Endogenous triacylglycerols represent an
important source of fuel for endurance exercise. Triacylglycerol
oxidation increases progressively during exercise; the specific
rate is determined by energy requirements of working muscles,
fatty acid delivery to muscle mitochondria, and the oxidation of
other substrates. The catecholamine response to exercise increases
lipolysis of adipose tissue triacylglycerols and, presumably, intramuscular
triacylglycerols. In addition, increases in adipose tissue
and muscle blood flow decrease fatty acid reesterification and
facilitate the delivery of released fatty acids to skeletal muscle.
Alterations in fatty acid mobilization and the relative use of adipose
and intramuscular triacylglycerols during exercise depend,
in large part, on degree of fitness and exercise intensity. Compared
with untrained persons exercising at the same absolute
intensity, persons who have undergone endurance training have
greater fat oxidation during exercise without increased lipolysis.
Available evidence suggests that the training-induced increase in
fat oxidation is due primarily to increased oxidation of nonplasma-derived
fatty acids, perhaps from intramuscular triacylglycerol
stores. Fat oxidation is lower in high-intensity exercise
than in moderate-intensity exercise, in part because of decreased
fatty acid delivery to exercising muscles. Parenteral lipid supplementation
during high-intensity exercise increases fat oxidation,
but the effect of ingesting long-chain or medium-chain triacylglycerols
on substrate metabolism during exercise is less clear.
This review discusses the relation between fatty acid mobilization
and oxidation during exercise and the effect of endurance training,
exercise intensity, and lipid supplementation on these
responses.