A key regulatory point in the TCA cycle is the
reaction catalysed by citrate synthase. The activ-
ity of this enzyme is inhibited by ATP, NADH,
succinyl-CoA and fatty acyl-CoA; the activity of
the enzyme is also affected by citrate availability.
Hence, when cellular energy levels are high, flux
through the TCA cycle is relatively low, but can
be greatly increased when ATP and NADH uti-
lization is increased, as during exercise.
Hormones
Many hormones influence energy metabolism in
the body (for a detailed review, see Galbo 1983).
During exercise, the interaction between insulin,
glucagon and the catecholamines (adrenaline
and noradrenaline) is mostly responsible for fuel
substrate availability and utilization; cortisol and
growth hormone also have some significant
effects.
Insulin is secreted by the b-cells of the islets of
Langerhans in the pancreas. Its basic biological
effects are to inhibit lipolysis and increase the
uptake of glucose from the blood by the tissues,
especially skeletal muscle, liver and adipose
tissue; the cellular uptake of amino acids is also
stimulated by insulin. These effects reduce the
plasma glucose concentration, inhibit the release
of glucose from the liver, promote the synthesis
of glycogen (in liver and muscle), promote syn-
thesis of lipid and inhibit FFA release (in adipose
tissue), increase muscle amino acid uptake and
enhance protein synthesis. The primary stimulus
for increased insulin secretion is a rise in the
blood glucose concentration (e.g. following a
meal). Exercise usually results in a fall in insulin
secretion.
Glucagon is secreted by the a-cells of the pan-
creatic islets and basically exerts effects that are
opposite to those of insulin. It raises the blood
glucose level by increasing the rate of glycogen
breakdown (glycogenolysis) in the liver. It also
promotes the formation of glucose from non-
carbohydrate precursors (gluconeogenesis) in
the liver. The primary stimulus for increased
secretion of glucagon is a fall in the concentration
32 nutrition and exercise
of glucose in blood. During most types of exer-
cise, the blood glucose concentration does not
fall, but during prolonged exercise, when liver
glycogen stores become depleted, a drop in the
blood glucose concentration (hypoglycaemia)
may occur.
The catecholamines adrenaline and noradren-
aline are released from the adrenal medulla.
Noradrenaline is also released from sympathetic
nerve endings and leakage from such synapses
appears to be the main source of the noradrena-
line found in blood plasma. The catecholamines
have many systemic effects throughout the body,
including stimulation of the heart rate and con-
tractility and alteration of blood vessel diame-
ters. They also influence substrate availability,
with the effects of adrenaline being the more
important of the two. Adrenaline, like glucagon,
promotes glycogenolysis in both liver and
muscle (see Fig. 2.6). Adrenaline also promotes
lipolysis in adipose tissue, increasing the avail-
ability of plasma FFA and inhibits insulin secre-
tion. The primary stimulus for catecholamine
secretion is the activation of the sympathetic
nervous system by stressors such as exercise,
hypotension and hypoglycaemia. Substantial
increases in the plasma catecholamine concentra-
tion can occur within seconds of the onset of
high-intensity exercise. However, the relative
exercise intensity has to be above about 50%
V.
o2max. in order to significantly elevate the
plasma catecholamine concentration.
Growth hormone, secreted from the anterior
pituitary gland, also stimulates mobilization of
FFA from adipose tissue and increases in plasma
growth hormone concentration are related to
the intensity of exercise performed. During
prolonged strenuous exercise, cortisol secretion
from the adrenal cortex is increased. Cortisol is a
steroid hormone that increases the effectiveness
of the actions of catecholamines in some tissues
(e.g. its actions further promote lipolysis in
adipose tissue). However, its main effects are to
promote protein degradation and amino acid
release from muscle and to stimulate gluconeo-
genesis in the liver. The primary stimulus to