NUTRITION IN SPORT

(Martin Jones) #1
Conclusion

The carbohydrate stores of the body, liver and
muscle glycogen, are utilized immediately at
start of exercise. Glucose output from the liver
closely matches the increased glucose require-
ment of the contracting muscles, keeping the
blood glucose concentration unchanged during
submaximal exercise. Blood glucose levels are
normally seen only to increase in the initial
period of intense exercise and to fall when the
hepatic glycogen store is depleted near to
exhaustion. The regulation of the hepatic glucose
release is a complex process dependent on both
hormonal control and feedback signals from con-
tracting muscles.
Glucose uptake by exercising muscle is
directly related to exercise intensity and regu-
lated by muscle blood flow and facilitated by
increased glucose transport capacity of the
plasma membrane of the contracting muscle. The
maximal rate of glucose uptake at a normal blood
glucose concentration is about 0.4 mmol · min–1·
kg–1exercising muscle. Glucose utilization is also
dependent on the glucose phosphorylation
capacity mediated by the activity of hexokinase.
The major carbohydrate store of the body is
muscle glycogen, which is used in concert with
the hepatic glycogen store to provide the exercis-
ing muscle with energy.
The rate of utilization is low at rest and during
low-intensity exercise, when blood-borne glu-
cose and free fatty acids are the major sources of
fuel for ATP resynthesis. With increasing exercise
intensity, the use of carbohydrate as an energy
substrate increases gradually to cover almost all
the energy demand of contraction at exercise
intensities near the subject’s maximal oxygen
uptake. The maximal rate of oxidative energy
production from muscle glycogen is of the order
of 35 mmol ATP · min–1·kg–1exercising muscle,
corresponding to a glycogen degradation rate of
1 mmol · min–1·kg–1 wet muscle. The mecha-
nism(s) controlling the integration of fat and car-
bohydrate utilization during exercise are poorly
understood and, as yet, unresolved.
The muscle glycogen store can also produce


94 nutrition and exercise


ATP anaerobically and at a rate that is twice that
of oxidative ATP regeneration. Anaerobic energy
delivery can be activated within milliseconds,
while the aerobic energy production needs
several minutes to reach a steady state. Thus,
anaerobic carbohydrate utilization will be im-
portant as an energy provider during the transi-
tion period between rest and exercise and during
periods of intense exercise when the energy
demand of contraction exceeds the capacity of
oxidative ATP regeneration.
It can be concluded that carbohydrate is used
as fuel at onset of exercise at all intensities and is
an obligatory fuel for the continuation of exercise
at intensities above 50–60% of the subject’s
maximal oxygen uptake. Depletion of the muscle
carbohydrate stores will impair exercise perfor-
mance at this range of exercise intensities.
Exhaustion of the liver glycogen store during
prolonged exercise results in hypoglycaemia
which also impairs continued exercise
performance.
Carbohydrate metabolism in exercising
muscle is initiated by Ca^2 +release from the sar-
coplasmic reticulum and thereafter is regulated
by the rate of ATP degradation via the phospho-
rylation state of the high-energy phosphate pool
(ATP, ADP, AMP, PCr) and Pi. AMP and Pi
concentrations regulate the flux through the
glycolytic pathway while Ca^2 +and pyruvate con-
centrations are the main regulators of PDH activ-
ity which, together with the intramitochondrial
concentration of ADP, determines the rate of car-
bohydrate oxidation. The result is a tight match-
ing of ATP generation from carbohydrate sources
with the ATP demand of contracting muscle.
Other influences on carbohydrate metabolism
during exercise include diet, training status and
hormonal balance.

References

Ahlborg, G. & Felig, P. (1982) Lactate and glucose
exchange across the forearm, legs and splanchnic
bed during and after prolonged leg exercise. Journal
of Clinical Investigation 69 , 45–54.
Ahlborg, G., Felig, P., Hagenfeldt, L., Hendler, R. &
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