regulated by malonyl-CoA (Winder et al.1989).
During exercise, malonyl-CoA formation is
reduced and therefore the capacity to transport
FAs across the mitochondrial inner membrane is
enhanced.
The rate of oxidation of FA is the result of three
processes:
1 Lipolysis of TG in adipose tissue and circulat-
ing TG and transport of FA from blood plasma to
the sarcoplasm.
2 Availability and rate of hydrolysis of intramus-
cular TG.
3 Activation of the FA and transport across the
mitochondrial membrane.
It is likely that the first two processes pose the
ultimate limitations to fat oxidation observed
during conditions of maximal FA flux. This is
most evident during both short-term intense
exercise or during the initial phase of a long-term
exercise. In this condition, lipolysis in adipose
tissue and in muscle TG is insufficiently upregu-
lated to result in enhanced FA supply. The result
will be that the rate of FA oxidation exceeds the
rate at which FAs are mobilized, leading to a fall
in plasma FAs and intracellular FAs in muscle. As
a consequence, the use of CHO from glycogen
must be increased to cover the increased energy
demand.
Direct evidence that the rate of FA oxidation
can be limited by a suppression of lipolysis, at
least during low-to-moderate intensity (44% of
V
.
o2max.) exercise, comes from a recent investiga-
tion by Horowitz et al. (1997). They showed that
CHO ingestion (0.8 g · kg–1 body mass) before
exercise, which resulted in a 10–30mU·ml–1
elevation in plasma insulin concentration, was
enough to reduce fat oxidation duringexercise,
primarily by a suppression of lipolysis. They also
showed that fat oxidation could be elevated (by
about 30%) when plasma FA concentration was
increased via Intralipid and heparin infusion,
even when CHO was ingested. However, the
increase in lipolysis was not sufficient to restore
fat oxidation to those levels observed after
fasting. Taken collectively, these results suggest
that CHO ingestion (and the concomitant eleva-
tion in plasma insulin concentration) has another
(additional) effect on reducing the rates of FA
oxidation by exercising skeletal muscle.Conclusion
In contrast to body CHO reserves, fat stores are
abundant in humans and represent a vast source
of fuel for exercising muscle. FAs stored both in
peripheral adipose tissue and inside the muscle
cells serve as quantitatively important energy
sources for exercise metabolism. During low-
intensity work (25% of V.
o2max.), plasma FA liber-
ated from adipose tissue represents the main
source of fuel for contracting muscle, with little
or no contribution from intramuscular lipolysis
to total energy metabolism. On the other hand,
during moderate-intensity exercise (65% of
V.
o2max.), fat metabolism is highest, with the con-
tribution of lipolysis from peripheral adipocytes
and of intramuscular TG stores contributing
about equally to total fat oxidation. During high-
intensity exercise (85% of V.
o2max.), there is a
marked reduction in the rate of entry of FA into
the plasma, but no further increase in intramus-
cular TG utilization. At such workrates, muscle
glycogenolysis and the accompanying increased
lactate concentration suppress the rates of
whole-body lipolysis.
The major hormonal changes which promote
lipolysis during exercise are an increase in cate-
cholamine concentration and a decline in insulin
levels, both of which facilitate activation of LPL.
The rate of FA oxidation is also regulated indi-
rectly by the oxidative capacity of the working
muscles and the intramuscular concentration
of malonyl-CoA. The muscle tissue level of
malonyl-CoA is dependent on the prevailing
concentrations of plasma glucose and insulin:
elevated circulating levels of these two com-
pounds is associated with elevated concentra-
tions of malonyl-CoA. Any increase in glycolytic
flux therefore may directly inhibit long-chain FA
oxidation, possibly by inhibiting its transport
into the mitochondria (Sidossis & Wolfe 1996;
Sidossiset al. 1996; Coyle et al. 1997).