary endpoints will include comparisons of changes in dietary intake, adiposity, arterial stiffness, lipoprotein metabolites/functionality, insulin sensitivity and markers of inflammation in blood between subjects randomized to exercise coupled with weight-loss intervention versus those randomized to exercise alone, with exploratory analyses of minorities and age/hormonal status interactions.
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