In practice, this is usually exercise intensities
between 60% and 85% of maximal oxygen con-
sumption. Continuous exercise of any longer
duration (i.e. an intensity of less than 60% of
maximal oxygen consumption) is probably not
limited by substrate availability and, providing
adequate hydration is maintained, can probably
be sustained for several hours or even days!
Unlike maximal intensity exercise, the rate of
muscle ATP production required during pro-
longed exercise is relatively low (<2.5 mmol · kg–1
dm · s–1) and therefore PCr, carbohydrate and fat
can all contribute to ATP resynthesis. However,
carbohydrate is without question the most
important fuel source.
It can be calculated that the maximum rate
of ATP production from carbohydrate oxidation
will be approximately 2.0–2.8 mmol · kg–1
dm · s–1(based upon a maximum oxygen con-
sumption of 3–4 l · min–1), which corresponds to
a glycogen utilization rate of approximately
4 mmol · kg–1dm · min–1. Therefore, it can be seen
that carbohydrate could meet the energy require-
ments of prolonged exercise. However, because
the muscle store of glycogen is in the region of
350 mmol · kg–1dm, under normal conditions, it
can be calculated that it could only sustain in the
region of 80 min of exercise. This was demon-
strated in the 1960s by Bergström and Hultman
(1967). The authors also demonstrated that if the
glycogen store of muscle was increased by
dietary means, exercise duration increased in
parallel (Bergström et al. 1967). Of course, carbo-
hydrate is also delivered to skeletal muscle from
hepatic stores in the form of blood glucose and
this can generate ATP at a maximum rate of
approximately 1 mmol · kg–1dm · s–1.
The majority of hepatic glucose release during
exercise (1.5–5.5 mmol · min–1) is utilized by
skeletal muscle. Only 0.5 mmol · min–1is utilized
by extramuscular tissue during exercise. Muscle
glucose utilization is dependent on glucose
supply, transport and metabolism. If blood
glucose is unchanged, as in the majority of exer-
cise conditions, glucose supply to muscle is dic-
tated by muscle blood flow, which increases
linearly with exercise intensity and can increase
90 nutrition and exercise
by 20-fold from rest to maximal exercise. The
increase in muscle glucose delivery as a result of
the exercise- mediated increase in blood flow is
probably more important for muscle glucose
uptake during exercise than the insulin and con-
traction-induced increase in membrane glucose
transport capacity (see Richter & Hespel 1996).
As exercise continues, plasma insulin concentra-
tion declines, which facilitates hepatic glucose
release and reduces glucose utilization by extra-
muscular tissue. However, insulin supply to
muscle probably remains elevated above basal
supply due to the contraction-induced elevation
in muscle blood flow.
Hexokinase is responsible for the phosphory-
lation of glucose by ATP when it enters the
muscle cell. The enzyme is allosterically inhib-
ited by glucose-6-phosphate, the product of the
hexokinase reaction and an intermediate of gly-
colysis. Thus, during short-term high-intensity
exercise and at the onset of prolonged sub-
maximal exercise, glucose phosphorylation by
hexokinase will be inhibited by glucose-6-
phosphate accumulation. This will increase the
concentration of glucose in the extra- and intra-
cellular water and will contribute to the increase
in blood glucose observed during high-intensity
exercise. However, as submaximal exercise
continues, the decline in muscle glucose-6-
phosphate results in an increase in glucose
phosphorylation.
In comparison with muscle glycogen metabo-
lism, relatively little is known about the inter-
action between exercise and hepatic glycogen
metabolismin man. This is not because of a lack of
interest but because of the invasive nature of the
liver biopsy technique. The few studies that have
been performed in healthy volunteers using this
technique have demonstrated that the rate of
liver glucose release in the postabsorptive state is
in the region of 0.8 mmol glucose · min–1, which
is sufficient to meet the carbohydrate demands
of the brain and obligatory glucolytic tissues.
Approximately 60% of this release (0.5 mmol ·
min–1) is derived from liver glycogen stores and
the remainder is synthesized by gluconeogenesis
in the liver using lactate, pyruvate, glycerol and