sugars. Fructose metabolism takes place pre-
dominantly in the liver (Zakin et al. 1969),
whereas the majority of glucose appears to
bypass the liver and be stored or oxidized by the
muscle (Maehlum et al. 1978). When infused,
fructose has been found to result in a four times
greater liver glycogen storage than glucose
(Nilsson & Hultman 1974). On the other hand, a
considerably higher glycogen storage rate has
been demonstrated in skeletal muscle after
glucose than after fructose infusion (Bergström &
Hultman 1967c).
The similar rates of glycogen storage for the
sucrose and glucose supplements could not be
accounted for by Blom et al. (1987). Sucrose con-
tains equimolar amounts of glucose and fructose.
If muscle glycogen storage was chiefly depen-
dent on the glucose moiety of the disaccharide,
one should expect a lower rate of glycogen
storage from sucrose than from a similar amount
of glucose. One possible explanation provided
by Blom et al. (1987) was that fructose, by virtue
of its rapid metabolism in the liver, compared
with that of glucose, inhibits the postexercise
hepatic glucose uptake, thereby rendering a large
proportion of absorbed glucose available for
muscle glycogen resynthesis.
solid vs. liquid supplements
The form in which the carbohydrate is provided
has also been investigated. Keizer et al. (1986)
found that providing approximately 300 g of
carbohydrate in either liquid or solid form
after exercise resulted in a glycogen storage rate
of approximately 5mmol·g–1wet weight · h–1over
the first 5 h of recovery. However, these solid
feedings contained a substantial amount of fat
and protein that is typically not found in liquid
supplements. Therefore, Reed et al. (1989) com-
pared the postexercise glycogen storage rates
following liquid and solid carbohydrate supple-
ments of similar compositions. Again there were
no differences noted between the two treatments.
The average glycogen storage rates for the liquid
and solid supplements were 5.1 and 5.5mmol·g–1
wet weight · h–1, respectively.
influence of type of exercise
As previously indicated, during prolonged bouts
of exercise in which muscle and liver glycogen
concentrations are reduced and hypoglycaemia
results, muscle glycogen synthesis is typically
5–6mmol · g–1wet weight · h–1, provided an ade-
quate carbohydrate supplement is consumed.
However, if the exercise rapidly reduces the
muscle glycogen concentration, resulting in
elevated blood and muscle lactate, synthesis of
glycogen can be very rapid even in the absence of
a carbohydrate supplement. Hermansen and
Vaage (1977) depleted the muscle glycogen levels
of their subjects by multiple 1-min maximal exer-
cise bouts on a cycle ergometer. During the first
30 min of recovery, the rate of muscle glycogen
synthesis averaged 33.6mmol·g–1wet weight ·
h–1. The increase in muscle glycogen was found
to parallel the decline in muscle lactate, which
had increased to 26.4mmol·g–1wet weight after
the last exercise bout. MacDougall et al. (1977)
also found a relatively rapid rate of storage after
muscle glycogen depletion when subjects per-
formed 1-min cycling sprints at 150% of V.
o2max.
to exhaustion. The difference in storage rates fol-
lowing prolonged exercise, as opposed to high-
intensity exercise, can probably be explained by
the availability of substrate for muscle glycogen
synthesis. With multiple high-intensity sprints,
glycogen depletion is accompanied by hypergly-
caemia and elevated blood and muscle lactate
concentrations, which can be used immediately
as substrate for glycogen synthesis. By contrast,
prolonged sustained exercise severely reduces
the endogenous precursors of muscle glycogen,
thereby requiring an exogenous carbohydrate
source for rapid muscle glycogen synthesis.
Exercise that results in muscle damage also
affects muscle glycogen synthesis. Sherman et al.
(1983) found that after a marathon, restoration of
muscle glycogen was delayed and that this delay
was related to muscle damage caused by the run
(Hikidaet al. 1983; Sherman et al. 1983). Eccentric
exercise which involves the forced lengthening
of active muscles and the transfer of external
power from the environment to the muscle