only the central nervous system. Approximately
70% of this release is derived from liver CHO
stores and the remainder from liver gluconeoge-
nesis. During exercise, the rate of hepatic glucose
release has been shown to be related to exercise
intensity. Ninety percent of this release is derived
from liver CHO stores, ultimately resulting in
liver glycogen depletion.
Thus, CHO ingestion during exercise could
also delay fatigue development by slowing the
rate of liver glycogen depletion and helping
to maintain the blood glucose concentration.
Central fatigue is a possibility during prolonged
exercise and undoubtedly the development of
hypoglycaemia could contribute to this.
Metabolic adaptation to
exercise training
Adaptations to aerobic endurance training
include increases in capillary density and mito-
chondrial size and number in trained muscle.
The activity of TCA cycle and other oxidative
enzymes are increased with a concomitant
increase in the capacity to oxidize both lipid and
CHO. Training adaptations in muscle affect
substrate utilization. Endurance training also
increases the relative cross-sectional area of type
I fibres, increases intramuscular content of tri-
acylglycerol, and increases the capacity to use fat
as an energy source during submaximal exercise.
Trained subjects also appear to demonstrate an
increased reliance on intramuscular triacylglyc-
erol as an energy source during exercise. These
effects, and other physiological effects of train-
ing, including increased maximum cardiac
output and V
.
o2max., improved oxygen delivery to
working muscle (Saltin 1985) and attenuated
hormonal responses to exercise (Galbo 1983),
decrease the rate of utilization of muscle glyco-
gen and blood glucose and decrease the rate of
accumulation of lactate during submaximal exer-
cise. These adaptations contribute to the marked
improvement in endurance capacity following
training.
Alterations in substrate use with endurance
training could be due, at least in part, to a lesser
degree of disturbance to ATP homeostasis during
exercise. With an increased mitochondrial oxida-
tive capacity after training, smaller decreases in
ATP and PCr and smaller increases in ADP and Pi
are needed during exercise to balance the rate of
ATP synthesis with the rate of ATP utilization. In
other words, with more mitochondria, the
amount of oxygen as well as the ADP and Pi
required per mitochondrion will be less after
training than before training. The smaller
increase in ADP concentration would result in
less formation of AMP by the myokinase reac-
tion, and also less IMP and ammonia would be
formed as a result of AMP deamination. Smaller
increases in the concentrations of ADP, AMP, Pi
and ammonia could account for the slower rate
of glycolysis and glycogenolysis in trained than
in untrained muscle.
Training for strength, power or speed has little
if any effect on aerobic capacity. Heavy resistance
training or sprinting bring about specific changes
in the immediate (ATP and PCr) and short-term
(glycolytic) energy delivery systems, increases in
muscle buffering capacity and improvements in
strength and/or sprint performance. Heavy
resistance training for several months causes
hypertrophy of the muscle fibres, thus increasing
total muscle mass and the maximum power
output that can be developed. Stretch, contrac-
tion and damage of muscle fibres during exercise
provide the stimuli for adaptation, which
involves changes in the expression of different
myosin isoforms.References
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