posted May-16-2006 10:21 AM
Wow. Talk about redefining the rules. According to a Cal/Berkeley professor, lactic acid is actually a fuel, not a caustic waste product.
posted May-16-2006 10:28 AM
Owen Anderson from Running Research news has been talking about ths for while. He also wrote a book called "Lactate LIftoff" that gives you specific workouts for improving you lactate threshold. Also, there are a number articles on Peak Performance Online about this.
posted May-16-2006 11:01 AM
This appears to be the case of a narrow-minded biochemist not looking at the whole picture.
Yes, lactic acid can be used as a fuel, however, not directly by the mitochondria as he asserts. It must be converted back to glucose or pyruvate to be used. The purpose of lactate production is to regenerate NAD+ and allow glycolysis to continue in the absence of oxygen...this is why it accumulates only when we exert ourselves at a level that exceeds our ability to supply our muscles with sufficient oxygen. This cannot go on forever, and producing lactate requires the cell to stop producing pyruvate...which with oxygen would produce 18X as much energy as produced without oxygen and using lactate as the end product.
If his hypothesis were true, wouldn't we be able to run FASTER when lactate levels rise??
He says increasing muscle mitochondria mass enables them to burn more lactic acid, but what he ignores is that it allows a higher level of AEROBIC metabolism, which doesn't use lactate (only produced in the absence of oxygen). And that lactate must be converted before it can be burned in mitochondria.
Add this guy to the list of useless PhDs (like the guy who convinced the South African gov't that HIV drugs CAUSE AIDS).
posted May-16-2006 03:27 PM
Or Fereydoon Batmanghelidj, who in writing "Your Body's Many Cries for Water" created one of the greatest food myths ever.
His suggestion that the US was chronically dehydrated and we should all be drinking 8 x 8 ounce glasses of water a day was based on no scientific basis whatsoever.
quote:Originally posted by Desert Tortoise: Wow, very misleading article. It's filled with half-truths and just plain silly conclusions.
I agree it's misleading. I suspect the article was dumbed down for the general public, who really believe lactate causes muscle soreness and who also believe high levels cause muscle fatigue. The article also ignores the difference between endurance sports and highly anaerobic ones like sprints. The good doctor may well be embarrassed by this simple characterization of his work. Of course that's an inference on my part; one based on what I've said to reporters in the past and what they have actually written that I said.
posted May-16-2006 09:02 PM
Tigger you're very right. When I was doing cancer research our lab put out a big breakthrough that made CNN. I watched them film the segment in our lab and interview people, then went home to set the VCR and tape the segment. I was HORRIFIED to watch their "expert" get the finding completely wrong and totally misconstrue the implications of our work. To this day I never listen to mainstream media about anything of that sort, but look up the original article (haven't done that on this one yet).
posted May-17-2006 01:36 AM
At this moment, it is the most e-mailed article at the NY Times. I've invited the journalist to come here and discuss it with us. I know it's a long shot, but I did this once before and the author of the article in question showed up and held a very good discussion with a group.
I had the most trouble with these paragraphs:
quote:Coaches and personal trainers tell athletes and exercisers that they have to learn to work out at just below their "lactic threshold," that point of diminishing returns when lactic acid starts to accumulate. Some athletes even have blood tests to find their personal lactic thresholds.
But that, it turns out, is all wrong. Lactic acid is actually a fuel, not a caustic waste product. Muscles make it deliberately, producing it from glucose, and they burn it to obtain energy. The reason trained athletes can perform so hard and so long is because their intense training causes their muscles to adapt so they more readily and efficiently absorb lactic acid.
Without those two paragraphs, the article is not far off base.
Lactate thresholds are real, and I think most folks here know this. Distance runners from the 800 to the 10,000 do need to be able to utilize lactic acid, but they also bog down when its production outstrips the muscle's ability to tolerate elevated levels of the stuff.
posted May-17-2006 09:32 AM
I read a more technical article...yes, the reporter got some things wrong, but the article is still, at the very least, strongly misleading.
First, their "proof" is confocal microscopy showing colocalization of lactate dehydrogenase and an oxygen-utilizing complex on the mitochondrial membrane...colocalization is proof of nothing, just an interesting bit of circumstantial evidence. Proof would show direct interaction. The most obvious experiement would be a pulse-chase, where lactate would be radioactively labeled and then the researcher would follow what it was converted into to prove it went to pyruvate and then through aerobic metabolism.
Second, the fact that mitochondria might be able to use lactate directly as fuel changes NOTHING with regards to training. It is not more efficient than using glucose...it requires two extra steps, conversion of pyruvate (which comes from glucose) to lactate, transport of the lactate to the mitochondria, and then conversion of the lactate back to pyruvate. Nothing gained there. Most importantly, The conversion of lactate to pyruvate leads to aerobic metabolism....if the cell was short enough on oxygen to start anaerobic metabolism and produce lactate to begin with, where is the oxygen coming from to utilize lactate as a fuel??
The impact on training here is NOTHING. Increasing mitochondria is done not to use lactate better, but to increase the amount of aerobic metabolism possible before anaerobic metabolism is necessary and lactate begins to accumulate. Just like the colocalization of the proteins, the correlation of increased mitochondria with and lactate usage does NOT prove one has anything to do with the other....there is a much more logical explanation.
I'm not sure what is going on here....if this researcher is really ignorant of running enough to believe that this data somehow has some revelation on training, or if it is being accidentally misconstrued by them or someone else. I do know as a former researcher myself that any finding that reaches mainstream media is usually sensationalized....how many times do you hear on CNN about some finding that will lead to a cure to cancer yet we have none yet?
"Lactate doesn’t cause fatigue – it helps prevent fatigue
Recall that it has long been believed by the running community that lactate causes fatigue. It is this core belief that has caused runners to focus so intently on lactate threshold - lactate causes fatigue and the lactate threshold is the point where there is suddenly enough lactate in the body to cause fatigue to increase rapidly. There is no doubt that blood lactate levels increase with increasing exercise intensity. If lactate causes fatigue then it wouldn't matter if muscles become anaerobic or how lactate increases in the body - these points do not negate the idea that lactate causes fatigue. Lactate does increase with increasing exercise intensity and if it causes fatigue, then the other points are ancillary. Does lactate cause fatigue? Absolutely not!
"Lactate is a totally innocuous substance that, if infused into the bloodstream, has no noticeable effects."(5)
To top off the facts about lactate is this kicker – lactate not only does not cause fatigue as it has long been believed to, but there is reason to believe it actually helps prevent fatigue. How’s that for a complete turnaround of everything you ever believed about lactate?
Researchers examining muscle fatigue in rats caused by a reduced pH and loss of potassium found that the “subsequent addition of…lactic acid led, however, to an almost complete force recovery.” These researchers write:
“In contrast to the often suggested role for acidosis as a cause of muscle fatigue, it is shown that in muscles where force was depressed by high (potassium), acidification by lactic acid produced a pronounced recovery of force. Since intense exercise is associated with increased (potassium), this indicates that acidosis may protect against fatigue rather than being a cause of fatigue.”(6)
What they are saying in the above quote is that lactic acid in the muscles is likely to protect against fatigue, allowing the muscle to work longer and/or harder before fatigue sets in."
[This message has been edited by fredurie (edited May-17-2006).]
"kp9597 Cool Runner posted May-17-2006 11:59 AM -------------------------------------------------------------------------------- Science: Studied under Dr. Gladden at Auburn, where I got my Master's in exercise science, if you can access it you need to read Dr. Gladden's excellent paper: "Lactate metabolism: a new paradigm for the third millenium" from the Journal of Physiology, 2004
he reviews the literature and the previous theories and then expounds on the topic in the NY Times article. Excellent science, pretty technical though. One of the top 2 most accessed articles from the journal for almost 1.5-2 years.
If you can't access it online, email me (on profile) and I can forward it to in in PDF format.
------------------ Kevin"
[This message has been edited by fredurie (edited May-17-2006).]
"This means that workouts that range from longer repeats at just below 10K pace to shorter workouts at 5K pace or better are ideal for LT improvements. While these paces are great for improving the ability of your body to deliver and process oxygen and lactate, even faster paces are needed to improve levels of MCT1. Remember that MCT1 is needed to transport lactate into working muscles. While research into MCT1 is in early stages, it appears that MCT1 levels are only increased during very high intensity exercise. This means short repeats at 3K pace or faster. A couple of examples of MCT1 workouts are 3 minute intervals at 3K pace with 2 minute recovery in between or 2 minute repeats at near maximum pace with 4 minute recovery in between.
It appears that training paces faster than LT make the most improvements. But that does not mean that all workouts should be at that pace. You cannot maintain faster than LT paces for long periods of time. So longer repeats at LT pace or slower are necessary in order to train your body to maintain a quality pace for long periods of time."
[This message has been edited by fredurie (edited May-17-2006).]
posted May-17-2006 01:19 PM
I read the article at Power Running and have to say that these people seem to be making a far bigger claim for their research than they can support. The dismissal of the term "lactate threshold" on the grounds that there isn't an exact threshold is just silly. There is a clear and limited range at which lactate levels rise exponentially and that's agreed upon by all. This need to dismiss "lactate threshold" is simply semantics and nothing more.
What really seems to be going on is a refinement of the notions we have regarding lactic acid, but there are researchers out there who seem to want to grab some head lines by puffing up the claims for their research.
I am certainly no biologist, but I'd like to put up a few paragraphs from a book from 2001 called Lactate Threshold Training by Peter Jannsen, an MD who works with athletes. It is five years old, but the basic points are still good:
quote:High lactate values cause muscle fatigue. When an athlete begins an endurance run at a pace that is too high or begins the final sprint too soon, lactic acid content will increase to high values. The fatigue that follows increased lactic acid will cause the athlete to lose the race.
High lactate values cause acidosis in and around the muscle cells. This acidosis may seriouslyt disturb various mechanisms within the muscle cells. The system of aerobic enzymes in the muscle cell may be seen as a factory where aerobic energy supply is generated. This enzyme system is damaged by acidosis, which decreases aerobic endurance capacity. After acidosis damage, it may take days before the system recovers sufficiently and regains aerobic capacity. When the exercise is repeatedly too intensive (i.e., without sufficient recovery), aerobioc endurance capacity decreases considerably. These overly-intensive workouts then lead to a complex of complaints called overtraining. Acidosis damages the wall of the muscle cell, causing a leakage from the muscle cell into the blood. The day after a heavy workout all kinds of abnormalities can be seen in the blood, especially higher values of ureum, creatine kinase, aspartate aminotransferase, and alanine aminotransferase, which all indicate damage of the muscle cell wall.
posted May-17-2006 06:32 PM
I've already spent more time discussing this on letsrun than I care to dedicate, so if anyone is interested they can look there for my biochemical opinion.
The secondary sources listed above make dangerous leaps of half-logic. Few people say anymore that lactate is a "metabolic bad guy" responsible for nefarious acts. At the end of glycolysis, you have pyruvate and NADH. NAD+ must be replenished to continue glycolysis. If aerobic respiration (pyruvate going to CO2 and ATP) is keeping up, no problem. But in a shortage of oxygen, lactate must be produced because the reaction gives off NAD+ to continue glycolysis. So lactate serves an important function. Nobody is mentioning muscle fatigue here...it's energy metabolism, a totally different subject!
Finally, the significance of lactate threshhold is being totally misconstrued. The point at which lactate rapidly accumulates signals the exertion level at which one's aerobic systems are running all-out...additional exertion requires increased non-sustainable anaerobic respiration. THIS is the significance....nothing to do with muscle fatigue or bad effects of lactate itself...lactate is just a reporter molecule signaling that the athlete's aerobic capacity is tapped out.
Within the same cell, lactate can give ZERO increase in efficiency because it comes from pyruvate, and must be converted back to pyruvate to give energy...and oxygen is required to do so, and if the cell is producing lactate to begin with that means oxygen is in short supply.
When transported to other cells nearby, you could get a proximity effect, whereby muscle fibers with excess oxygen receive lactate produced by nearby cells and have the oxygenn to use it. However, since the cells producing lactate can't do it for long before running out of glucose/glycogen (lactate production is 18X less efficient than aerobic respiration), this is hardly sustainable.
Edit: Additionally, unless the actual paper includes data not mentioned in any of these articles, this study proves nothing they claim it does. They used confocal microscopy to show colocalization of lactate dehydrogenase and oxygen-utilizing proteins on the mitochondrial membranes. While decent circumstantial evidence, it's hardly conclusive proof...there are hundreds of proteins on that membrane. In layman's terms, if you are standing next to a guy at the bus stop and he drops dead, are you guilty of murder for standing next to him? Of course not; you may be a prime suspect but you need to find a smoking gun. Now, if they isolated the mitochondria (doable) and exposed them to radioactively-labeled lactate, and followed the reactivity through the downsteam metabolites to prove it's doing what they say it's doing, the case would be iron-clad.
[This message has been edited by AndyHass (edited May-17-2006).]
posted May-16-2006 10:21 AM
