MCT's

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    MCT's


    Hey Stryder,

    Any possibility of carrying some MCT oil??Getting ready to order some lean extreme and glucophase and wouldnt mind ordering some MCT's as well.Thanks!

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    Quote Originally Posted by bigbody52
    Hey Stryder,

    Any possibility of carrying some MCT oil??Getting ready to order some lean extreme and glucophase and wouldnt mind ordering some MCT's as well.Thanks!
    Glad to see someone else that appreciates MCT oil...I think its a great supp, and have used it forever...everyone thinks I am nuts...
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    Glad to see someone else that appreciates MCT oil...I think its a great supp, and have used it forever...everyone thinks I am nuts...
    what do you think are the real benefits of MCT and how do you usually use it?
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    Studies are kind of older (2000ish), but MCT oil has been around for a long time.I always have a bottle of Cap-Tri around.It's old school stuff, but it's great stuff.I am always more vascular, and leaner...it burns and does not get stored, and creates almost a themogenic typr reaction...heated up, and you sweat.I think John Parillo was they guy who brought it to the for fron in the early 90's.It was basicall used in a Ketosis type diet,low carbs high protien, it gets used as an energy source, and save your muscle from catabolising.

    By Arthur E. Roberson, Ph.D

    I. Introduction
    Nomenclature of Fats
    Fats, or lipids, are found in all cells and perform a variety of functions essential for life. These include their roles in energy storage, membrane structure, and incorporation in vitamins, hormones, and prostaglandins (Zubay, 1983). Fats are used to cushion and insulate the body and function as electrical insulation in the nervous system. Triglycerides are the most common form of fat found in foods and stored in body fat depots. Triglycerides are comprised of three fatty acids (figure 1) esterified to a glycerol backbone (figure 2). Most naturally occuring triglycerides contain fatty acids 16-20 carbon atoms in length. Such fatty acids are called "long chain fatty acids" (LCFAs), and their corresponding triglycerides are called "long chain triglycerides" (LCTs). Medium chain triglycerides (MCTs) are comprised of medium chain fatty acids (MCFAs), which are 6-12 carbons in length. Although the carboxylic acid part of fatty acids is soluble in water, the hydrocarbon chain is not. Thus, LCFAs are not water soluble. Since the hydrocarbon chains of MCFAs are shorter, MCFAs are more water soluble than LCFAs. Likewise, MCTs are also relatively soluble in water, due to ionization of the carboxylic acid groups and the small size of the hydrocarbon chains. Their small molecular size and greater water solubility cause MCTs to undergo a different metabolic path than that experienced by LCTs (Bach and Babayan, 1982).

    Occurrence and Purification of MCTs
    Medium chain triglycerides occur naturally in small quantities in a variety of foods, and are present naturally in the blood of the human fetus and in human milk (Bach and Babayan, 1982; Souci, Fachmann, Kraut, 1989/90). In cow's milk, C6-C14 fatty acids together account for 20% of the total fatty acid composition (Christensen et al, 1989). Commercially, medium chain fatty acids are prepared by the hydrolysis of coconut oil (an abundant source) and are fractionated by steam distillation. The MCFAs so obtained consist of predominantly C8:0, with lesser amounts of C10:0, and minute amounts of C6:0 and C12:0. The fractionated MCFAs are re-esterified with glycerol to generate MCTs (Bach and Babayan, 1982). MCT oil softens or splits certain plastics such as polyethylene and polystyrene, but not polypropylene. It is recommended that MCT oil be stored in metal, glass, or ceramic containers (Sucher, 1986). MCT oil has a caloric density of 8.3 calories per gram; one tablespoon equals 14 grams and contains 115 calories. MCTs are not drugs and have no pharmacological effects (Bach and Babayan, 1982).

    Historical Uses of MCTs
    Since their introduction in 1950 for the treatment of fat malabsorption problems, medium chain triglycerides have enjoyed wide application in enteral and parenteral nutrition regimens (Bach and Babayan, 1982). Fat emulsions can be used to provide up to 60% of nonprotein calories. Before the availability of lipid emulsions suitable for intravenous use, glucose was used as the only nonprotein source of calories (Mascioli et al, 1987). Not only did this result in essential fatty acid deficiencies, but it was also undesirable because it increased hepatic lipogenesis and respiratory work. Although inclusion of LCTs in intravenous feedings represented an improvement, problems remained with slow clearance of LCTs from the bloodstream and interference with the RES component of the immune system. When medium chain triglycerides or structured lipids (triglycerides containing both MCFAs and LCFAs) are added to the regimen, calories are provided in a more readily oxidizable form (Schmidl, Massaro, and Labuza; 1988), and less interference with the RES is observed (Mascioli et al, 1987). In one case, MCT was fed as the exclusive source of fat (along with a small amount of LCT to provide essential fatty acids) to a patient with chyluria (a fat malabsorption disease) for over 15 years without producing side effects (Geliebter et al, 1983).

    Sports Nutrition
    Although MCTs have been used in hospital environments for years, their use by healthy individuals is relatively new. Recently, athletes have begun to use MCTs to increase caloric consumption, thereby providing energy and facilitating weight gain. Their low food efficiency, due to the thermogenic effect, means that MCTs have very little tendency to be converted to body fat. The calories from MCTs represent an additional energy source which (in contrast to conventional fats) can be used concurrently with glucose.

    II. Metabolism
    Digestion and Absorption of Fats
    Since LCTs are not very soluble in water, the body has to go through an elaborate digestive process in order to absorb these nutrients. Bile salts are secreted by the gall bladder to help dissolve the LCTs. Upon ingestion, LCTs interact with bile in the duodenum (upper small intestine) and are incorporated into mixed micelles (Record et al, 1986). Enzymes called lipases (pancreatic lipase and phospholipase A2) remove the fatty acid molecule from the glycerol backbone. The mixed micelles are passively absorbed into the intestinal mucosa where the free fatty acids are re-esterified with glycerol. The intestinal mucosa synthesizes a lipoprotein carrier called a chylomicron to transport the reformed triglyceride. Chylomicrons are secreted into the lymph and are released into the venous circulation via the thoracic duct. In the bloodstream, lipoprotein lipase again breaks down the triglycerides into two free fatty acids and a monoglyceride. The monoglycerides go to the liver to be further degraded, while many of the circulating free fatty acids are taken up and stored by adipocytes (fat cells). When carbohydrates are consumed insulin is released, and insulin stimulates adipocytes to re-esterify the fatty acids into triglycerides and store them as body fat. In general, body fat stores are not mobilized and used for energy to any significant extent in the presence of insulin.

    In contrast, since MCFAs are more water soluble they are more easily absorbed and do not require this complicated digestive process. MCTs can be absorbed intact and do not require the action of pancreatic lipase or incorporation into chylomicrons. Instead, a lipase within the intestinal cell degrades the MCT into free MCFAs and glycerol. The MCFAs are bound to albumin, released into the bloodstream, and transported directly to the liver by the portal vein. The vast majority of MCFAs are retained by the liver where they are rapidly and extensively oxidized. Whereas conventional fats are largely deposited in fat cells, MCTs are transported directly to the liver and used for energy. Very little of the MCFAs ever escape the liver to reach the general circulation (Bach and Babayan, 1982). Only 1-2% of MCTs are incorporated into depot fat (Geliebter et al, 1983; Baba, Bracco, and Hashim, 1982). Medium chain triglycerides are digested and absorbed much faster than conventional fats (in fact, as rapidly as glucose) and are immediately available for energy.

    References

    Baba, Bracco, and Hashim, Enhanced thermogenesis and diminished deposition of fat in response to overfeeding with diet containing medium chain triglyceride. Am. J. Clin. Nutr. 35: 678-682 (1982).
    Bach and Babayan, Medium chain triglycerides: an update. Am. J. Clin. Nutr. 36:950-962 (1982).
    Christensen, Hagve, Gronn, and Christophersen, Beta-oxidation of medium chain (C8-C14) fatty acids studied in isolated liver cells. Biochem. et Biophys. Acta 1004: 187-195 (1989).
    Geliebter, Torbay, Bracco, Hashim, and Van Itallie, Overfeeding with medium chain triglyceride diet results in diminished deposition of fat. Am. J. Clin. Nutr. 37: 1-4 (1983).
    Mascioli, Bistrian, Babayan, and Blackburn, Medium chain triglycerides and structured lipids as unique nonglucose energy sources in hyperalimentation. Lipids 22: 421-423 (1987).
    Record, Kolpek, and Rapp, Long chain versus medium chain length triglycerides - a review of metabolism and clinical use. Nutr. Clin. Prac. 1:129-135 (1986).
    Schmidl, Massaro, and Labuza, Parenteral and enteral food systems. Food Tech. 77-87 (July, 1988).
    Souci, Fachmann, and Kraut, Food Composition and Nutrition Tables 1989/90. Published by Wissenschaftliche Verlagsgesellschaft (1989).
    Sucher, Medium chain triglycerides: a review of their enteral use in clinical nutrition. Nutr. Clin. Prac. 44: 146-150 (1986).
    Zubay, Biochemistry, chapter 13: "Metabolism of Fatty Acids and Triacylglycerols," by Denis E. Vance. Published by Addison-Wesley Publishing Company (1983).
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    By Arthur E. Roberson, Ph.D

    Once inside a cell, fatty acids can be oxidized (burned) to release energy. The site of energy production within the cell is a membranous organelle called a mitochondrion. Long chain fatty acids cannot simply enter the mitochondria by themselves; they must be actively transported across the mitochondrial membrane (Record et al, 1986). First, the fatty acid is converted to its active form, acyl-CoA. The long chain acyl-CoA is then transesterified to L-carnitine by carnitine acyltransferase I (CAT I), generating acylcarnitine. A protein carrier embedded within the mitochondrial membrane acts as a shuttle to transport the LCFA-carnitine complexes into the inner mitochondrial space. Once there, carnitine acyltransferase II (CAT II) releases the fatty acid in its activated form, acyl-CoA (figure 1).

    The enzymes responsible for oxidation of fatty acids are located inside the mitochondria. Therefore, if fatty acids are not permitted to enter the mitochondria they cannot be burned for energy. Entry into the mitochondria is regulated by the activity of the carnitine shuttle. This transport system is not very active if carbohydrates are available because carbohydrate metabolism generates malonyl-CoA, which inhibits CAT I. In addition, glucagon (the hormonal antagonist of insulin) is involved in stimulating mobilization of body fat stores and use of fat for energy. Following carbohydrate ingestion insulin is released and glucagon is suppressed, so very little body fat is used for energy. After carbohydrate reserves have been diminished, the body releases glucagon as a signal to begin burning fat. These are the reasons why fat stores are drawn upon for energy only after glycogen has been depleted.

    The inhibition of CAT I by malonyl-CoA represents a regulatory mechanism to prevent the wasteful use of energy substrates. Generally speaking, the body uses carbohydrate fuels first and stores fat as an energy reserve. Fat contains twice the energy density of carbohydrate (9 calories per gram versus 4 calories per gram) and does not require water for storage, as does carbohydrate. Fat is thus a more efficient molecule for energy storage. Animals are able to store only a small amount of energy as carbohydrate (in the form of liver and muscle glycogen) but can store a virtually unlimited amount of energy as fat.

    In contrast to long chain fats, MCFAs are immediately available for energy. Medium chain fatty acids are retained by the liver, where they are rapidly and extensively oxidized (Bach and Babayan, 1982). Medium chain fatty acids can enter the mitochondria by passive diffusion and do not require the carnitine transport system (Record et al, 1986; Bach and Babayan, 1982). MCFAs thus can be used for energy even in the presence of carbohydrates, and in fact have a carbohydrate-sparing effect (Lavau and Hashim, 1978; Cotter et al, 1987). Once inside the mitochondria all fatty acids are burned in a process called beta-oxidation. During beta-oxidation, blocks of two carbon atoms are removed from the activated fatty acid (acyl-CoA) to form acetyl-CoA (figure 2). The intermediate acetyl-CoA can then undergo several metabolic fates: i) it can enter the Krebs cycle to generate ATP; ii) it can be used to generate ketone bodies; iii) it can be used as a substrate for fatty acid synthesis or elongation; or iv) it can be consumed in an energy transforming process known as reversed electron transfer (Bach and Babayan, 1982; Berry et al, 1985; Crozier et al, 1987).

    The vast majority of MCFAs are retained in the liver where they undergo beta-oxidation, producing acetyl-CoA. To enter the Krebs cycle (the body's central energy producing pathway) the acetyl-CoA combines with oxaloacetate, producing citrate. Medium chain fatty acids are oxidized in the liver so rapidly that the supply of oxaloacetate becomes limiting. As a result, the capacity of the Krebs cycle is overwhelmed and a large proportion of the acetyl-CoA is directed toward the synthesis of ketone bodies (Bach and Babayan, 1982). This process is known as "ketogenesis" (figure 3). Ketone bodies are released from the liver into the blood and are subsequebtly taken up by muscles and used as fuel. LCT ingestion also causes an increase in blood levels of ketone bodies during fasting, but only MCT will still produce ketone bodies if carbohydrates are concurrently ingested (Sucher, 1986). Once inside muscle cells, ketone bodies are converted back to acetyl-CoA, which then enters the Krebs cycle to produce ATP. The conversion of MCFAs to ketone bodies occurs even in the presence of carbohydrates. This additional source of energy decreases glucose uptake and utilization (Lavau and Hashim, 1978) and thus may extend endurance by sparing glycogen (Cotter et al, 1987).

    References

    Bach and Babayan, Medium chain triglycerides: an update. Am. J. Clin. Nutr. 36:950-962 (1982).
    Berry, Clark, Grivell, and Wallace, The contribution of hepatic metabolism to diet-induced thermogenesis. Metab. 34: 141-147 (1985).
    Cotter, Taylor, Johnson, and Rowe, A metabolic comparison of pure long chain triglyceride lipid emulsion (LCT) and various medium chain triglyceride (MCT)-LCT combination emulsions in dogs. Am. J. Clin. Nutr. 45: 927-939 (1987).
    Crozier, Bois-Joyeux, Chanez, Girard, and Peret, Metabolic effects induced by long-term feeding of medium chain triglycerides in the rat. Metabolism 36: 807-814 (1987).
    Lavau and Hashim, Effect of medium chain triglyceride on lipogenesis and body fat in the rat. J. Nutr. 108: 613-620 (1978).
    Record, Kolpek, and Rapp, Long chain versus medium chain length triglycerides - a review of metabolism and clinical use. Nutr. Clin. Prac. 1:129-135 (1986).
    Sucher, Medium chain triglycerides: a review of their enteral use in clinical nutrition. Nutr. Clin. Prac. 44: 146-150 (1986).
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    09/23/2000 - Report No. 3, Cellular Energy Production : The Krebs Cycle, Electron Transport, and Oxidative Phosphorylation

    By Arthur E. Roberson, Ph.D

    Introduction

    Humans and other animals obtain energy to support life, growth, and activity from food. The basic question is how is the energy contained in food extracted and transformed into a form which can be directly used as fuel by the body. The source of energy used by the body is the potential energy contained in the chemical bonds of food. Energy is either released or consumed during chemical reactions, depending on the relative energies of the reactants versus the products. The main foods used as energy substrates by the body are carbohydrates and fats. Carbohydrates and fats are different chemically, but have in common that they both contain carbon-hydrogen bonds. In this state, carbon is said to be reduced. In aerobic metabolism the carbon and hydrogen react with oxygen, forming CO2 and H2O. The reaction between hydrogen and oxygen to make water is extremely exergonic (this is the reaction that turned the Hindenburg into a fireball). This reaction releases energy because hydrogen and oxygen are more stable (i.e., have less energy) when they are joined together as water than when they exist separately. Most of the energy derived from the aerobic metabolism of foods is from this reaction. Fats provide twice the caloric density of carbohydrates - 9 calories per gram for fat as compared to 4 calories per gram for carbohydrate. The reason fat contains more energy than carbohydrate is that in fat the carbon is in a more reduced form (Zubay, 1983, p. 482) - more hydrogen is packed in per carbon atom.

    In aerobic metabolism the carbon and hydrogen in foods react with oxygen to produce CO2 and H2O. This reaction releases energy because carbon dioxide and water molecules contain less energy than the original food molecules and oxygen. The same reaction occurs when a piece of food burns in the camp fire. In that situation the energy released by the reaction is simply liberated as heat to the surroundings. In the body the reaction is broken down into many small steps and the energy which is released is captured in a molecule called adenosine triphosphate, or ATP. About 67% of the energy obtained in glucose (the body's chief fuel molecule) is captured by ATP and the rest is liberated as heat (Zubay, 1983, p. 395). This is a very impressive efficiency level compared to other machines. ATP is the immediate source of energy used to fuel nearly all cellular processes, including muscular contraction. The role of ATP is not to store energy (that is the role of body fat and glycogen) but rather to transfer energy from a food molecule to some other cellular molecule which is going to perform work (Vander, Sherman, Luciano, 1980, p. 80). Energy is the ability to do work. Potential energy is energy which is stored and has the potential to perform work if it is released. The energy contained in a chemical bond is a form of potential energy. The potential energy contained in the chemical bonds of food molecules is released during oxidation, and this energy is transferred via ATP to other molecules which perform cellular work - everything from muscular contraction to protein synthesis.

    Conceptually, it is convenient to break up this process into four stages, although in fact these stages are intimately linked in the cell. The first stage of carbohydrate metabolism is glycolysis and the first stage of fat metabolism is beta-oxidation. The following stages of energy production are common to both fats and carbohydrates, and are the Krebs cycle, electron transport, and oxidative phosphorylation.

    The Krebs Cycle
    The central energy producing pathway in the body is the Krebs cycle (figure 1), named for the German chemist Hans Krebs. Krebs originally postulated this process, also known as the TCA cycle, in 1937 and was later awarded the Nobel Prize in 1953 for this work. Energy substrates derived from carbohydrates or fatty acids enter the Krebs cycle as the intermediate acetyl-CoA. The ultimate end of the process is to convert the chemical energy contained in foods into ATP. Adenosine triphosphate is an unstable molecule containing a high energy phosphate bond. When ATP is split, the energy contained in this phosphate bond is released and is available to perform work inside the cell. ATP is the immediate source of energy for nearly all cellular processes, and thus has earned its reputation as "the energy currency of the cell."

    Carbohydrates are initially metabolized via an anaerobic process known as glycolysis. Glucose enters the glycolytic pathway and is converted into two molecules of pyruvate, generating a net yield of two ATP molecules. Under anaerobic conditions, as may be temporarily experienced in muscular tissue during weight training, pyruvate is reduced to lactate, or lactic acid, which causes a burning sensation in the muscle. Glycolysis is a relatively inefficient process, yielding only two ATPs per glucose molecule. The two lactate molecules account for roughly 93% of the energy present in the original glucose molecule, so only about 7% of the energy embodied in glucose is made available for use. Of this, about 50% is captured in ATP (Zubay, 1983, p. 305). In the presence of oxygen a different metabolic fate is available to pyruvate. Instead of being converted into lactate, pyruvate is decarboxylated to generate acetyl-CoA. Acetyl-CoA is also produced by beta-oxidation of fatty acids, as discussed Technical Report #2.

    The basic point of the Krebs cycle is to provide the chemical means of completely oxidizing the carbon of glucose or fatty acids to CO2 and the hydrogen to H2O. This allows much more of the energy contained in the food molecule to be extracted and used by the cell, as compared to anaerobic metabolism. In each turn of the Krebs cycle two carbons enter as acetate and two carbons exit as CO2. The cycle involves eight intermediates, each of which is converted into the next by an enzyme specific for that step (figure 1). These reactions are localized in the mitochondria, the site of aerobic energy production within the cell.

    The first stage of carbohydrate metabolism, glycolysis, occurs in the cytoplasm and does not require oxygen. The end-product of glycolysis, pyruvate, enters the mitochondria to be further metabolized. In the mitochondria pyruvate is converted into acetyl-CoA by pyruvate dehydrogenase. Fats are oxidized to produce acetyl-CoA within the mitochondria. Long chain fatty acids must be ferried across the mitochondrial membrane by the carnitine shuttle, while medium chain fatty acids can transverse the membrane by passive diffusion.

    Acetyl-CoA donates the two-carbon compound acetate to a four-carbon acceptor oxaloacetate thereby generating citrate, a six-carbon compound. During one turn of the cycle two molecules of carbon dioxide are liberated, ultimately regenerating oxaloacetate. The Krebs cycle intermediates are not consumed in the cycle and there is no net loss of carbon in the process, ignoring any side reactions which may occur. The cycle can thus be viewed as catalytic, since a relatively small amount of oxaloacetate can be used to metabolize an arbitrary amount of acetyl-CoA.

    The activity of this pathway is controlled by the levels of its substrates and products, so that its level of energy production matches the energy needs of the cell. As the concentration of substrates increases, or the concentration of end products decreases, the activity of the cycle increases. The most sensitive factors which directly regulate the cycle's activity are the NAD/NADH ratio and the ATP/ADP ratio. The activity of the first step in the pathway is also sensitive to the concentration of oxaloacetate.

    Under normal conditions the concentration of intermediates such as oxaloacetate is not limiting. Medium chain triglycerides enter mitochondria independent of the carnitine shuttle, and thus bypass an important regulatory step in fatty acid oxidation (refer to Technical Report #2). Medium chain triglycerides are oxidized so rapidly that the acetyl-CoA which is produced can overwhelm the amount of oxaloacetate available to accept it (Bach and Babayan, 1982). Some portion of the acetyl-CoA is then diverted to another metabolic fate - ketogenesis. In ketogenesis two molecules of acetyl-CoA combine to form ketone bodies, primarily acetoacetic acid and beta-hydroxybutarate (refer to Technical Report #2). This process is diminished if oxaloacetate precursors, such as aspartate and pyruvate, are co-administered with the MCTs (Bach and Babayan, 1982; Crozier, 1988). This suggests that the ketogenic properties of MCTs are due, in fact, to their ability to overwhelm the capacity of the Krebs cycle at the level of oxaloacetate.

    Only one ATP molecule is produced directly by each turn of the Krebs cycle. This is referred to as "substrate level phosphorylation" since the generation of ATP is directly coupled to a specific chemical reaction. In other words, ADP participates as a substrate in the reaction. Most of the energy derived from aerobic metabolism comes from subsequent oxidation of the NADH and FADH2 produced by the cycle. This is referred to as "oxidative phosphorylation" since here ATP synthesis is coupled to the oxidation of NADH and FADH2. Aerobic metabolism can the be thought of as having two phases: the oxidative phase in which electrons (in the form of hydrogen atoms) are removed from organic substrates and transferred to coenzyme carriers (FAD and NAD), followed by the reoxidation of the reduced coenzymes (FADH and NADH2) by the transfer of electrons (again in the form of hydrogen) to oxygen, generating H2O (Zubay, 1983, p. 325). The reduction of oxygen to water to extremely exergonic and most of the ATP is generated during this process. The oxidation of acetyl-CoA involves removal of electrons (as hydrogen) from the Krebs cycle intermediates and transfer of hydrogen to the coenzymes FAD and NAD. In the process, these coenzymes are reduced to FADH and NADH2. (In chemistry, "oxidation" is the removal of electrons and "reduction" is the addition of electrons.) Subsequently, the reduced coenzymes are reoxidized by transfer of the hydrogens to oxygen in the "electron transport chain." Ultimately, ATP is synthesized by oxidative phosphorylation of ADP, which is driven by a proton gradient generated in the process of electron transport (Zubay, 1983, p. 325).

    The most important points are (Zubay, 1983, p. 335):

    Acetate enters as acetyl-CoA by condensation onto a four-carbon acceptor, oxaloacetate.
    Decarboxylation occurs at two steps so that the input of carbon as acetate is balanced by the loss of two carbons as CO2.
    Oxidation occurs at fours steps, by the way of transfer of hydrogen atoms. In three cases NAD is converted to NADH and in one case FAD is converted to FADH2.
    One molecule of ATP is generated directly.
    Oxaloacetate is regenerated to complete the cycle.
    Two carbons enter as acetate and exit as CO2, producing ATP, NADH, and FADH2 as byproducts. The FADH and NADH2 in turn enter the electron transport chain to be further metabolized.Electron Transport and Oxidative Phosphorylation

    Although some ATP is directly generated by the Krebs cycle, more significant products of the cycle are the reduced coenzymes NADH and FADH2. Most of the energy contained in the starting material is still present in these coenzymes. The primarily energy yield of aerobic metabolism occurs when NADH and FADH2 are re-oxidized to NAD and FAD. This process is known as electron transport because electrons from NADH and FADH2 are transported via a chain of electron carriers and are ultimately transferred to molecular oxygen. Oxygen is a very electronegative element, meaning that it has a strong affinity for electrons. In essence, oxygen and hydrogen combine to form water because oxygen has a high affinity for electrons, and hydrogen represents an easy source. Hydrogen does not have a strong affinity for electrons and basically gets trapped into sharing its electrons with oxygen.

    The reduced coenzymes NADH and FADH2 serve as donors of electrons (as hydrogen) which combine with oxygen to form water. The delta-G expression indicates that the reaction will proceed spontaneously with the release of energy. Enough energy is released to drive the synthesis of several ATPs. Therefore, rather than wasting energy, the above reaction is divided up into several small steps. The energy release is thus parcelled out in small packets to allow ATP to be generated more efficiently (Zubay, 1983, p. 365). To achieve this, electrons are transported from the reduced coenzymes to oxygen via a series of carriers, arranged in the order of increasing electron affinity (figure 2). These electron carriers are molecules (some of them proteins) capable of undergoing reversible oxidation-reduction reactions.

    These electron transporters are embedded within the mitochondrial inner membrane (mitochondria are double-membraned structures). The energy which is released as electrons are transported down the chain to acceptors of ever increasing electron affinity is not directly used to synthesize ATP. Instead, the energy is used to generate a proton gradient across the inner mitochondrial membrane. This results in an electric field across the membrane (about 0.14 V) as well as a pH gradient (about 1.4 units). Protons are actively pumped across the inner mitochondrial membrane using the energy derived from electron transport. In order to establish a proton concentration gradient across the membrane, the membrane must be impermeable to passive diffusion of protons. Protons re-enter the mitochondrial matrix (driven by the concentration gradient) through a protein structure embedded within the membrane known as F0. F0 is physically attached to another protein structure known as F1-ATPase, which directly synthesizes ATP from ADP and phosphate. The precise mechanism by which energy is transferred from F0 to F1 and subsequently used to drive ATP synthesis is still under investigation, but may involve protein conformational changes or channeling of protons through the enzyme active site (Zubay, 1983, p. 393).

    In summary, ATP is a molecule used to transfer energy from fuel substrates to cellular machinery performing work. The specific way in which this is accomplished is simple in principle but complicated in its actual execution. In principle, energy is derived from foods by their reaction with oxygen, just as when food is burned in a fire. Instead of being released as heat to the surroundings, some of the energy is captured as ATP. To achieve this efficiently, the process is broken down into several small steps. The first stage is to convert food molecules into a two-carbon compound, acetyl-CoA. For carbohydrates this is achieved by glycolysis followed by decarboxylation of pyruvate; fatty acids are converted to acetyl-CoA by beta-oxidation. The acetyl-CoA, whether derived from carbohydrate or fat, is next metabolized in the Krebs cycle. One ATP molecule is generated per acetyl-CoA directly in the Krebs cycle, by "substrate level phosphorylation." The carbon entering the Krebs cycle is released as CO2. Hydrogen present in the original food is now in the form of the reduced coenzymes NADH or FADH2. Most of the energy from aerobic metabolism is derived from oxidation of these reduced coenzymes in the electron transport chain. The summary reactions of the electron transport chain suggest that the hydrogen from NADH and FADH2 combine with oxygen to form water, a well known exergonic reaction. However, this does not happen directly. Instead, the energy released as electrons are transported down the chain (to electron acceptors of increasing electron affinity) is used to generate a proton gradient across the mitochondrial membrane. The movement of protons back inside the membrane through the F0-F1 complex provides the driving force for ATP synthesis by F1. This is referred to as "oxidative phosphorylation" because the phosphorylation of ADP to form ATP is coupled to the oxidative events occurring in the electron transport chain.

    Energy Production and the Athlete
    Athletes experience increased energy need as compared to sedentary people. Bicycle racers and other endurance athletes can require as much as 10,000 calories per day to support their activity level. Bodybuilders commonly consume in excess of 8,000 calories daily to fuel their training and support gains in body weight. The body draws on three different types of food as energy substrates: fats, carbohydrates, and protein. Of these, carbohydrate is the most preferred. Carbohydrates are easily digested and rapidly enter the bloodstream as glucose. Glucose is immediately used as fuel by the cell. A byproduct of glucose metabolism is malonyl-CoA, which inhibits carnitine acyltransferase I. Since long chain fatty acids require the carnitine shuttle in order to be transported inside the mitochondria, they are not used as fuel to a significant extent until the carbohydrates are depleted. Similarly, amino acids can be also oxidized to produce energy but are not used as fuel to a significant extent until carbohydrate is depleted.

    Of course, one of the primary goals of bodybuilders is to increase muscle mass. Therefore amino acids are more valuable to use as protein rather than as fuel. Conventional fats are not a good energy source for bodybuilders either since they cannot be metabolized anaerobically and are not burned rapidly enough to meet the energy demands of high intensity exercise such as weight lifting (Coleman, 1991). Medium chain triglycerides are absorbed and metabolized much more rapidly than conventional fats and are immediately available for energy (Bach and Babayan, 1982). MCTs are an excellent quick energy source, harnessing the caloric density of fat but being metabolized as rapidly as glucose (Bach and Babayan, 1982). Furthermore, MCTs and the ketone bodies they produce decrease glucose uptake and utilization (Lavau and Hashim, 1978) and this seems to result in a glucose-sparing effect (Cotter et al, 1987). MCTs also have a protein-sparing effect and may reduce skeletal muscle protein catabolism, leaving amino acids available for use as protein instead of being oxidized as fuel (Babayan, 1987; Haymond, Nissen, and Miles, 1983). Medium chain triglycerides are an excellent energy source for anyone experiencing increased energy needs (Bach and Babayan, 1982) and are ideally suited to the special needs of athletes.

    References
    Babayan. Medium chain triglycerides and structured lipids. Lipids 22: 417-420 (1987).
    Bach and Babayan. Medium chain triglycerides: an update. Am. J. Clin. Nutr. 36:950-962 (1982).
    Coleman. Carbohydrates: the master fuel. In: Sports Nutrition for the 90s, eds. Berning and Steen. Aspen Publishers, 1991.
    Cotter, Taylor, Johnson, and Rowe, A metabolic comparison of pure long chain triglyceride lipid emulsion (LCT) and various medium chain triglyceride (MCT)-LCT combination emulsions in dogs. Am. J. Clin. Nutr. 45: 927-939 (1987).
    Crozier. Medium chain triglyceride feeding over the long term: the metabolic fate of C-14 octanoate and C-14 oleate in isolated rat hepatocytes. J. Nutr. 118: 297-304 (1988).
    Guyton. Textbook of Medical Physiology. Published by W.B. Saunders, 1976.
    Haymond, Nissen, and Miles, Effects of ketone bodies on leucine and alanine metabolism in normal man. In: Amino Acids - Metabolism and Medical Applications, Eds. Blackburn, Grant, and Young. Published by John Wright PSG Inc., pages 89-95 (1983).
    Lavau and Hashim, Effect of medium chain triglyceride on lipogenesis and body fat in the rat. J. Nutr. 108: 613-620 (1978).
    Vander, Sherman, and Luciano. Human Physiology - The Mechanisms of Body Function. Published by McGraw-Hill Book Company, 1980.
    Zubay. Biochemistry. Addison-Wesley Publishing Company, 1983.
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    By Arthur E. Roberson, Ph.D

    Introduction

    Even during rest the human body is constantly metabolizing energy to maintain itself. The rate at which energy is expended by the body, expressed in calories per hour (or more rigorously normalized to calories expended per kg body mass per hour), is known as the metabolic rate. The basal metabolic rate (BMR) is the body's rate of energy ex-penditure while at rest. This represents just the energy requirements of maintaining life, consisting mostly of maintenance of body temperature, heart rate, breathing, nerve transmission, and electrochemical gradients across cell membranes. The basal meta-bolic rate accounts for 65-75% of daily energy requirements (Van Zant, 1992). Other compo-nents of metabolic rate in-clude the thermic effect of feeding (TEF; also re-ferred to as diet-induced ther-mogenesis, or DIT), the thermic effect of activity (TEA), and adaptive thermogenesis (AT); Van Zant (1992). The components of energy expenditure are illustrated in figure 1. Metabolic rate is affected by many parameters such as eating (caloric consumption as well as dietary composition), activity (dependent on type, inten-sity, and duration of activity), lean body mass, age, sex, hor-mones, and drugs.

    Since all of the energy expended by the body is ul-timately converted to heat (except when work is performed outside the body), metabolic rate can be determined by the amount of heat energy liberated by the body (Guyton, 1976). A calo-rimeter can be used to directly measure the heat given off by the body. However, since greater than 95% of the energy liberated by the body is derived from the reaction of foods with oxy-gen, the metabolic rate can also be calculated from the rate of oxygen con-sumption (Guyton, 1976). In many studies metabolic rate, or energy expenditure, is expressed in terms of oxygen consumption.

    Thermic Effect of Feeding Medium Chain Triglycerides

    After consuming a meal the food is digested, released into the bloodstream, and trans-ported to all the cells of the body. There, it reacts with oxygen to produce energy. Some of the energy is captured in ATP, the energy source used directly by cellular machinery performing work. Calories consumed in excess of energy requirements will be stored as body weight. About 55% of the energy contained in food is liberated as heat during the process of ATP formation (Guyton, 1976). This release of heat energy from the oxida-tion of foods represents an increase in metabolic rate and is accompanied by increased oxygen consumption.

    Feeding different dietary items while maintaining caloric intake affects oxygen con-sumption (Baba, Bracco, and Hashim, 1982). That different foods, normalized for en-ergy content, increase the metabolic rate to different extents probably reflects the ten-dency of a particular food to be burned for energy versus being stored as body weight, as well as its extent of digestion and absorption. That protein increases the metabolic rate more than carbohydrate and conventional fat suggests that certain amino acids may di-rectly stimulate thermogenesis (Guyton, 1976). The increase in energy expenditure caused by feeding is known as diet-induced thermogenesis or the thermic effect of feed-ing (Van Zant, 1992). MCTs cause profound postprandial ther-mogenesis because they are very caloric dense and are absorbed and metabolized very rapidly. The rapid oxida-tion of MCFAs in the liver causes an increase in postprandial oxygen consumption, i.e. metabolic rate. The in-crease in metabolic rate resulting from MCT ingestion has been measured in humans as well as in rats, using LCTs as controls (Seaton et al, 1986; Hill et al, 1989; Baba, Bracco, and Hashim, 1982). The data seem straight forward, well con-trolled, and statistically significant.

    Baba, Bracco, and Hashim (1982) observed that rats overfed MCT gained significantly less fat than rats fed an isocaloric diet containing LCT as the fat source. This was at-tributed to higher resting oxygen consumption (metabolic rate) in the MCT group. The authors explained this by pointing out that while conventional fats are transported as chylomicrons and are largely stored as body fat, MCTs are transported directly to the liver where they are oxidized extensively to produce energy. The rapid oxidation of MCTs results in increased oxygen consumption, increased heat generation, and increased metabolic rate.

    In 1986 Seaton and colleagues demonstrated in humans that a meal contain-ing MCTs in-creased oxygen consumption 12% above basal levels for 6 hours following the meal, while the LCT-containing meal increased oxygen consumption by only 4%. This indi-cates that MCTs are burned faster than conventional fats and increase the meta-bolic rate more. The increase in energy expenditure accounted for 13% of the energy contained in the MCT meal and 4% of the energy contained in the LCT meal.

    Hill and coworkers (1989) also compared the thermogenic effect of medium chain tri-glycerides with that of long chain triglycerides. Ten male volunteers were hospitalized and fed diets containing 30% of calories from either MCT or LCT. Metabolic rate was measured before, during, and after the experiment. Each subject was studied for one week on each diet in a double-blind crossover design. The thermic effect of food (TEF) is defined as the difference between metabolic rate during a six hour period after eating and the resting metabolic rate. That is, it is a measure of the increase in metabolic rate caused by eating the test meal. On day one of the experiment, the TEF of the meal con-taining MCT accounted for 8% of the ingested energy, while the TEF of the LCT meal accounted for 5.5% of the ingested energy. On day six of the experiment, the TEF of the MCT meal had increased to 12% of ingested energy, and the TEF of the LCT meal was 6.6% of ingested energy (figure 2). This means that the MCT-enhancement of the metabolic rate increased during the course of the experiment as the subjects became acclimated to the MCTs. On the last day of the trial the subjects were fed a liquid diet by continuous tube feeding. During this experiment it was found that the TEF of the MCT meal increased to 15.7% of ingested energy, and the TEF of the LCT meal was 7.3% of ingested energy. So the increase in metabolic rate was even greater when MCT was administered con-tinually.

    Mechanisms of Thermogenesis
    The chemical mechanism underlying this thermogenic effect is unknown at present, but several suggestions have been advanced. Hill and coworkers (1989 and 1990) demon-strated that MCT overfeeding results in increased hepatic de novo fatty acid synthesis in man. This process is energetically costly and could account for the lesser efficiency of storage of MCT-derived energy. The observed increase in thermogenesis agrees well with the en-ergy cost associated with de novo lipogenesis (Hill et al, 1990). This obser-vation was corroborated by Crozier (1988) working with isolated rat hepatocytes.

    Alternatively, if electron transport is uncoupled from oxidative phosphorylation the en-ergy spent to establish an electrochemical potential gradient across the mitochondrial membrane is dissipated as heat instead of being conserved as ATP (Baba, Bracco, and Hashim, 1987). For example, in brown adipose tissue a pathway exists allowing proton leakage across the mitochondrial membrane (Nicholls, 1979).

    Another means of dissipat-ing energy as heat, believed to occur in liver mitochondria, is redox cycling in-volving the glycerophosphate and malate shuttles (Berry et al, 1985; Crozier et al, 1987). In the glycerophosphate shuttle, energy is spent to pump reducing equivalents outside the mitochondria to drive the reduction of dihydroxyacetone phos-phate to glycerol-3-phos-phate in the cytoplasm. The glycerol-3-phosphate then diffuses into the mitochondria and is oxidized to reform dihydroxyacetone phosphate, which then diffuses out of the mitochondria to complete the cycle. The net result is the shuttle of glycerol-3-phosphate and dihydroxyacetone phosphate across the mitochondrial mem-brane (Berry et al, 1985; Crozier et al, 1987; Zubay, 1983, p. 401). Free energy is con-sumed to drive the cycle, but since no net work is performed the energy ultimately ap-pears as heat (Berry et al, 1985). The malate/aspartate shuttle is analogous.

    Finally, increased activity of Na-K ATPase has also been suggested as a thermogenic mechanism for wasting energy as heat (Levin and Sullivan, 1985). It is estimated that 10-40% of the total energy expended by the cell is used to maintain the concentration gradient of sodium and potassium ions across the cell membrane (Vander, Sherman, and Luciano, 1980). Since these ions also can cross the membrane by passive diffusion, an increase in the activity of the enzyme could be a mechanism for spending ATP.

    In all of the models - de novo fatty acid synthesis, proton leakage, redox cycling (or other futile cycles), and Na-K ATPase - the MCFAs are rapidly oxidized (explaining increased oxygen consumption), energy is consumed (explaining the low ef-ficiency of storage of MCT-derived energy) and heat is produced as a by-product (explaining the thermogenic effect). Considerable evidence exists to support the in-volvement of de novo fatty acid synthesis as a mechanism for MCT-induced ther-mogenesis (Hill et al, 1989; Hill et al, 1990; Crozier, 1988) but other mechanisms may be involved as well. The reader is re-ferred to Levin and Sullivan (1985) and Van Zant (1992) for reviews on thermogenesis and energy balance.

    References

    Baba, Bracco, and Hashim, Enhanced thermogenesis and diminished deposition of fat in response to overfeeding with diet containing medium chain triglyceride. Am. J. Clin. Nutr. 35: 678-682 (1982).
    Baba, Bracco, and Hashim, Role of brown adipose tissue in thermogenesis induced by overfeeding a diet containing medium chain triglyceride. Lipids 22: 442-444 (1987).
    Berry, Clark, Grivell, and Wallace, The contribution of hepatic metabolism to diet-induced thermogenesis. Metab. 34: 141-147 (1985).
    Crozier, Medium chain triglyceride feeding over the long term: the metabolic fate of C-14 octanoate and C-14 oleate in isolated rat hepatocytes. J. Nutr. 118: 297-304 (1988).
    Crozier, Bois-Joyeux, Chanez, Girard, and Peret, Metabolic effects induced by long-term feeding of medium chain triglycerides in the rat. Metabolism 36: 807-814 (1987).
    Guyton, Textbook of Medical Physiology. Published by W.B. Saunders, chapter 71 (1976).
    Hill, Peters, Yang, Sharp, Kaler, Abumrad, and Greene, Thermogenesis in humans during overfeeding with medium chain triglycerides. Metabolism 38: 641-648 (1989).
    Hill, Peters, Swift, Yang, Sharp, Abumrad, and Greene, Changes in blood lipids during six days of overfeeding with medium or long chain triglycerides. J. Lipid Res. 31: 407-416 (1990).
    Levin and Sullivan, Regulation of thermogenesis in obesity. In: Novel Approaches and Drugs for Obesity, eds. Sullivan and Garattini, John Libbey and Co. Ltd. (1985).
    Nicholls, Brown adipose tissue mitochondria. Biochim. Biophys. Acta 549: 1-29 (1979).
    Seaton, Welle, Warenko, and Campbell, Thermic effect of medium chain and long chain triglycerides in man. Am. J. Clin. Nutr. 44: 630-634 (1986).
    Vander, Sherman, and Luciano, Human Physiology - The Mechanisms of Body Function, p. 236. Published by McGraw-Hill Book Company, 1980.
    Van Zant, Influence of diet and exercise on energy expenditure - a review. Int. J. Sports Nutr. 2: 1-19 (1992).
    Zubay, Biochemistry. Addison-Wesley Publishing Company (1983).
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    Don't use MCT oil on a carb cycling diet though. You'll end up using the MCTs for energy instead of the long chain fatty acids that make up most body fat. They can be great for you high carb folks though.
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    Quote Originally Posted by T-Bone
    Don't use MCT oil on a carb cycling diet though. You'll end up using the MCTs for energy instead of the long chain fatty acids that make up most body fat. They can be great for you high carb folks though.
    You talking about a low carb diet?....Parillo uses it specifically for low carb diets, for the most part high protein and lots of fiberous carbs.It's great for cutting up.
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    I know some old school BB'ers that use MCT oil during their cutting phase (zero carb) to keep energy up but also to keep their muscles looking fuller and more vascular as well...they swear by it, but personally I've never used it.

    Hey bigbody52, any particular brands you interested in?
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    Willieman, good info on the MCT's...I am actually planning on using it as part of a low-carb diet/cutter(UD 2.0 to be exact)Great book by the way and Lyle McDonald recommends it for that diet and the reasons willieman mentioned.(so thats why t-bone)

    Stryder, I have been looking at the 32oz bottle from Ultimate Nutrition and Twinlab also has a 16oz bottle as well.Those are the only two I have really looked at but any would be fine.(i trust your judgement)

    Thanks
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    I'm familiar with Twin Lab's. They are both good companies...I'll get some in and let you know when it's available on the site.
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    Thanks Stryder!I'll be waiting!
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    Any idea on ETA Stryder?
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    Ultimate Nutrition MCT Gold now in stock!
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    Thanks alot Stryder, I will be ordering some tonite!!
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    how would you supplement MCT's before v02 training? 30mins?1hour?what about if i am taking a cordyceps supplement from MST for my AM running (6am)
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    6 years. Impressive bump
  

  
 

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