The first purpose of the study was to examine whether combined ingestion of glucose and sucrose at an intake rate of 1.2 g/min would lead to higher oxidation rates compared with the ingestion of an isocaloric amount of glucose or sucrose alone. The second aim of the study was to investigate whether a mixture of glucose and sucrose when ingested at a high rate (2.4 g/min) would result in exogenous CHO oxidation rates higher than 1.2 to 1.3 g/min. Eight trained cyclists (maximal oxygen consumption: 64 +/- 2 mL . kg -1 . min -1 , mean +/- SE) performed 5 exercise trials in random order. Each trial consisted of 120 minutes of cycling at 50% maximum power output (63% +/- 2% maximal oxygen consumption), whereas subjects received a solution providing either 1.2 g/min of glucose (GLU), 1.2 g/min of sucrose (SUC), 0.6 g/min of glucose + 0.6 g/min of sucrose (M-GLU+SUC), 1.2 g/min of glucose + 1.2 g/min of sucrose (H-GLU+SUC), or water (WAT). Peak exogenous CHO oxidation rates in the H-GLU+SUC trial (1.20 +/- 0.07 g/min) were significantly higher ( P < .01) compared with the GLU, M-GLU+SUC, and SUC trials (0.77 +/- 0.04, 0.90 +/- 0.07, 0.98 +/- 0.04 g/min, respectively). Furthermore, peak exogenous CHO rates in M-GLU+SUC and SUC trials were significantly higher ( P < .05) compared with the GLU trial. In conclusion, combined ingestion of moderate amounts of glucose and sucrose (144 g) during cycling exercise resulted in approximately 21% higher exogenous CHO oxidation rates compared with the ingestion of an isocaloric amount of glucose. Furthermore, when a mixture of glucose and sucrose was ingested at high rates (2.4 g/min), exogenous CHO oxidation rates reached peak values of approximately 1.20 g/min.
"The effects of different conditions of substrate source and particularly exercise are beyond the scope of this review but there is, again, a good deal of variability as seen even in the effects on rates of oxidation of different sugars (Review: ). As noted above, the presence of fructose tends to increase the levels of plasma lactate but, generally, differences between dietary glucose vs. fructose + glucose tends to become smaller and, as in other conditions, fructose alone is not desirable . "
[Show abstract][Hide abstract] ABSTRACT: Whether dietary fructose (as sucrose or high fructose corn syrup) has unique effects separate from its role as carbohydrate, or, in fact, whether it can be considered inherently harmful, even a toxin, has assumed prominence in nutrition. Much of the popular and scientific media have already decided against fructose and calls for regulation and taxation come from many quarters. There are conflicting data, however. Outcomes attributed to fructose --- obesity, high triglycerides and other features of metabolic syndrome --- are not found in every experimental test and may be more reliably caused by increased total carbohydrate. In this review, we try to put fructose in perspective by looking at the basic metabolic reactions. We conclude that fructose is best understood as part of carbohydrate metabolism. The pathways of fructose and glucose metabolism converge at the level of the triose-phosphates and, therefore, any downstream effects also occur with glucose. In addition, a substantial part of ingested fructose is turned to glucose. Regulation of fructose metabolism per se, is at the level of substrate control --- the lower Km of fructokinase compared to glucokinase will affect the population of triose-phosphates. Generally deleterious effects of administering fructose alone suggest that fructose metabolism is normally controlled in part by glucose. Because the mechanisms of fructose effects are largely those of a carbohydrate, one has to ask what the proper control should be for experiments that compare fructose to glucose. In fact, there is a large literature showing benefits in replacing total carbohydrate with other nutrients, usually fat, and such experiments sensibly constitute the proper control for comparisons of the two sugars. In terms of public health, a rush to judgement analogous to the fat-cholesterol-heart story, is likely to have unpredictable outcome and unintended consequences. Popular opinion cannot be ignored in this problem and comparing fructose to ethanol, for example, is without biochemical correlates. Also, nothing in the biochemistry suggests that sugar is a toxin. Dietary carbohydrate restriction remains the best strategy for obesity, diabetes and metabolic syndrome. The specific contribution of the removal of fructose or sucrose to this effect remains unknown.
"Earlier tracer studies observed that blood lactate concentration was increased after fructose or fructose + glucose ingestion compared to that after glucose ingestion alone
[56,66,68,79,80]. It was also observed that sucrose ingestion also caused a higher blood lactate response than did glucose
[67,81]. However, no detailed data were reported to clarify how much of the ingested fructose was converted into the lactate in these studies. "
[Show abstract][Hide abstract] ABSTRACT: Fructose consumption and its implications on public health are currently under study. This work reviewed the metabolic fate of dietary fructose based on isotope tracer studies in humans. The mean oxidation rate of dietary fructose was 45.0% +/- 10.7 (mean +/- SD) in non-exercising subjects within 3--6 hours and 45.8% +/- 7.3 in exercising subjects within 2--3 hours. When fructose was ingested together with glucose, the mean oxidation rate of the mixed sugars increased to 66.0% +/- 8.2 in exercising subjects. The mean conversion rate from fructose to glucose was 41% +/- 10.5 (mean +/- SD) in 3--6 hours after ingestion. The conversion amount from fructose to glycogen remains to be further clarified. A small percentage of ingested fructose (<1%) appears to be directly converted to plasma TG. However, hyperlipidemic effects of larger amounts of fructose consumption are observed in studies using infused labeled acetate to quantify longer term de novo lipogenesis. While the mechanisms for the hyperlipidemic effect remain controversial, energy source shifting and lipid sparing may play a role in the effect, in addition to de novo lipogenesis. Finally, approximately a quarter of ingested fructose can be converted into lactate within a few of hours. The reviewed data provides a profile of how dietary fructose is utilized in humans.
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