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      Lactate, Fructose and Glucose Oxidation Profiles in Sports Drinks and the Effect on Exercise Performance

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          Exogenous carbohydrate oxidation was assessed in 6 male Category 1 and 2 cyclists who consumed CytoMax™ ( C) or a leading sports drink ( G) before and during continuous exercise (CE). C contained lactate-polymer, fructose, glucose and glucose polymer, while G contained fructose and glucose. Peak power output and VO 2 on a cycle ergometer were 408±13 W and 67.4±3.2 mlO 2·kg −1·min −1. Subjects performed 3 bouts of CE with C, and 2 with G at 62% VO 2peak for 90 min, followed by high intensity (HI) exercise (86% VO 2peak) to volitional fatigue. Subjects consumed 250 ml fluid immediately before (−2 min) and every 15 min of cycling. Drinks at −2 and 45 min contained 100 mg of [U- 13C]-lactate, -glucose or -fructose. Blood, pulmonary gas samples and 13CO 2 excretion were taken prior to fluid ingestion and at 5,10,15,30,45,60,75, and 90 min of CE, at the end of HI, and 15 min of recovery. HI after CE was 25% longer with C than G (6.5±0.8 vs. 5.2±1.0 min, P<0.05). 13CO 2 from the −2 min lactate tracer was significantly elevated above rest at 5 min of exercise, and peaked at 15 min. 13CO 2 from the −2 min glucose tracer peaked at 45 min for C and G. 13CO 2 increased rapidly from the 45 min lactate dose, and by 60 min of exercise was 33% greater than glucose in C or G, and 36% greater than fructose in G. 13CO 2 production following tracer fructose ingestion was greater than glucose in the first 45 minutes in C and G. Cumulative recoveries of tracer during exercise were: 92%±5.3% for lactate in C and 25±4.0% for glucose in C or G. Recoveries for fructose in C and G were 75±5.9% and 26±6.6%, respectively. Lactate was used more rapidly and to a greater extent than fructose or glucose. CytoMax significantly enhanced HI.

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          Role of mitochondrial lactate dehydrogenase and lactate oxidation in the intracellular lactate shuttle.

          To evaluate the potential role of mitochondrial lactate dehydrogenase (LDH) in tissue lactate clearance and oxidation in vivo, isolated rat liver, cardiac, and skeletal muscle mitochondria were incubated with lactate, pyruvate, glutamate, and succinate. As well, alpha-cyano-4-hydroxycinnamate (CINN), a known monocarboxylate transport inhibitor, and oxamate, a known LDH inhibitor were used. Mitochondria readily oxidized pyruvate and lactate, with similar state 3 and 4 respiratory rates, respiratory control (state 3/state 4), and ADP/O ratios. With lactate or pyruvate as substrates, alpha-cyano-4-hydroxycinnamate blocked the respiratory response to added ADP, but the block was bypassed by addition of glutamate (complex I-linked) and succinate (complex II-linked) substrates. Oxamate increased pyruvate (approximately 10-40%), but blocked lactate oxidation. Gel electrophoresis and electron microscopy indicated LDH isoenzyme distribution patterns to display tissue specificity, but the LDH isoenzyme patterns in isolated mitochondria were distinct from those in surrounding cell compartments. In heart, LDH-1 (H4) was concentrated in mitochondria whereas LDH-5 (M4) was present in both mitochondria and surrounding cytosol and organelles. LDH-5 predominated in liver but was more abundant in mitochondria than elsewhere. Because lactate exceeds cytosolic pyruvate concentration by an order of magnitude, we conclude that lactate is the predominant monocarboxylate oxidized by mitochondria in vivo. Mammalian liver and striated muscle mitochondria can oxidize exogenous lactate because of an internal LDH pool that facilitates lactate oxidation.
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            Oxidation of combined ingestion of glucose and fructose during exercise.

            The purpose of the present study was to examine whether combined ingestion of a large amount of fructose and glucose during cycling exercise would lead to exogenous carbohydrate oxidation rates >1 g/min. Eight trained cyclists (maximal O(2) consumption: 62 +/- 3 ml x kg(-1) x min(-1)) performed four exercise trials in random order. Each trial consisted of 120 min of cycling at 50% maximum power output (63 +/- 2% maximal O(2) consumption), while subjects received a solution providing either 1.2 g/min of glucose (Med-Glu), 1.8 g/min of glucose (High-Glu), 0.6 g/min of fructose + 1.2 g/min of glucose (Fruc+Glu), or water. The ingested fructose was labeled with [U-(13)C]fructose, and the ingested glucose was labeled with [U-(14)C]glucose. Peak exogenous carbohydrate oxidation rates were approximately 55% higher (P < 0.001) in Fruc+Glu (1.26 +/- 0.07 g/min) compared with Med-Glu and High-Glu (0.80 +/- 0.04 and 0.83 +/- 0.05 g/min, respectively). Furthermore, the average exogenous carbohydrate oxidation rates over the 60- to 120-min exercise period were higher (P < 0.001) in Fruc+Glu compared with Med-Glu and High-Glu (1.16 +/- 0.06, 0.75 +/- 0.04, and 0.75 +/- 0.04 g/min, respectively). There was a trend toward a lower endogenous carbohydrate oxidation in Fruc+Glu compared with the other two carbohydrate trials, but this failed to reach statistical significance (P = 0.075). The present results demonstrate that, when fructose and glucose are ingested simultaneously at high rates during cycling exercise, exogenous carbohydrate oxidation rates can reach peak values of approximately 1.3 g/min.
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              Active muscle and whole body lactate kinetics after endurance training in men.

              We evaluated the hypotheses that endurance training decreases arterial lactate concentration ([lactate](a)) during continuous exercise by decreasing net lactate release () and appearance rates (R(a)) and increasing metabolic clearance rate (MCR). Measurements were made at two intensities before [45 and 65% peak O(2) consumption (VO(2 peak))] and after training [65% pretraining VO(2 peak), same absolute workload (ABT), and 65% posttraining VO(2 peak), same relative intensity (RLT)]. Nine men (27.4 +/- 2.0 yr) trained for 9 wk on a cycle ergometer, 5 times/wk at 75% VO(2 peak). Compared with the 65% VO(2 peak) pretraining condition (4.75 +/- 0.4 mM), [lactate](a) decreased at ABT (41%) and RLT (21%) (P < 0.05). decreased at ABT but not at RLT. Leg lactate uptake and oxidation were unchanged at ABT but increased at RLT. MCR was unchanged at ABT but increased at RLT. We conclude that 1) active skeletal muscle is not solely responsible for elevated [lactate](a); and 2) training increases leg lactate clearance, decreases whole body and leg lactate production at a given moderate-intensity power output, and increases both whole body and leg lactate clearance at a high relative power output.

                Author and article information

                Role: Academic Editor
                PLoS ONE
                PLoS ONE
                Public Library of Science (San Francisco, USA )
                26 September 2007
                : 2
                : 9
                Exercise Biology Laboratory, Department of Kinesiology, California State University Chico, Chico, California, United States of America
                University of Louisville, United States of America
                Author notes
                * To whom correspondence should be addressed. E-mail: JLAzevedo@

                Conceived and designed the experiments: JA. Performed the experiments: JA ET TT JP. Analyzed the data: JA KC. Contributed reagents/materials/analysis tools: JA. Wrote the paper: JA.

                Azevedo Jr, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
                Page count
                Pages: 8
                Research Article
                Biochemistry/Membrane Proteins and Energy Transduction
                Physiology/Muscle and Connective Tissue



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