| Popis: |
Impaired lipid metabolism at rest has been linked to the development of insulin resistance and an attenuation of plasma concentration of the hormone adiponectin. However, it has been suggested that increasing fatty acid oxidation at rest, via exercise or otherwise, may augment plasma adiponectin. The current literature addressing changes substrate utilization and possible direct effects on adiponectin during and following exercise is not well established. Therefore, the purpose of this dissertation was to examine concomitant changes in adiponectin and substrate utilization both at rest and during various exercise modalities, as this may provide implications for improving metabolic responses and in turn, affect insulin sensitivity. Pre-, mid-, and post-exercise measurements were obtained for five separate studies. Each study incorporated a single, unique exercise modality, which included: acute aerobic, chronic aerobic, acute resistance, chronic resistance, or acute stretching exercise. Chronic resistance training significantly increased adiponectin levels, although resting substrate utilization did not significantly change pre- to post-exercise. All acute exercise modalities significantly increased glucose utilization during exercise. However, none of the acute exercise modalities nor the chronic aerobic exercise modality elicited significant changes in adiponectin. First degree family history of type 2 diabetes mellitus had a significant inverse correlation with adiponectin concentration, whereas regular aerobic exercise had a significant direct correlation with adiponectin. Body fat percentage and body mass index did not have significant inverse correlations with adiponectin. These results suggest that substrate utilization does not directly affect adiponectin concentration and that the regulation of this hormone is likely dependent on other factors. The results do, however, highlight the importance of implementing a chronic exercise training program to limit the development of insulin resistance, especially in populations genetically predisposed to type 2 diabetes mellitus. |
