It has been proposed that exercise may confer protection against coronary heart disease by inducing changes in plasma lipoproteins and especially high density lipoprotein (HDL) subfractions that are associated with a reduced incidence of this condition. This thesis examines the effects of different forms of exercise and dietary variation on HDL, to determine whether exercise-induced changes in HDL subfractions are consistent with their role in providing protection against coronary heart disease. No changes were observed in the concentration of low density lipoprotein cholesterol (LDL-C), very low density lipoprotein cholesterol (VLDL-C), HDL-cholesterol (HDL-C) or HDL particle size after acute bouts of exercise. However, a significant increase in the concentration of HDL3-C and a significant decrease in HDL2-C was evident following a 21 km and a 42 km race. In a series of prolonged walks on different diets, progressive and significant increases in the concentration of HDL-C (HDL2) occurred during walking on mixed and high-fat diets. These changes were accompanied by significant reductions in the concentration of VLDL-C and increases in the particle size of HDL. In contrast, walking on a high-carbohydrate diet was followed by a significant decrease in the concentration of HDL-C and increase in the concentration of VLDL-C and VLDL-triglyceride (VLDL-TG). In the absence of exercise, a similar but less pronounced response was observed during and after the high-fat diet, whereas a greater decrease in the concentration of HDL-C occurred during the high-carbohydrate diet. Under each set of experimental conditions, changes in the proportion of apoprotein E-rich HDL, a subfraction of HDL that has been implicated in a direct mechanism of coronary protection, appeared to be unrelated to increases in HDL-C and HDL particle size. These results therefore indicated that variation in diet can profoundly influence the effects of exercise upon HDL subfractions and suggest that prolonged walking may, in part, confer health benefit through HDL facilitating the clearance of TG-rich lipoproteins.