Thesis (M.S.)--University of Wisconsin--La Crosse, 2003. / Includes bibliographical references.

Thesis (D.P.E.)--Springfield College, 2003. / Includes bibliographical references.

Thesis (M.A.)--University of North Carolina at Chapel Hill, 2004. / Includes bibliographical references (leaves 30-33).

Thesis (M.S.)--University of Wisconsin--La Crosse, 2002. / Includes bibliographical references.

Thesis (M.S.)--Michigan State University, 2005. / Includes bibliographical references (leaves 143-147)

Thesis (Ph.D.)--University of Nebraska-Lincoln, 2007. / Title from title screen (site viewed July 9, 2007). PDF text: vii, 77 p. UMI publication number: AAT 3247183. Includes bibliographical references. Also available in microfilm and microfiche formats.

Thesis (Ph. D.)--University of California, San Diego, 2007. / Title from first page of PDF file (viewed May 25, 2007). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 112-121).

Thesis (M. Sc.)(Biochemistry)--University of Pretoria, 2006. / Includes bibliographical references. Available on the Internet via the World Wide Web.

The overarching aim of this thesis was to examine factors that affect post-exercise glycaemia and contribute to minimising the risk of hypoglycaemia after exercise. An inability to regulate circulating insulin concentrations is considered the primary gluco-regulatory defect within T1DM. Therefore, the aim of chapter 3 was to examine the effects of pre-exercise rapid-acting insulin reductions on blood glucose responses before and after running in T1DM individuals, to test the hypothesis that reducing pre-exercise insulin dose may help preserve post-exercise glycaemia. The results demonstrate that a 75% reduction to pre-exercise rapidacing insulin dose best preserved blood glucose before and after exercise, without increasing the risk of ketoacidosis, and reduced the risk of hypoglycaemia in free living conditions for 24 hours following running. An important factor determining blood glucose concentrations and subsequent patterns of fuel oxidation is the rate of appearance of carbohydrate into the circulation. Potentially, low GI carbohydrates may raise blood glucose less and increase the percentage contribution of lipids as a fuel because of a slower digestion. Therefore, the aim of chapter 4 was to examine the metabolic and blood glucose responses to ingestion of a high or low GI carbohydrate, combined with a 75% reduced insulin dose, before, during and for 24 hours after running. The results demonstrate that compared to a high GI carbohydrate, the low GI carbohydrate increased blood glucose concentrations less before exercise and maintained blood glucose better for 24 hours after running, via lower carbohydrate and higher lipid oxidation rates during the latter stages of running. After manipulating both the insulin dose and the pre-exercise carbohydrate GI, to improve post-exercise blood glucose concentrations, the timing of the ingestion of carbohydrate (alongside a reduced insulin dose) before exercise is an important factor which may further refine these strategies. Therefore, chapter 5 examined the metabolic and blood glucose responses to alterations in the timing of carbohydrate feeding and insulin administration prior to running. Our results demonstrated that administration of both a reduced rapid-acting insulin dose and low GI carbohydrate 30 minutes before exercise improved glycaemia for 24 hours after running, by reductions in carbohydrate oxidation, leading to increased carbohydrate availability post-exercise.

The impact of acute resistance exercise (RE) on glycaemia in type 1 diabetes (T1DM) individuals is poorly understood. Yet, such knowledge would have great use in improving our understanding of blood glucose control during and after the performance of RE. Increasing research in this area might help minimise complications associated with blood glucose vulnerability and potentially maximise health benefits related to RE which are known to be obtained by people without diabetes. The overarching aim of this thesis was to examine the impact of acute RE on glycaemia in T1DM individuals, and promote confidence in people with T1DM to partake in this form of exercise and lead a more physically active lifestyle. Exercise volume, or the total weight lifted during a RE session, is a primary component in the design of a RE session. Therefore, Chapter 3 examined the acute impact of manipulating RE session volume in T1DM individuals. The results demonstrate that exercise volume is an important factor in determining the blood glucose responses to RE; specifically, blood glucose concentrations rose above rest for one hour after one and two sets of similar intensity RE, but this exercise-induced hyperglycaemia was attenuated by increasing the volume of exercise by addition of a similar intensity third set of RE. Additionally, performing morning RE after an overnight fast and in the absence of rapid-acting insulin, did not induce acute hypoglycaemia, ketoacidosis or raise a marker of muscle damage, but caused metabolic acidosis in a dose-dependent fashion. Exercise intensity is a characteristic that is integral to the design of a RE session, and this characteristic might play a role in explaining the exercise-induced hyperglycaemia caused by the thirty minute (two-set) RE sessions in Chapter 3. The aim of Chapter 4 was to examine the impact of manipulating exercise intensity in T1DM individuals. The findings from this study demonstrate that performing a low intensity RE session evoked a similar magnitude of post-exercise hyperglycaemia and metabolic acidosis than a higher intensity RE session, when sessions were matched for total weight lifted. In an attempt to alleviate the consistent exercise-induced hyperglycaemia presented by the two-set RE session, the aim of Chapter 5 was to implement a modified algorithm that delivers an individualized dose of rapid-acting insulin after morning RE, to counter acute post-exercise hyperglycaemia in T1DM individuals. The results demonstrate that post-exercise rapid-acting insulin injection delivered by means of an algorithm resulted in reductions to post-RE hyperglycaemia without the occurrence of hypoglycaemia during two hours after exercise. However, during the subsequent twenty hours of freely living conditions, T1DM individuals remained unprotected from post-exercise hypoglycaemia as per a control condition. Overall, the findings of this thesis underpin some important factors that determine the glycaemic and metabolic responses to acute performance of RE, which may facilitate the better management of blood glucose around this form of exercise, in T1DM individuals.