Thesis--Auburn University, 2005. / Abstract. Vita. Includes bibliographical references (leaves 76-90).

Thesis (MSc (Physiology))--University of Pretoria, 2007. / Includes bibliographical references. Also available in print format.

Thesis (doctoral)--Lund University, 1998. / Added t.p. with thesis statement inserted.

Thesis (M.S.)--Virginia Polytechnic Institute, 1946. / Includes bibliographical references (leaves 49-52). Also available via the Internet.

Thesis (doctoral)--Lund University, 1998. / Added t.p. with thesis statement inserted.

Thesis (Ph.D.) - University of Queensland, 2003. / Includes bibliography.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1966. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

No description available.

Low-fat, high-carbohydrate diets are recommended by various scientific bodies for the prevention of coronary heart disease. However, these diets increase postprandial lipaemia and so their net benefit for coronary heart disease risk has been the subject of vigorous debate. Exaggerated postprandial lipaemia has been implicated in the development of atherosclerosis. Previous research suggests that physical exercise improves triacylglycerol metabolic capacity. The present thesis investigated whether exercise, when simultaneously adopted with a high-carbohydrate diet, could prevent the augmentation of postprandial lipaemia observed with this dietary change.

Currently no previous study has isolated the independent influence of body fat (BF) on thermoregulatory responses from the confounding biophysical factors of body mass and metabolic heat production (Hprod). Therefore, seven lean (L, BF:10.7 ± 4.1%) and seven non-lean (NL, BF:32.2 ± 6.4%) males matched for total body mass (TBM, L: 87.8 ± 8.5 kg, NL: 89.4 ± 7.8 kg; P= 0.73), cycled for 60 min in a 28.2 ±0.2˚C and 27 ± 10% RH room at i) a Hprod of 546 W; and ii) a Hprod of 7.5 W·kg lean body mass (LBM). Rectal (Tre) and esophageal (Tes) temperatures, and local sweat rate (LSR) were measured continuously; while whole body sweat loss (WBSL) was measured from 0-60 mins. At 546 W, changes in Tre (L: 0.74 ± 0.16ºC, NL: 0.83 ± 0.14ºC), mean local sweat rate (MLSR) based on an average of upper-back and forearm local sweat rates (L: 0.65 ± 0.25, NL: 0.59±0.12 mgcm-2min-1) and WBSL (L: 568 ± 28 mL, NL: 567 ± 29 mL) were similar (P>0.58). At 7.5 W·kg LBM, the L group had greater changes in Tre (L: 0.87 ± 0.16ºC, NL: 0.55 ± 0.11ºC), MLSR (L: 0.83 ±0 .38, NL: 0.41 ± 0.13 mgcm-2min-1) and WBSL (L: 638 ± 19 mL, NL: 399 ± 17 mL) (P<0.05). In conclusion, i) body fat does not independently alter thermoregulatory responses during exercise; ii) core temperature comparisons between groups differing in BF should be performed using a Hprod normalized for TBM, not LBM.