Ae. Jeukendrup et R. Jentjens, Oxidation of carbohydrate feedings during prolonged exercise - Current thoughts, guidelines and directions for future research, SPORT MED, 29(6), 2000, pp. 407-424
Although it is known that carbohydrate (CHO) feedings during exercise impro
ve endurance performance, the effects of different feeding strategies are l
ess clear. Studies using (stable) isotope methodology have shown that not a
ll carbohydrates are oxidised at similar rates and hence they may not be eq
ually effective. Glucose, sucrose, maltose, maltodextrins and amylopectin a
re oxidised at high rates. Fructose, galactose and amylose have been shown
to be oxidised at 25 to 50% lower rates. Combinations of multiple transport
able CHO may increase the total CHO absorption and total exogenous CHO oxid
ation. Increasing the CHO intake up to 1.0 to 1.5 g/min will increase the o
xidation up to about 1.0 to 1.1 g/min. However, a further increase of the i
ntake will not further increase the oxidation rates. Training status does n
ot affect exogenous CHO oxidation. The effects of fasting and muscle glycog
en depletion are less clear.
The most remarkable conclusion is probably that exogenous CHO oxidation rat
es do not exceed 1.0 to 1.1 g/min. There is convincing evidence that this l
imitation is not at the muscular level but most likely located in the intes
tine or the liver. intestinal perfusion studies seem to suggest that the ca
pacity to absorb glucose is only slightly in excess of the observed entranc
e of glucose into the blood and the rate of absorption may thus be a factor
contributing to the limitation. However, the liver may play an additional
important role, in that it provides glucose to the bloodstream at a rate of
about 1 g/min by balancing the glucose from the gut and from glycogenolysi
s/gluconeogenesis. It is possible that when large amounts of glucose are in
gested absorption is a limiting factor, and the liver will retain some gluc
ose and thus act asa second limiting factor to exogenous CHO oxidation.