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The purpose of this study was to examine the caloric intake and energy output of swimmers and runner during normal daily activities and training. Daily and energy expenditure of twenty college varsity swimmers and runners were measured. Four groups of subjects were categorized as male runners, female runners, male swimmers, and female swimmers with five subjects in each group. An additional twenty runners and swimmers recorded only dietary intake. Despite a large difference in body weight and body fat, the mean daily caloric intake was similar for the two groups (male swimmers: 3377 Kcal/d-1, male runners: 3463 Kcal/d-1, female swimmers: 2491 Kcal/d-1, female runners: 2037 Kcal/d-1). Comparison of data normalized for body weight showed that male runners were more active than swimmers. Male runners burned more calories (53.3 Kcal/kg. d-1) in a twenty four hour period than swimmers (47.6 Kcal/kg.d-1). In the case of the females, the trend was reversed. Female swimmers expended more calories (45 Kcal/kg .d-1) than runners (38.9 Kcal/kg.d-1) despite a lower food intake. Consequently, caloric intake and life style does not seem to explain body fat difference between runners and swimmers. The data in this study suggest that the greater body fat found in swimmers may be related to a physiological adaptation induced by swim training.

Thesis (Ph. D.)--University of Washington, 1999. / Vita. Includes bibliographical references (leaves 75-77).

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SIRT1 (sirtuin 1), a mammalian ortholog of the longevity regulator yeast Sir2p, elicits diversified functions by mediating NAD+ -dependent deacetylation of protein targets. SIRT1 contributes to the beneficial effects of calorie restriction, the non-genetic intervention capable of promoting longevity and reducing the incidence of age-related disorders. In mammals, SIRT1 acts as a metabolic regulator in response to environmental stress signals. Activation of SIRT1 protects mice against diet-induced obesity and insulin resistance. However, the tissue specific metabolic functions of SIRT1 remain to be defined. The present study shows that over-expression of human SIRT1 selectively in adipose tissue decreases circulating lipid levels, reduces whole body fat mass, and elevates systemic insulin sensitivity. By contrast, over-expression of a dominant-negative human SIRT1 mutant H363Y in adipose tissue accelerates the development of aging-associated insulin resistance. Activation or down-regulation of adipose SIRT1 promotes lipid mobilization towards different metabolic organs and alters biotin homeostasis in opposite manners. Adipose SIRT1 positively regulates lipid metabolism, genes expression and adipokines secretion which are negatively influenced by SIRT1 H363Y mutant. Biotin is a water soluble vitamin and plays an important role in energy metabolism. The present study shows that biotin and its metabolites are the endogenous inhibitors of SIRT1 enzymatic activity. Chronic biotin supplementation abolishes adipose SIRT1-mediated beneficial effects on lipid metabolism. These effects are partly explained by the regulation of acetyl-CoA carboxylase (ACC), a key regulator of lipid metabolism and biotin homeostasis. SIRT1 selectively deacetylates and negatively regulate the protein stability of ACC. Over-expression of SIRT1 in fat cells persistently down-regulates ACC expression. The direct interaction between SIRT1 and ACC are subjected to rapid regulation by nutrient status which can explain the beneficial effect of SIRT1 in energy homeostasis. In mice subjected to chronic treatment with biotin, the interactions between SIRT1 and ACC were significantly inhibited. Taken in conjunction, the above findings reveal that SIRT1 in adipose tissue functions to regulate systemic energy metabolism and insulin sensitivity. In particular, it plays a critical role in modulating ACC protein levels and biotin homeostasis in adipose tissue, which in turn facilitate lipid storage and utilization in response to nutrient level changes. / published_or_final_version / Pharmacology and Pharmacy / Doctoral / Doctor of Philosophy

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Diss. (sammanfattning) Uppsala : Uppsala universitet, 2009. / Härtill 4 uppsatser.