Oxidation of carbohydrate feedings during prolonged exercise - Current thoughts, guidelines and directions for future research

Citation
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
Citations number
88
Categorie Soggetti
Ortopedics, Rehabilitation & Sport Medicine
Journal title
SPORTS MEDICINE
ISSN journal
01121642 → ACNP
Volume
29
Issue
6
Year of publication
2000
Pages
407 - 424
Database
ISI
SICI code
0112-1642(200006)29:6<407:OOCFDP>2.0.ZU;2-Z
Abstract
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.