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atavistclimer
May 18, 2006, 5:47 PM
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Evidently, lactic acid isn't necessarily a bad thing after all. Wierd. http://www.nytimes.com/2006/05/16/health/nutrition/16run.html?ex=1148097600&en=1d44fa0b49133c03&ei=5087%0A
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circello
May 18, 2006, 6:43 PM
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There's a lot of bad science in that article.
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jt512
May 18, 2006, 7:12 PM
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It's true that lactate itself does not cause muscle fatigue. Muscle fatigue is caued by the increased acidity in the muscle cell caused by the anaerobic breakdown of glucose. Whether or not lactate itself is used as a muscle fuel is subject to debate, as far as I can tell from the literature. What I gather is that Brown has shown that muscles (mitochondria, specifically) can burn lactate, but whether or not they actually do burn lactate (at least to a significant degree) in living muscle tissue is unclear. In fact there is evidence that they don't.* The conventional view is that lactate is transported out of the muscle cell and carried to the liver, where it is converted to glucose. This glucose can then be transported back to the muslces for fuel. -Jay *Sahlin K, Fernstrom M, Svensson M, Tonkonogi M. No evidence of an intracellular lactate shuttle in rat skeletal muscle. J Physiol. 2002 Jun 1;541(Pt 2):569-74. PMID: 12042360
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bill413
May 18, 2006, 7:19 PM
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In reply to: Yet, Dr. Brooks said, even though coaches often believed in the myth of the lactic acid threshold, they ended up training athletes in the best way possible to increase their mitochondria. "Coaches have understood things the scientists didn't," he said. No. If the premise (about the role of lactate ) is correct, then coaches have been equally wrong about lactic acid. If the premise is incorrect, then the scientists did (more or less) understand it. Coaches have understood how to train, by looking at the results. Not necessarily by being correct, or understanding, the underlying theory.
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lemon_boy
May 18, 2006, 7:35 PM
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I read the article and laughed my ass off. Brooks must be a fat ass that wouldn't know lactic acid if it slapped him in the face. the article says he ran collegiate track back in the day, but i have a hunch he was just the water boy. the article makes it sound like athletes are going to start some revolutionary training/performance method by getting pumped out of their gourds and THEN getting down to business. ummmmmm, survey says......... no f'n way.
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karma
May 18, 2006, 8:11 PM
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I think it is hilarious that because none of you are capable of reading through the article and attempting to understand it, you simply ignore what it says and assume that the scientist behind the study was nothing more than a fat ass. Brilliant. Truly brilliant. The article recognizes the fact that coaches have been doing the right thing for years and that science was behind because no one had set out to examine the evidence and the physiology with new methods. Think about it: The first study on this involved frog legs and a battery in the early 1900s. Its not like this just came up out of nowhere, Brooks started his research in the 1970s! Rather than simply assume you know everything and that any new evidence or study is automatically false because it bucks the trend, why not examine the facts, educate yourself and produce an intelligent opinion?
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helios
May 18, 2006, 8:17 PM
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For a science related story in a newspaper, I thought it was actually pretty decent. It had two sources, Brooks and Gladden, both are at respectable institutions and they aren't co-authors either. That's much better than most science articles. Sure, it oversimplifies things, leans too much on an unchallenged hypothesis, and makes scientists look dumber than jocks, but at least it does one thing well: Gets us to rethink a long held notion that didn't have a lot of evidence in the first place. As far as the Sahlin group goes, they ground up muscle tissue, ripped out the mitochondria from cells in the presence of protein-eating enzymes, then looked for a lactate shuttling protein. And low, they didn't find one:roll: Jay, I think that was a good summary, but wouldn't showing that cells can't transport lactate out of them be evidence FOR being able to burn lactate? I guess this means my gym is going to take down the route "Lactic Acid Attack" soon. Might want to redpoint that one tonight...
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zivo
May 18, 2006, 8:45 PM
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since I bike a bit, here's some food for thought: Lance A has been claimed to be able to work more before lactic acid builds up AND to get rid of it faster than other competitors. He trains like a maniac (disregarded pain that turned out to be cancer because he thought it's normal for the training he does) so maybe he has trained his muscle cells to use / burn lactic acid for fuel interesting article
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korporal
May 18, 2006, 11:34 PM
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WARNING: Everything in this post is based on my AP (college level course during high school) Biology class. I have done no research, only read books. The Technical / Abstractl: Lactic acid is a product of fermentation. Fermentation happens when there is no oxygen present to process glucose into ATP (cellular energy). Depending on the structure and function of the cell, fermentation can produce either alchohol or lactic acid. Muscle cells produce lactic acid. The first step of cellular respiration (process which converts glucose to ATP) is splitting glucose, a six carbon sugar, into two three carbon sugars called pyruvate. This happens regardless of the presence of oxygen. In fermentation, an electron is removed from one of pyruvate's hydrogens and stored at its energy level in an electron carrier to be used later in cellular respiration. The product of this electron "theft" is lactic acid. During regular cellular respiration (when oxygen is present) pyruvate is broken down and processed further untill all of its hyrogen ions are "stolen." Fermentation produces 2 of these captured electrons for every glucose molecule, regular cellular respiration produces many more (15?). The number of ATP produced is directly related to the number of these excited electrons are produced. The more electrons, the more ATP. When oxygen is present again, the cell converts the lactic acid to pyruvate again. And the cell processes it into plentiful amounts of ATP. I have never heard anything about lactic acid being transprorted to the liver. The application / the meat: When you exersize heavly you body demands more oxygen than your heart and lungs can provide. All the available oxygen in your body is consumed, and they start fermenting glucose into lactic acid as a result. Less ATP (cellular energy) is produced as a result, and the lactic acid build up in the muscle cells. The muscle cells do not have as much energy and don't function as well. The build of lactic acid could also affect the cells function by increasing the cells size and internal pressure. When you stop/reduce your exersize more oxygen becomes present and more efficent processes convert the lactic acid to cellular energy and the muscles return to normal. How this relates to training I'm not so sure. The only way I train is running and doing ab workouts untill I can't move, then resting for twoish days for dryland before ski season.
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ccarver99
May 19, 2006, 1:17 AM
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I thought this article was very well written, and simplified a complicated subject without losing any of the value. Being a current biochemistry major in college and a competitive swimmer for the last five years, most everything he says seems to fall in line with personal experiences and stuff I have been taught.
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jt512
May 19, 2006, 3:58 AM
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In reply to: As far as the Sahlin group goes, they ground up muscle tissue, ripped out the mitochondria from cells in the presence of protein-eating enzymes, then looked for a lactate shuttling protein. And low, they didn't find one:roll: Jay, I think that was a good summary, but wouldn't showing that cells can't transport lactate out of them be evidence FOR being able to burn lactate? First of all, muscle cells can and do transport lactate out of the cell. The lactate gets picked up by the liver, which from it synthesizes glucose, which becomes available to muscle cells as fuel. This is the well known "Cori cycle." Secondly, as I understand it, Brooks discovered a lactate transport protein in mitochondrial membrane of skeletal muscle cells as well as LDH, the enzyme needed for utilization of lactate as fuel, inside mitochondria. He also demonstrated that isolated mitochondria will readily burn lactate. So, in principle, it appears that muscle cells could burn lactate aerobically. The question remains, do they? Sahlin's group as well as another lab were unable to reproduce Brooks' finding that mitochondria will burn lactate in vitro. Thus it appears unclear at present, whether they do in vivo. Jay
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angry
May 19, 2006, 4:24 AM
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I did some interesting studies on occlusion. When I did something that pumped my forearms, my grip strength was significantly reduced by blood occlusion long before lactic acid built up in significant quantities. So getting pumped isn't only lactic acid, it's your muscles inability to get replentished with oxygen quick enough. I didn't read the article.
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ed
May 19, 2006, 5:15 AM
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I think this article can fit fine into current knowledge. Most enzymes, in this case Lactate dehydrogenase (responsible for conversion of pyruvate to lactic acid), work in both directions depending on the abundance of reactants and products. I don't believe it is the case that in the presence of oxygen LDH just shuts off, but more likely converts lactic acid back into pyruvate and that is then transported to the mitochondria for oxidative phosphorylation, where the real energy is made. So it would stand to reason that there is no lactate transporter for the mitochondria because they use pyruvate, not lactic acid. Most of these topics don't interest me too much but I think some interesting discussion has been sparked. jt512 is correct about the Cori cycle, but the presence of this mechanism doesn't mean another system couldn't be active under different conditions. I haven't read the actual research articles by the scientists interviewed so I don't know the the conditions they used in their studies. In fact, from my experience as a biochem major and a physical therapy student currently, the body is full of backups, compensations and checks and balances for just about everything, otherwise one thing going wrong can throw everything out of wack. This concept is called homeostasis, or keeping a balance. As for the point of performing our best after a strong pump, I think the NY times article didn't do a good job of explaining that well. I think what was meant by that is that during a training cycle, the last phase before a desired peak performance involves short fast bouts of exercise with rest. This is not done immediately before that big race/onsight attempt. Don't post much so please excuse the volume...just wanted to contribute. Ed
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fluxus
May 19, 2006, 5:17 AM
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I thing the article was a mess, but that's not a judgement of Brook's work. Jay I'd love to get your thoughts on these claims from the NYT article: "The understanding now is that muscle cells convert glucose or glycogen to lactic acid. The lactic acid is taken up and used as a fuel by mitochondria, the energy factories in muscle cells. Mitochondria even have a special transporter protein to move the substance into them, Dr. Brooks found. Intense training makes a difference, he said, because it can make double the mitochondrial mass." and later: "Through trial and error, coaches learned that athletic performance improved when athletes worked on endurance, running longer and longer distances, for example. That, it turns out, increased the mass of their muscle mitochondria, letting them burn more lactic acid and allowing the muscles to work harder and longer." I've never read anything other than the NYT bit that acted as if it was settled science. Am I worng about this? It certainly does not show up in the many physiological and kinesiological texts that I read. I'm not sure of the relationship of the NYT article and Brook's published work. Here is part of the abstract from Brook's paper titled "Endurance training, expression, and physiology of LDH, MCT1, and MCT4 in human skeletal muscle" it can be found here: http://www3.baylor.edu/HHPR/faculty/Kreider/Courses/AJP278-571-9-00.pdf ACCORDING TO THE CELL-CELL lactate shuttle hypothesis, lactate is more a metabolic intermediate than an end product (7, 8). Lactate is continuously formed in and released from diverse tissues such as skeletal muscle, skin, and red blood cells (RBCs). Lactate also serves as an energy source in highly oxidative tissues such as the heart and a gluconeogenic precursor for the liver. Lactate exchanges between these tissues appear to occur under various conditions ranging from postprandial to sustained exercise (11, 13, 18, 36). In humans, arterial lactate concentration is low at rest and increases little during moderate exercise because lactate oxidation and gluconeogenesis match production (5, 11, 15, 36). The cell-cell lactate shuttle is therefore a central means by which the intermediary metabolism in diverse tissues is coordinated (8). Cell-cell lactate exchanges are facilitated by membrane- bound monocarboxylate transporters (MCT; see Refs. 17, 30, 33). In skeletal muscle, two MCT isoforms (MCT1 and MCT4) with different kinetic properties have been described (17, 37). Recently, the existence of an intracellular lactate shuttle was hypothesized and demonstrated (9, 12), suggesting that cytosolic lactate produced in myocytes and hepatocytes can be transported and oxidized in mitochondria of the same cell. Direct lactate oxidation by mitochondria is dependent on the presence of mitochondrial lactate dehydrogenase (LDH) and a pyruvate/lactate transporter (9). Endurance training decreases muscle lactate concentrations by increasing lactate clearance (15) and by decreasing lactate production at low but not high power outputs (5). MCT1 expression increases after shortterm training in humans (6) and chronic electrical stimulations in rats (25) and decreases after denervation in rats (37). We hypothesized that during endurance training, regulation of MCT expression would occur to adapt membrane lactate transport capacity to maintain lactate exchanges despite attenuated lactate concentrations. For that purpose, we determined the effect of 9 wk of leg cycle endurance training on expressions of MCT1 and MCT4 in human vastus lateralis muscle. Also, we evaluated the effects of training on glucose and lactate fluxes and muscle exchange (4, 5). Because the mitochondrial lactate/pyruvate transporter has been shown to be MCT1 (10), and because training has been shown to increase muscle mitochondrial mass (14, 20), muscle mitochondrial MCT1 content was evaluated. Furthermore, we determined if changes in muscle lactate release and oxidation were associated with training-induced changes in MCT expression.
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helios
May 19, 2006, 3:08 PM
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In reply to: First of all, muscle cells can and do transport lactate out of the cell. Yeah, I think I was getting confused between the transporter and LDH. It was LDH that Sahlin didn't find, right?
In reply to: Sahlin's group as well as another lab were unable to reproduce Brooks' finding that mitochondria will burn lactate in vitro. Thanks Jay. But it was my understanding that the methods they used were more distructive to the mitochondrial membrane proteins then the methods Brooks employed. Brooks made a point in his paper that they didn't used trypsin or proteolytic digestion. They confirmed their findings of LDH in mitos with electron microscopy. Although I agree that someone should definitely verify the findings of Brooks, I find it odd that these groups did not use the same procedures for mito prep.
In reply to: Thus it appears unclear at present, whether [mitochondria] do [burn] in vivo. Word. So, if lactic acidosis isn't responsible for muscle soreness what is?
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timmay
May 19, 2006, 3:48 PM
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Another option that might be causing muscle fatigue other than the lactic acid hypothesis is the accumulation of inorganic phosphate. In a paper by Westerblad et al, (2002 - Muscle Fatigue: Lactic Acid or inorganic phophate the major cause?) he says that an increase in inorganic phosphate from creatine phosphate may depress contractile function, especially in high-intensity exercise (lasting only minutes). He also listed a few papers that show a drop in pH in the muscles does not affect contraction in mammalian muscle at physiological temperatures. However during even more intense activation, such as a continuous maximal contraction, failure of action potential propagation is going to become more important in fatigue.
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jt512
May 19, 2006, 6:45 PM
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In reply to: In reply to: First of all, muscle cells can and do transport lactate out of the cell. Yeah, I think I was getting confused between the transporter and LDH. It was LDH that Sahlin didn't find, right? I don't recall, and I don't have time today to re-read the paper. My main recollection was that he observed no oxidation of lactate in mitochondria. Whether that was because of no LDH or other reasons, I can't recall.
In reply to: In reply to: Sahlin's group as well as another lab were unable to reproduce Brooks' finding that mitochondria will burn lactate in vitro. Thanks Jay. But it was my understanding that the methods they used were more distructive to the mitochondrial membrane proteins then the methods Brooks employed. That was Brooks' argument. I'm not a lab bench scientist, so I'm not in a position to judge that for myself.
In reply to: In reply to: Thus it appears unclear at present, whether [mitochondria] do [burn] in vivo. Word. So, if lactic acidosis isn't responsible for muscle soreness what is? First of all "lactic acidosis" is a misnomer. Under anaerobic conditions lactate and acid each accumulate in the cell. The distinction is not trivial or semantic because the "extra" step in glycolysis in which lactate is produced from pyruvate under anaerobic conditions actually reduces the H+ concentration in the cell. Thus production of lactate is thus alkalyzing, not acidifying. It is known that lactate does not cause muscle fatigue. Experiments have shown that muscle cells do not fatigue when lactate concentration is high when the pH of the cell is controlled. It is the drop in pH under anaerobic conditions that causes muscle fatigue. Presumably, glycolytic enzymes don't function well under lower pH. Jay
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jt512
May 19, 2006, 7:02 PM
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In reply to: Jay I'd love to get your thoughts on these claims from the NYT article: "The understanding now is that muscle cells convert glucose or glycogen to lactic acid. The lactic acid is taken up and used as a fuel by mitochondria, the energy factories in muscle cells. That is Brooks' claim. It is controversial. I think most scientists in the field are calling it the "lactate shuttle hypothesis." Conventional wisdom is that lactate leaves the muscle cell and is recycled into glucose in the liver. Apparently, Brooks' has also shown -- and this appears to be less controversial -- that other muscle cells can also absorb this lactate and convert burn it. Whether this conversion occurs in mitochondria, though, is controversial.
In reply to: Mitochondria even have a special transporter protein to move the substance into them, Dr. Brooks found. It's not that "special" because, as I understand it, it is the same transporter that transports pyruvate. Conventional wisdom is that it is pyruvate that gets transported; Brooks' controversial claim is that it's mostly lactate. In reply to: Intense training makes a difference, he said, because it can make double the mitochondrial mass." That's what I learned in school.
In reply to: That, it turns out, increased the mass of their muscle mitochondria, letting them burn more lactic acid and allowing the muscles to work harder and longer." Again, it's controversial as to what those mitochondria are burning.
In reply to: I've never read anything other than the NYT bit that acted as if it was settled science. Am I worng about this? The article is poor, in part, because it is confounding two distinct subjects, one well settled, the other controversial. Lactate doesn't cause muscle fatigue. That is known. Whether mitochondria burn lactate is controversial, and probably has no practical importance to training. When you increase the mitochondrial mass by training you are increasing the muscle's aerobic capacity. It's just not clear whether the mitochondria are burning lactate or pyruvate. Jay
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bill413
May 19, 2006, 8:36 PM
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Jay - as a former biochemist - that felt like a wonderful summary. Thanks.
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karl_hungus
May 19, 2006, 9:20 PM
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Jay, et al, Here's the source article, which probably has more credence than some NYT hack re-hashing scientific terminology that they most likely don't understand enough to write about. Of course, that doesn't mean I understand it either way. http://www.berkeley.edu/news/media/releases/2006/04/19_lactate.shtml -Bob
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fargoan
Jun 26, 2006, 11:39 PM
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In reply to: In reply to: So, if lactic acidosis isn't responsible for muscle soreness what is? First of all "lactic acidosis" is a misnomer. Under anaerobic conditions lactate and acid each accumulate in the cell. The distinction is not trivial or semantic because the "extra" step in glycolysis in which lactate is produced from pyruvate under anaerobic conditions actually reduces the H+ concentration in the cell. Thus production of lactate is thus alkalyzing, not acidifying. Jay One point for the sake of semantics-- "Lactic acidosis" is a broader term that refers to the pH state of the extracellular compartment (ie blood) of the body. Under anaerobic conditions in the muscle, where there is production of large quantities of lactic acid, lactic acid is transported from muscle cells to the liver via the bloodstream. In the liver, it is used to produce additional glucose molecules and eliminate lactate (this is known as the Cori Cycle, although it would appear that the study under discussion argues that myocytes/RBCs can bypass the Cori Cycle somewhat by processing their own lactate in their mitochondria-- this concept is controversial, the Cori Cycle is well accepted). When large amounts of lactic acid/lactate are in the blood stream (headed to the liver), the pH of the bloodstream drops, creating a situation refered to as "anion-gap metabolic acidosis." This is lactic acidosis. An example would be someone who has never trained or exercised and decides to put down their Cheetos, get off the couch, and run a marathon. HUGE amounts of lactate are produce and overwhelm the buffering capacity of the system. Severe lactic acidosis can be fatal. Local lactate accumulation would be a more specific way of describing what happens when you get the muscle burn during a workout, although I've not spent any time looking into whether lactic acid is directly or indirectly related to somatic pain generation, or unrelated to the pain entirely. Jonathan
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jt512
Jun 27, 2006, 2:11 AM
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In reply to: In reply to: In reply to: So, if lactic acidosis isn't responsible for muscle soreness what is? First of all "lactic acidosis" is a misnomer. Under anaerobic conditions lactate and acid each accumulate in the cell. The distinction is not trivial or semantic because the "extra" step in glycolysis in which lactate is produced from pyruvate under anaerobic conditions actually reduces the H+ concentration in the cell. Thus production of lactate is thus alkalyzing, not acidifying. Jay One point for the sake of semantics-- "Lactic acidosis" is a broader term that refers to the pH state of the extracellular compartment (ie blood) of the body. Under anaerobic conditions in the muscle, where there is production of large quantities of lactic acid, lactic acid is transported from muscle cells to the liver via the bloodstream. In the liver, it is used to produce additional glucose molecules and eliminate lactate (this is known as the Cori Cycle, although it would appear that the study under discussion argues that myocytes/RBCs can bypass the Cori Cycle somewhat by processing their own lactate in their mitochondria-- this concept is controversial, the Cori Cycle is well accepted). When large amounts of lactic acid/lactate are in the blood stream (headed to the liver), the pH of the bloodstream drops, creating a situation refered to as "anion-gap metabolic acidosis." This is lactic acidosis. An example would be someone who has never trained or exercised and decides to put down their Cheetos, get off the couch, and run a marathon. HUGE amounts of lactate are produce and overwhelm the buffering capacity of the system. Severe lactic acidosis can be fatal. Local lactate accumulation would be a more specific way of describing what happens when you get the muscle burn during a workout, although I've not spent any time looking into whether lactic acid is directly or indirectly related to somatic pain generation, or unrelated to the pain entirely. Jonathan Thank you for confusing the subject by restating the century-old misconception that the cell produces lactic acid under anaerobic condittions. It doesn't. It produces acid and lactate in separate steps of glycolysis; and, in fact - since I love repeating myself - the lactate-producing step in glycolysis is alkalyzing. Jay
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joshy8200
Jun 27, 2006, 2:50 AM
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Interesting that this topic made the frontpage today. My professor just covered this is my physiology class today. He stated that lactic acid causing fatigue is a myth and the research has been around for 20 years that has shown that. Again this is a professor at the University of North Carolina at Chapel Hill teaching in the Nutrition and Exercise and Sport Sciences departments...and he stated that lactic acid does not cause fatigue or soreness or acidity. The research for this has been around for 20 years, but as shown on this website many people just haven't come learned about it.
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papizjb
Jun 27, 2006, 3:49 AM
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In reply to: In reply to: In reply to: In reply to: So, if lactic acidosis isn't responsible for muscle soreness what is? First of all "lactic acidosis" is a misnomer. Under anaerobic conditions lactate and acid each accumulate in the cell. The distinction is not trivial or semantic because the "extra" step in glycolysis in which lactate is produced from pyruvate under anaerobic conditions actually reduces the H+ concentration in the cell. Thus production of lactate is thus alkalyzing, not acidifying. Jay One point for the sake of semantics-- "Lactic acidosis" is a broader term that refers to the pH state of the extracellular compartment (ie blood) of the body. Under anaerobic conditions in the muscle, where there is production of large quantities of lactic acid, lactic acid is transported from muscle cells to the liver via the bloodstream. In the liver, it is used to produce additional glucose molecules and eliminate lactate (this is known as the Cori Cycle, although it would appear that the study under discussion argues that myocytes/RBCs can bypass the Cori Cycle somewhat by processing their own lactate in their mitochondria-- this concept is controversial, the Cori Cycle is well accepted). When large amounts of lactic acid/lactate are in the blood stream (headed to the liver), the pH of the bloodstream drops, creating a situation refered to as "anion-gap metabolic acidosis." This is lactic acidosis. An example would be someone who has never trained or exercised and decides to put down their Cheetos, get off the couch, and run a marathon. HUGE amounts of lactate are produce and overwhelm the buffering capacity of the system. Severe lactic acidosis can be fatal. Local lactate accumulation would be a more specific way of describing what happens when you get the muscle burn during a workout, although I've not spent any time looking into whether lactic acid is directly or indirectly related to somatic pain generation, or unrelated to the pain entirely. Jonathan Thank you for confusing the subject by restating the century-old misconception that the cell produces lactic acid under anaerobic condittions. It doesn't. It produces acid and lactate in separate steps of glycolysis; and, in fact - since I love repeating myself - the lactate-producing step in glycolysis is alkalyzing. Jay Jay, I'm not aware of any step in glycolysis that produces acid. I'm saying this nicely, trying not to offend anyone's intellect. The only place I'm aware of lactate being produced is from pyruvate using NADH and is catylyzed by LDH. I would also appreciate any legitimate literature demonstrating that lactate is not produced intracellularly. Also, concerning the "destructive techniques" used to isolate mitochondria: To the layperson, grinding cells may sound destructive, but to isolate intracellular compartments, you first grind the cells, and then spind down the mixture. What collects at the bottom are cell membrane components, i.e., big lipids and intergral proteins. The stuff floating in the liquid layer is intracellular organells. (I spend a large part of my day, every day, at a bench in the lab).
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