strenuous, continuous cycling exercise have
observed no effect of increased blood glucose
availability on net muscle glycogen utilization,
either measured directly from biopsy samples
(Fig. 8.2) (Fielding et al.1985; Coyle et al.1986,
1991; Flynn et al.1987; Hargreaves & Briggs 1988;
Mitchellet al.1989; Widrick et al.1993; Bosch et al.
1994) or estimated from total CHO oxidation and
tracer-determined glucose uptake (Jeukendrup
et al.1998). Decreases in glycogen use during
cycling have been reported (Erikson et al.1987),
during the latter stages of prolonged exercise
(Boschet al.1996), with a large increase in blood
glucose (Bergström & Hultman 1967) and during
intermittent exercise protocols (Hargreaves et al.
1984; Yaspelkis et al.1993). In two of these studies
(Hargreaves et al.1984; Erikson et al.1987), the
results are potentially confounded by higher pre-
exercise muscle glycogen levels in the control
trial which influences the subsequent rate of
degradation (Hargreaves et al.1995). It is possible
that during intermittent exercise with periods of
rest or low-intensity exercise, CHO ingestion
may result in glycogen synthesis (Kuipers et al.
1987) and a reduction in net muscle glycogen use.
On balance, however, the effects of CHO inges-
tion on muscle glycogen use during prolonged,
strenuous cycling exercise appear relatively
small. In contrast, recent studies during treadmill
running indicate that CHO ingestion reduces net
muscle glycogen use, specifically in the type I
fibres (Tsintzas et al.1995, 1996a), and that the
114 nutrition and exercise
increase in muscle glycogen availability late in
exercise contributed to the enhanced endurance
capacity that was observed (Tsintzas et al.1996a).
The ingestion of CHO results in lower plasma
free fatty acid levels during prolonged exercise
(Coyleet al.1983, 1986; Murray et al.1989a, 1989b,
1991; Davis et al.1992; Tsintzas et al.1996a). The
effects of CHO ingestion during exercise on fat
oxidation do not appear to be as great as those
observed with pre-exercise CHO ingestion, most
likely as a consequence of the smaller increases in
plasma insulin levels which, while still blunting
lipolysis and the exercise-induced increase in
plasma free fatty acid levels (De Glisezinski et al.
1998; Horowitz et al.1998), may result in a
smaller initial increase in muscle glucose uptake
and relatively less inhibition of intramuscular
lipid oxidation (Horowitz et al.1998).Practical aspects of CHO ingestion
during exercise
Type of CHO
There appear to be relatively few, if any, differ-
ences between glucose, sucrose and malto-
dextrins in their effects on metabolism and
performance when ingested during exercise
(Massicotte et al. 1989; Murray et al. 1989a;
Hawleyet al.1992; Wagenmakers et al.1993). In
contrast, fructose alone is not as readily oxidized
as other CHO sources (Massicotte et al.1989) due(a) (b) (c)
*Hepatic glucose productionMuscle glucose uptake (g)Net muscle glycogen utilization (mmol.kg–1
)
120100806040200*120100806040200*120100806040200Fig. 8.2(a) Total hepatic glucose
production, (b) muscle glucose
uptake, and (c) net muscle
glycogen utilization during 2 h of
exercise at 70–74% V.
o2peakwith
( ) and without ( ) ingestion of
CHO. Values are means±SEM
(n=6 – 7). *, difference from no
ingestion of CHO, P<0.05. Data
from Coyle et al.(1986) and
McConellet al.(1994).