NUTRITION IN SPORT

glycogen levels decline. The utilization of blood
glucose is greater at higher workrates and
increases with exercise duration during pro-
longed submaximal exercise and peaks after
about 90 min (Fig. 2.9). The decline in blood
glucose uptake after this time is attributable to
the increasing availability of plasma FFA as fuel
(which appears to directly inhibit muscle glucose
uptake) and the depletion of liver glycogen
stores.
At marathon-running pace, muscle CHO
stores alone could fuel about 80 min of exercise
before becoming depleted (Table 2.3). However,
the simultaneous utilization of body fat and
hepatic CHO stores enables ATP production to
be maintained and exercise to continue. Ulti-
mately, though, ATP production becomes com-
promised due to muscle and hepatic CHO stores
becoming depleted and the inability of fat oxida-
tion to increase sufficiently to offset this deficit.
The rate of ATP resynthesis from fat oxidation
alone cannot meet the ATP requirement for exer-
cise intensities higher than about 50–60% V

.
o2max..
It is currently unknown which factor limits the
maximal rate of fat oxidation during exercise (i.e.

36 nutrition and exercise

why it cannot increase to compensate for CHO

depletion), but it must precede acetyl-CoA for-

mation, as from this point fat and CHO share the

same fate. The limitation may reside in the rate of

uptake of FFA into muscle from blood or the

transport of FFA into the mitochondria rather

than in the rate of b-oxidation of FFA in the

mitochondria.

It is generally accepted that the glucose–fatty

acid cycle regulates the integration of CHO

and fat oxidation during prolonged exercise.

However, whilst this may be true of resting

muscle, recent evidence (Dyck et al. 1993) sug-

gests that the cycle does not operate in exercising

muscle and that the site of regulation must reside

elsewhere (e.g. at the level of phosphorylase

and/or malonyl-CoA). From the literature, it

would appear that the integration of muscle

CHO and fat utilization during prolonged exer-

cise is complex and unresolved.

The glycogen store of human muscle is fairly

insensitive to change in sedentary individuals.

However, the combination of exercise and

dietary manipulation can have dramatic effects

on muscle glycogen storage. A clear positive rela-

tionship has been shown to exist between muscle

glycogen content and subsequent endurance

performance. Furthermore, the ingestion of CHO

during prolonged exercise has been shown to

decrease muscle glycogen utilization and fat

mobilization and oxidation, and to increase the

rate of CHO oxidation and endurance capacity. It

is clear therefore that the contribution of orally

ingested CHO to total ATP production under

these conditions must be greater than that nor-

mally derived from fat oxidation. The precise

biochemical mechanism by which muscle glyco-

gen depletion results in fatigue is presently unre-

solved (Green 1991). However, it is plausible that

the inability of muscle to maintain the rate of ATP

synthesis in the glycogen depleted state results in

ADP and Piaccumulation and consequently

fatigue development.

Unlike skeletal muscle, starvation will rapidly

deplete the liver of CHO. The rate of hepatic

glucose release in resting postabsorptive individ-

uals is sufficient to match the CHO demands of

Fig. 2.9Changes in the relative contributions of the
major fuel sources to ATP resynthesis during
prolonged submaximal exercise at an intensity
equivalent to about 70% V

.
o2max.(approximately 10
times the resting metabolic rate). , blood glucose;
, plasma free fatty acids;
, muscle glycogen and
triacylglycerol.

Rate of ATP resynthesis

0

(rest) Exercise duration (min)

30 60 90 120

25%

25%

50%

33%

36%

31%

41%

45%

14%

30%

62%

8%