Although the hypotriacylglycerolemic effect of exercise was described more than 40 years ago, the mechanisms responsible for triacylglycerol (TAG)-lowering have just recently started to be elucidated. Delayed-onset hypotriacylglycerolemia in the basal state, 1 day after a single bout of endurance exercise is due to augmented efficiency of very low-density lipoprotein (VLDL)-TAG removal from the circulation, likely mediated by the secretion of fewer but TAG-richer VLDL particles from the liver; exercise-induced changes in skeletal muscle lipoprotein lipase are more likely a contributing rather than the primary factor of TAG-lowering. This illustrates, in vivo, how changes in VLDL-apolipoprotein B-100 metabolism in the liver can effect changes in VLDL-TAG metabolism in the periphery. The exercise-induced increase in basal VLDL-TAG clearance rate plateaus at approximately 40%, whereas the threshold of energy that needs to be expended during endurance exercise lies near or above 500-600 kcal. Resistance exercise is more potent than endurance exercise in this respect. Exercise-induced changes in basal hepatic VLDL-TAG secretion 12-24h after exercise are not negligible but span around zero; available data indicates that reduced hepatic VLDL-TAG secretion rate may be responsible for the persistence of hypotriacylglycerolemia at later time points (>or=48 h) after exercise cessation, or following training. Our understanding of the mechanisms leading to TAG-lowering after exercise has advanced considerably in recent years, but much remains to be learned.