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Essay on Lactate Experiment

The aim of the experiment was to examine the effects of consuming lactate before and during a prolonged exercise. The data shows that the consumption of the lactate actually did work and the performance of the subject was better than the previous three experiments of dieting. This was due to the lactate that was consumed in the CytoMax. Azevedo, Tietz, Two- Feathers, Paull, and Chapman (2007) state that CytoMax contains polylactate which speeds up the delivery of substrates and is thought to help with prolonged exercise. They believe that polylactate will the delay of fatigue and provide energy for he body.

In the experiment this can be observed because after the initial drop of blood glucose in the first fifteen minutes of exercise from 77. 2mg/dL to 65. 6 mg/dL the blood glucose actually increased. At the end of the 90 minute run the blood glucose level reached 91 mg/dL. Out of the four experiments, this experiment was the only one where blood glucose rose during exercise. As previously stated, the blood glucose started at 77. 2 mg/dL and ended with 91 mg/dL at the end of the 90 minutes. In the baseline experiment, the blood glucose was at 80 mg/dL and dropped to 61. 9 mg/dL.

In the CHO loaded xperiment, the blood glucose was 107 mg/dL then dropped 76. 2 mg/dL. In the lipid loaded experiment, the blood glucose was 71 mg/dL and dropped to 49. 6 mg/dL. In all the experiments that have been run in lab, it has been shown the positives and negatives of diets and how it effects aerobic exercise. In lactate supplementations the positives show that blood glucose is spared. The findings were supported by Donovan and Brooks (1983) that claimed that polylactate spares the bodies glycogen (muscle and liver) and can used to generate glucose. In Fahey et al. 1991) had a study they want to see if lucose polymer or polylactate had an effect on blood glucose, lactate, pH, and bicarbonate on five trained male cyclists exercising for two hours. In the study the blood glucose levels stayed stable while the control group’s blood glucose levels dropped significantly.

The study shows that polylactate did play a role in maintaining blood glucose even though the data from this study did not match what was found in this experiment. The study also showed that the polylactate did have an effect on the blood lactate. In their study, the blood lactate was maintained in the range of 1 mmol/L to 1. throughout the 2 hour study while the range for the blood lactate for the control group was 1. 2 to 1. 6 mmol/L. The study showed that lactate was being consumed and not accumulating. In our experiment, the blood lactate is low this can be seen in the first thirty minutes of exercise. From the start the blood lactate was 1. 17 and there is very little change even thirty minutes in where the blood lactate reaches 1. 28 mmol. In the experiment the peak of blood lactate is 2. 28 and that is sixty minutes into the run. In all of the experiments, blood lactate was higher than in this experiment.

In the baseline xperiment the blood lactate started at 2. 06 and peaked at 3. 55mmol. For the CHO loaded experiment, the blood lactate peaked at 3. 4 an hour into the experiment and stayed relatively constant to 3 mmol for the rest of the 90 minute run. Finally the lipid loaded experiment, peaked at 3. 13 mmol. When comparing the blood lactate levels of the subject on CytoMax to the previous experiments it is clear that CytoMax plays a role. 2) Before the 1970’s lactate was just thought of as waste product when the body has insufficient amount of oxygen during exercise.

That lactate did nothing but impair the exercisers erformance but now it is known that lactate can be used to create energy and possible help improve anaerobic and aerobic performance. As stated in the introduction, lactate is now known to be constantly being produced and removed. Brooks (2002) suggested that when the body is exercising roughly seventy-five percent of lactate that is formed is removed through oxidation. Coming from a biochemical stand point, glucose is broken down to form pyruvate which can have two main reactions happen.

The first is that it can enter into the mitochondria to form ATP the other option pyruvate has is, orming lactate. This reaction occurs when lactate dehydrogenase using NADH to form lactate. This reaction has some benefits because it supports the glyceraldehyde 3 phosphate NAD+ substrate reaction. Robergs, Ghiasvand, and Parker (2004) claim that the lactate that is formed can be removed by monocarboxylate transporters away from the cell or other tissues can receive the lactate and be used for metabolism. The sites where this can occur are in the skeletal muscle cells, cardiac cells, and the brain.

The name of the two concepts were cell-cell lactate shuttle and intracellular lactate shuttle. The cell-cell lactate shuttle’s main idea is that lactate is formed in type Il tissues and the lactate is moved from these type II fibers to type I fibers. This makes sense because type II fibers are high glycolytic fibers and type I fibers are oxidative fibers. Brooks (1985) showed this concept by using isotope racers to follow lactate. The study was conducted on rats, where a lactate tracer was infused into the blood of the rats. He took blood from the rats at rest and during exercise to see what happens to the rats blood lactate.

The observation that was made was the lactate was being produced and consumed. He elieved that about half of the lactate that was produced at rest was being oxidized. In Brooks et al. (1991) the study was performed on men and women to find the same result, that at rest the lactate produced and about half was oxidized. The only difference in this study it was shown that at 50-75% of the VO2 max the body can oxidize about 75-80% of the lactate. Messonnier et al. (2013) explained that the metabolic clearance rate is influenced by the intensity the body is working at.

From light to moderate intensity, the body’s rate is high meaning the body can consume the amount of lactate that is being produced ut when the body moves from moderate to high intensity the clearance rate decreases. With the increase in intensity causes more type Il fibers to be activated causing more lactate to potentially to be formed. This means the body can no longer consume the lactate at the same rate as being produced. Messonnier et al. (2013) mentioned that the sites where lactate uptake and oxidation is in the muscle fibers, liver, heart, and brain.

To explain how lactate could be oxidized the intracellular lactate shuttle concept was the key. The problem that many scientist had with the cell to cell shuttle concept was how does actate move from the cytosol to the mitochondria because the mitochondria has a bi-layer wall that prevents things from entering it. In a research article Schruers and Schaafsma (2010) talked about how the lactate is transported from the cytosol to the mitochondria and the transporter is called monocarboxylate transporter (MCT). This transporter has various forms and varies in different areas in the body.

In the article, they mentioned that the body has three main MCT: MCT1, MCT2, and MCT4. The location of MCT4 is in the fiber type II (fast twitch muscle) and not in type I fibers. It is known to be involved in the efflux of actate from muscle fibers. MCT1 is different, because this MCT is found in type 1 fibers and type Ila fibers. This transporter is the transporter that consumes the lactate. MCT2 is the transporter that helps consume the lactate that is formed at rest and is thought to be in the heart. In the review article Cruz et al. 2012) examined two main areas where lactate consumption occurs the heart and skeletal muscle.

In the article, they combed through studies to examine what is occurring in these sites. They concluded that the mitochondria are able to oxidize the lactate directly because of the MCT1. That the lactate hat is being produced in the muscle can be transported because of the MCT1 and once in the mitochondria the lactate can turn into pyruvate because of lactate dehydrogenase-1. In the fast twitch cells, the MCT4 allows for the lactate to leave and be picked up by the blood.

Robergs, Ghiasvand, and Parker (2004) explain that blood cells do not have mitochondria and need energy from glycolysis and is necessary to prevent acidosis. Acidosis can occur because during glycolysis, glyceraldehyde 3 phosphate gets dehydrogenated which forms NADH and H+. With an increase in this reaction can cause pH to increase. What the formation of lactate uses NADH preventing the proton to be released. In the article, they discussed metabolic acidosis and what they claim was metabolic acidosis is not just because the proton is released but a problem with the balance of buffering.

In the body there are many buffering agents and two of the main agents are bicarbonate and lactate. What bicarbonate does is bind to the proton allowing the body to maintain its pH. The point of this is there is a need to have a balance in the acid base and if the balance cannot be maintain it will cause problems in the body. So after understanding how actate is consumed by the muscle how does supplementation have an effect on exercise? In a review article, Morris (2012) explains that lactate acts as an alkalinizing agent causing a rise in bicarbonate and pH.

This allows the muscle to oxidize the lactate allowing for glucose sparing to occur. In the article, the problem with supplementing lactate is it can cause gastrointestinal issues and has to be diluted. This theory was backed up Fahey et al. (1991), in the study they concluded that polylactate played a role in the pH and bicarbonate. That lactate is hydrogen acceptor because lactate is a weak base.

What polylactate allows does is it allows the body to keep a reserve of bicarbonate so for endurance exercise there is an enhanced buffer capacity. 3) Maassen et al. 2004) describes diabetes as a disease that is known for by chronic hyperglycemia. The body has a need to maintain normal glucose levels and the pancreas is responsible for monitoring the level. The pancreas has a B-cells that can detect an increase in the glucose levels and can tell the body to secrete insulin. The insulin will cause the body to suppress glucose output and all for the muscle and adipose tissue to take up glucose. The problem is that diabetics have problems with insulin because the body maybe insulin resistant causing hyperglycemia.

A major problem that diabetics have to deal with when in a hyperglycemic state is called diabetic ketoacidosis (DKA). DKA has the possibility of being life threatening and is very serious. Diabetics have insulin deficiency and when they exercise the catecholamines increase which causes an increase glucose into the body. Which sounds like a good thing for exercise but the tissues have trouble disposing the glucose because of this insulin resistance and/or deficiency. This stresses the kidney which can lead to glycosuria, dehydration, and osmotic diuresis. Lu et al. 2010) reported that in DKA the body is in metabolic acidosis which can be seen because of a large concentration of anions.

They believe that the anions are present because of acetone, acetoacetate, B-hydroxybutyrate, and lactate. In the article, it was mentioned that new studies are showing that this form of lactate might have a larger role in forming the metabolic acidosis. This lactate is D-lactate which is an stereoisomer. In the body, there are two forms of lactate: Dlactate and L-lactate. The L-lactate is the thought of as the lactate that causes metabolic acidosis; while the D-lactate occurs but in a low concentration.

The two stereoisomers are formed in two different ways. The L-lactate is formed when the body goes through glycolysis and the D-lactate is formed when it goes through methylglyoxal metabolism. When the body is in hyperglycemic the D-lactate increases causing the metabolic acidosis. So would lactate supplementation help buffer the blood and allow diabetics to exercise without suffering from DKA? Schreurs and Schaafsma (2010) reported that the lactate metabolism in diabetics are more active than non-diabetics.

That providing lactate would cause local hypoxia in fat tissue because there would be a decrease in vascularization in the cells. The result would be that the body would rely more on anaerobic glycolysis causing for the body to increase the amount of lactate to be produced. With an increase in lactate produced can cause the body to become more insulin resistant. The point of supplementation is to allow the body to remove lactate from the body and not accumulate. So the answer is lactate supplementation is not appropriate for diabetics.

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