Lactate Lab Report

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Introduction
Lactic acid which exists in the body as lactate was first discovered by a Swedish chemist, Carl Wilhelm Schede, who first isolated the compound in 1780 from sour milk and gave it a name based on its origins (Armstrong RB, 1998). With reference to much of the 20th century, lactate was largely reflected as a metabolic dead end waste product of glycolysis due to hypoxia, the major cause of the oxygen debt, the major cause of muscle exhaustion and an important factor in acidosis prompted tissue damage. Recently however, experimental evidence proves the existence of a cell to cell lactate shuttle, along with other evidence for astrocyte-neuron, lactate alanine, peroxisomal lactate shuttles and spermatogenic lactate shuttles. The greater
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Due its molecular mass and metabolic capacity, skeletal muscle is the major component of the lactate shuttle, not with reference to lactate production but also in the net absorption and utilization as well. Some of the Lactate leaks into the circulation; this lactate diffuses to neighbouring oxidative muscle fibres which can oxidize it. The majority of the lactate taken up by muscles, as mentioned before, is cleared via oxidation with dependence on the metabolic rate of both exercising and resting muscles. Increase in Lactate oxidation is supplemented by a decrease in glucose oxidation; hence the conclusion is that Lactate competes with glucose as a carbohydrate fuel source, therefore sparing blood glucose for use by other tissues like the red blood cells. During exercise, Lactate and H+ move out of the muscles primarily via mono-carboxylate transporters (MCT) MCT1 and MCT4 (Armstrong RB, 1998).
Lactate metabolism in cardiac muscle
As a principle, cardiac muscle is highly oxidative than the most oxidative skeletal muscle, it therefore goes without saying that the heart is an active lactate utiliser. Evidence from several experimental approaches propose that as blood concentration of Lactate, myocardial blood flow increase, Lactate becomes the ideal fuel for the heart, accounting for 60% of the substrate used. Studies
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The integral principle of the intracellular lactate shuttle is that lactate is an inevitable product of glycolysis, predominantly during rapid glycolysis; this is because lactate dehydrogenase (LDH) has the highest Vmax of any enzyme in the glycolytic pathway (Brooks, 2000).
In muscle. Evidence for the important components of the intracellular lactate shuttle in skeletal muscle include the direct absorption and oxidation of lactate by isolated mitochondria without prior extra-mitochondrial conversion of lactate, the availability of an intra-mitochondrial pool of LDH, and finally the presence of MCT1 in mitochondria, apparently in the inner mitochondrial membrane. Lactic acid (lactate) would be produced continuously in the cytosol and its production rate would be directly proportional to the glycolytic rate. With reference to its higher concentration, lactate would be the primary monocarboxylate diffusing to mitochondria with the use of MCT1 as mentioned above. Once in the mitochondria, namely in the matrix, mitochondrial LDH catalyses the conversion of lactate back to pyruvate. The pyruvate is oxidized through the PDH (pyruvate dehydrogenase) reaction to acetyl-CoA. The acetyl-CoA would then continue through the TCA cycle so as to provide energy. (Kowalchuk JM et al,

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