Bacterial translocation and profound fluid shifts contribute to circulatory collapse. Global oxygen delivery falls. Endogenous catecholamine release attempts to support the circulation but will also increase glycolysis and lactate formation.
As shock develops hepatic blood flow falls and intracellular acidosis inhibits gluconeogenesis from lactate. The liver produces rather than clears lactate. Intestinal bacteria metabolize glucose and carbohydrate to d -lactate.
This is only slowly metabolized by human LDH and contributes to the escalating lactic acidosis. Google Scholar. Google Preview. Please see multiple choice questions 28— Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide.
Sign In or Create an Account. Sign In. Advanced Search. Search Menu. Article Navigation. Close mobile search navigation Article Navigation. Volume 6. This article was originally published in. Article Contents Normal lactate production. Measurement of lactate. Lactate and lactic acidosis.
Normal lactate metabolism. Causes of hyperlactaemia. Lactate and critical illness. Lactate physiology in health and disease. Oxford Academic. Select Format Select format. Open in new tab Download slide. Glycolysis, Kreb's cycle and oxidative phosphorylation. Principle modes of lactate removal from plasma. Table 1 Causes of hyperlactaemia considered in terms of increased production and decreased clearance.
This fraction may rise during hyperlactaemia. Open in new tab. Google Scholar Crossref. Measuring Lactic Acid Levels. Lactic Acid — The Truth. Lactic Acid — Misconceptions and Myths. Lactic Acid — Commercial Applications. Lactate Threshold. Lactate is actually a product of cellular metabolism and is produced in various cells throughout the body including muscles, brain cells and red blood cells.
Lactate and lactic acid are actually used as a fuel by some tissues in the body including neurons and cardiac heart muscle. In those cases, the working muscles generate energy anaerobically. This energy comes from glucose through a process called glycolysis, in which glucose is broken down or metabolized into a substance called pyruvate through a series of steps.
When the body has plenty of oxygen, pyruvate is shuttled to an aerobic pathway to be further broken down for more energy. But when oxygen is limited, the body temporarily converts pyruvate into a substance called lactate, which allows glucose breakdown—and thus energy production—to continue. The working muscle cells can continue this type of anaerobic energy production at high rates for one to three minutes, during which time lactate can accumulate to high levels.
A side effect of high lactate levels is an increase in the acidity of the muscle cells, along with disruptions of other metabolites. The same metabolic pathways that permit the breakdown of glucose to energy perform poorly in this acidic environment. On the surface, it seems counterproductive that a working muscle would produce something that would slow its capacity for more work.
In reality, this is a natural defense mechanism for the body; it prevents permanent damage during extreme exertion by slowing the key systems needed to maintain muscle contraction. Contrary to popular opinion, lactate or, as it is often called, lactic acid buildup is not responsible for the muscle soreness felt in the days following strenuous exercise.
Rather, the production of lactate and other metabolites during extreme exertion results in the burning sensation often felt in active muscles, though which exact metabolites are involved remains unclear. This often painful sensation also gets us to stop overworking the body, thus forcing a recovery period in which the body clears the lactate and other metabolites.
Researchers who have examined lactate levels right after exercise found little correlation with the level of muscle soreness felt a few days later.
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