Browsing by Subject "Glucose - Metabolism"

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    Limits to exogenous glucose oxidation by skeletal muscle during prolonged, moderate-intensity exercise in man
    (1993) Hawley, John Alan; Noakes, Timothy D; Dennis, Steve
    Several factors may determine the rate. at which exogenous carbohydrate (CHO) is utilised by the human working muscles during prolonged (> 90 min moderate-intensity (63% of peak sustained power output [PPO]) exercise. These include i) the rate of gastric emptying of an ingested fluid, ii) the rate of digestion, absorption and subsequent transport of glucose into the systemic circulation, and iii) the rate of glucose uptake and oxidation by the working muscles. To test the hypothesis that the rate of gastric emptying is the primary factor limiting the rate of CHO delivery to the working muscles during exercise, uniformly labelled ¹⁴carbon (U-¹⁴C) tracer techniques were used in association with conventional gas exchange measurements and post-exercise gastric aspiration to compare the rates of gastric emptying, intestinal CHO delivery and ingested CHO oxidation from 15 g/100 ml solutions of glucose, maltose, a 22 chain-length glucose polymer, and an isocaloric 'soluble' starch preparation. Two groups of six highly-trained male cyclists or triathletes each ingested two of the test drinks which were given as a 400 ml loading bolus immediately before and then as eight 100 ml feedings at 10 min intervals during 90 min of continuous cycling at a work rate of 63% of PPO (~70% of maximal oxygen consumption [VO₂ₘₐₓ]).
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    Metabolism in myocardial ischaemia and reperfusion with specific reference to the role of glucose
    (1996) King, Linda Mary; Opie, Lionel H
    Hypothesis: Glucose is known to be protective in moderate low flow ischaemia due to the production of glycolytic ATP. However, it is questioned whether glucose would still be protective in ultra-low flow ischaemia. Firstly, glycolysis is thought to be inhibited, and secondly, deleterious glycolytic metabolites accumulate. Our hypothesis was that in ultra-low flow ischaemia, glucose utilisation is not inhibited at the level of glycolysis, but by delivery. Increased delivery of glucose should result in increased production of protective glycolytic ATP, but the rate of metabolite accumulation would also increase. Using ultra low flow rates, I wished to investigate how to achieve optimal rates of glycolysis, and how such rates would be balanced by any detrimental component of metabolite accumulation. Methods: The isolated Langendorff-perfused rat heart, with a left ventricular balloon to record ischaemic contracture and reperfusion stunning, was used, with severe flow restriction. Glucose concentrations were changed and pre-ischaemic glycogen contents were altered by perfusion with different substrates (acetate - depletion~ glucose + insulin - loading) or by preconditioning, with 5 min ischaemia and 5 min reperfusion prior to sustained ischaemia. Results: Analysis of glucose uptake relative to delivery showed that in severe low flow ischaemia, the extraction of glucose was increased, and glycolysis was thus limited more by substrate supply than by enzyme inhibition. Analysis of metabolites confirmed this concept. The optimal glucose concentration during severe low flow ischaemia was 11 mM, giving maximal recovery on reperfusion. Both lower and higher glucose concentrations increased ischaemic contracture. Changes in pre-ischaemic glycogen levels correlated with the time to onset of contracture, such that a reduction in glycogen accelerated contracture. Prior glycogen depletion or loading did not improve functional recovery. The benefits of preconditioning on reperfusion function following sustained total global ischaemia could not be related to glycogen depletion. If preconditioning were followed by sustained low flow ischaemia, glucose uptake was increased, but no benefit was found, possibly because a low residual flow abolished the effects of preconditioning. Many of the above results are consistent with the hypothesis that too low a rate of glycolysis results. in insufficient ATP production for protection, while excess glycolytic rates lead to excess metabolite accumulation with detrimental effects. Conclusions: Provision of glucose at the correct concentration, when the benefit associated with glycolytic ATP outweighs the detriment associated with moderate metabolite accumulation, is protective to the low-flow ischaemic myocardium, which can upregulate its ability to extract glucose. Improved residual flow enhances this benefit. Prior glycogen depletion is not beneficial, despite a reduced metabolite accumulation. This mechanism cannot be related to the protective effect of preconditioning.