Exercise exerts both acute and chronic effects on plasma lipid and lipoprotein concentrations. Much of the triglyceride-lowering effect is an acute response, with the changes in cholesterol having a greater chronic component. The acute Tg decrease seems to be due to accelerated catabolism resulting from increased LPL activity. Following exercise, and on a more chronic basis, decreased VLDL-Tg synthesis may also occur in response to an increase in tissue insulin sensitivity. The low body fat content of endurance-trained athletes also contributes to lower Tg concentrations, through this same mechanism. The magnitude of the plasma Tg response to acute or chronic exercise is highly influenced by preexercise values--decreases in plasma Tg occur only when preexercise values are elevated. The major exercise effect on plasma cholesterol appears to be an increase in HDL-C as a result of endurance training, very likely related to the increase in LPL activity and Tg catabolism. This response is not always achieved with exercise training, and has been especially difficult to demonstrate in previously sedentary women. Exercise effects on HDL-C may be augmented by weight loss or changes in nutrient intake, but these interrelationships are not well established. A dose-response relationship exists, with the lower threshold influenced by baseline HDL-C values and exercise status. The higher HDL-C associated with endurance training is the result of increases in the less dense HDL2 subfraction, with elevations in both the lipid and protein components. Relatively small decreases in LDL-C occur with training. The biological mechanisms for these exercise effects have not been established.