mation of adenosine triphosphate, which fuels
muscle contraction, increases enormously (New-
sholme & Leech 1983). The formation of adeno-
sine triphosphate is driven by increased flux
through glycolysis and the tricarboxylic cycle.
Exercise mobilizes intramuscular fuels in the
form of glycogen and triacylglycerol to supply
glucose moieties and fatty acids, respectively.
Exogenous fuels, in the form of glucose and non-
esterified fatty acids (NEFA), are also taken up
from the blood and oxidized together with intra-
muscular fuels.
The glucose concentration in the blood,
however, remains relatively stable because the
rate of peripheral glucose uptake is matched by
the rate of release of glucose into the circulation.
Regulation of blood glucose concentration is
complex and, in addition to exercise, several hor-
mones participate in this regulation. Insulin is
the major hormone regulating the removal of
glucose from the blood. Glucose entering the
circulation may be absorbed from the intestine
(from food or glucose drinks) but most of the
time glucose is released from the liver as a result
of glycogen breakdown or glucose synthesized
via gluconeogenesis. During exercise, the con-
centrations of glucagon, catecholamines, cortisol
and growth hormone all increase and these
hormones stimulate glucose release from the
liver and ensure that blood glucose concentra-
tion remains relatively constant (Cryer & Gerich
1985). The hormones that stimulate glucose
release into the blood (and inhibit glucose
uptake) are often called counter-regulatory
hormones.
The rate of glucose uptake is elevated in skele-
tal muscle during exercise, although the insulin
concentration decreases during exercise. Several
studies have shown that glucose uptake is stimu-
lated by exercise, even in the absence of insulin
(Richter 1996) and the reduction of insulin con-
centration during exercise may be important for
avoiding hypoglycaemia (Cryer & Gerich 1985).
Insulin is a strong inhibitor of lipolysis in fat cells
and of glucose release from the liver. A fall in the
insulin concentration is important to optimize
the supply of NEFA to the contracting muscles.
458 special considerations
The decrease in basal insulin concentration
aids the release of NEFA from adipose tissue and
glucose from the liver.
During prolonged exercise, the concentration
of glycogen in skeletal muscles decreases and
glucose uptake from the blood becomes gradu-
ally more important. When skeletal muscles
are depleted of glycogen, glucose uptake may
account for nearly all carbohydrate oxidation
(Wahren et al.1971). When the liver is depleted of
glycogen, glucose is released at much lower rates
and the blood glucose concentration decreases. A
decrease in blood glucose concentration is well
recognized as a major factor in the fatigue
that accompanies endurance exercise, and the
reduced supply of carbohydrate to the central
nervous system and to the muscle may both be
factors in the fatigue process (Costill & Harg-
reaves 1992).
The intensity of exercise is also an important
determinant of the rate of carbohydrate utiliza-
tion. During exercise of an intensity of about 50%
ofV.
o2max., the energy comes equally from fat and
carbohydrate metabolism and, as the intensity
of the exercise increases, the percentage contri-
bution from carbohydrates rises. At intensities
of exercise above 80% V.
o2max., carbohydrates
become the major metabolic fuel. At this inten-
sity of exercise, glucose uptake is also much
higher, and depletion of liver glycogen will occur
in 1–2 h followed by a decrease in concentration
of blood glucose. During exercise of short dura-
tion and high intensity, on the other hand, the
hepatic glucose output can exceed the rate of
glucose uptake and lead to hyperglycaemia.Regulation of carbohydrate and
fat metabolism after exercise
The ability to convert chemical energy to fuel
skeletal muscle contraction is essential for
human movement. Skeletal muscles have,
however, also an important role for regulation of
the blood glucose concentration, as most of the
glucose disposal stimulated by insulin occurs in
skeletal muscle (Shulman et al.1990).
After a carbohydrate-rich meal, the increased