Fructose–Maltodextrin Ratio Governs Exogenous and Other CHO Oxidation and Performance

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Fructose coingested with glucose in carbohydrate (CHO) drinks increases exogenous-CHO oxidation, gut comfort, and physical performance.


This study aimed to determine the effect of different fructose–maltodextrin–glucose ratios on CHO oxidation and fluid absorption while controlling for osmolality and caloricity.


In a crossover design, 12 male cyclists rode 2 h at 57% peak power then performed 10 sprints while ingesting artificially sweetened water or three equiosmotic 11.25% CHO-salt drinks at 200 mL·15 min−1, comprising weighed fructose and maltodextrin–glucose in ratios of 0.5:1 (0.5 ratio), 0.8:1 (0.8 ratio), and 1.25:1 (1.25 ratio). Fluid absorption was traced with D2O, whereas 14C-fructose and 13C-maltodextrin–glucose permitted fructose and glucose oxidation rate evaluation.


The mean exogenous-fructose and exogenous-glucose oxidation rates were 0.27, 0.39, and 0.46 g·min−1 and 0.65, 0.71, and 0.58 g·min−1 in 0.5, 0.8, and 1.25 ratio drinks, representing mean oxidation efficiencies of 54%, 59%, and 55% and 65%, 85%, and 86% for fructose and glucose, respectively. With the 0.8 ratio drink, total exogenous-CHO oxidation rate was 18% (90% confidence interval, ±5%) and 5.2% (±4.6%) higher relative to 0.5 and 1.25 ratios, respectively, whereas respective differences in total exogenous-CHO oxidation efficiency were 17% (±5%) and 5.3% (±4.8%), associated with 8.6% and 7.8% (±4.2%) higher fructose oxidation efficiency. The effects of CHO ratio on water absorption were inconclusive. Mean sprint power with the 0.8 ratio drink was moderately higher than that with the 0.5 ratio (2.9%; 99% confidence interval, ±2.8%) and 1.25 ratio (3.1%; ±2.7%) drinks, with total- and endogenous-CHO oxidation rate, abdominal cramps, and drink sweetness qualifying as explanatory mechanisms.


Enhanced high-intensity endurance performance with a 0.8 ratio fructose–maltodextrin–glucose drink is characterized by higher exogenous-CHO oxidation efficiency and reduced endogenous-CHO oxidation. The gut-hepatic or other physiological site responsible requires further research.

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