The aim of the present study was to compare the metabolic fate of repeated doses of fructose or glucose ingested every 30 min during long-duration moderate-intensity exercise in men. Healthy volunteers exercised for 3 h on a treadmill at 45% of their maximal oxygen consumption rate. "Naturally labeled" [13C]glucose or [13C]fructose was given orally at 25-g doses every 30 min (total feeding: 150 g; n = 6 in each group). Substrate utilization was evaluated by indirect calorimetry, and exogenous sugar oxidation was measured by isotope ratio mass spectrometry on expired CO2. Results were corrected for baseline drift in 13C/12C ratio in expired air due to exercise alone. Fructose conversion to plasma glucose was measured combining gas chromatography and isotope ratio mass spectrometry. Most of the ingested glucose was oxidized: 81 +/- 4 vs. 57 +/- 2 g/3 h for fructose (2P < 0.005). Exogenous glucose covered 20.8 +/- 1.4% of the total energy need (+/- 6.7 MJ) compared with 14.0 +/- 0.6% for fructose (2P < 0.005). The contribution of total carbohydrates was significantly higher and that of lipids significantly lower with glucose than with fructose. The blood glucose response was similar in both protocols. From 90 to 180 min, 55-60% of circulating glucose was derived from ingested fructose. In conclusion, when ingested repeatedly during moderate-intensity prolonged exercise, fructose is metabolically less available than glucose, despite a high rate of conversion to circulating glucose.

This study attempted to induce a major shift in the utilization of endogenous substrates during exercise in men by the use of a potent inhibitor of adipose tissue lipolysis, Acipimox, and to see to what extent this affects the 13C/12C ratio in expired air CO2. Six healthy volunteers exercised for 3 h on a treadmill at approximately 45% of their maximum O2 uptake, 75 min after having ingested either a placebo or 250 mg Acipimox. The rise in plasma free fatty acids and glycerol was almost totally prevented by Acipimox, and no significant rise in the utilization of lipids, evaluated by indirect calorimetry, was observed. Total carbohydrate oxidation averaged 128 +/- 17 (placebo) and 182 +/- 21 g/3 h (Acipimox). Conversely, total lipid oxidation was 84 +/- 5 (placebo) and 57 +/- 6 g/3 h (Acipimox; P < 0.01). Under placebo, changes in expired air CO2 delta 13C were minimal, with only a 0.49/1000 significant rise at 30 min. In contrast, under Acipimox, the rise in expired air CO2 delta 13C averaged 1/1000 and was significant throughout the 3-h exercise bout; in these conditions calculation of a "pseudooxidation" of an exogenous sugar naturally or artificially enriched in 13C, but not ingested, would have given an erroneous value of 19.8 +/- 2.6 g/3 h. Thus under conditions of extreme changes in endogenous substrate utilization, an appropriate control experiment is mandatory when studying exogenous substrate oxidation by 13C-labeled substrates and isotope-ratio mass spectrometry measurements on expired air CO2.

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The measurement of breath 13CO2/12CO2 is commonly used during exercise to evaluate the oxidation rate of exogenous carbohydrates enriched in 13C. The aim of this study was to investigate whether exercise itself affects the 13C/12C ratio in expired air CO2 in relation to exercise intensity. The relative abundance of 13C and 12C in expired air CO2 was determined by isotoperatio mass spectrometry and expressed as delta 13C (in %o) by using Craig's formula and calibrated standards. Five healthy young men exercised on a treadmill after an overnight fast during > or = 105 min on four occasions and in a randomized order. Work rates were performed at approximately 30, 45, 60, and 75% of their maximal O2 uptake (VO2max). Delta 13C in expired air CO2 and respiratory exchange ratio (RER) were determined every 15 or 30 min during exercise. At 30 and 45% VO2max, a slight and not statistically significant increase in delta 13C was observed at 30 min. In contrast, at 60 75% VO2max, the rise was statistically significant and averaged 0.83 and 0.99%o, respectively. Average delta 13C (between 0 and 105 min) progressively increased with the intensity of exercise. Individual values of delta 13C and RER were positively correlated (r = 0.653, P = 0.002) as were values of delta 13C and endogenous carbohydrates utilized (r = 0.752, P < 0.001). Factitious or "pseudooxidation" of a 13C-enriched exogenous glucose load (indeed noningested) was calculated from the changes in expired air delta 13C. Over the whole period of exercise it was not statistically significant at 30 and 40% VO2max. However, over the first 60 min of exercise, such pseudooxidation of exogenous glucose was significant at 30 and 45% VO2max. In conclusion, by modifying the mix of endogenous substrates oxidized, exercise at 60% VO2max and above significantly increases the 13C/12C ratio in expired air CO2. At these intensities, this could lead to overestimation of the oxidation of 13C-labeled substrates given orally. At lower intensities of exercise, such overestimation is much smaller an affects mainly the values recorded during the initial part of the exercise bout.

No abstract