Concept2 Forum

I saw this article in this morning's NYT and am interested in any thoughts that anyone might have on the subject.

http://www.nytimes.com/2006/05/16/healt ... 16run.html

Will

I was just about to post a link it myself.

Even if the scientists got it wrong on the role of lactic acid, the training we've been advised to do has been in the ballpark: endurance combined with interval work.

This is old news to Xeno's fans and to those junkies of the WP Level 4. I'm finding it hard to believe that US scientists are regarding this understanding as "new", or controversial. There's plenty of reading material from Europe to support it and coaches there have been on board longer than here it seems. To anyone who's remotely familiar with "red meat" and "white meat" types of muscle, a simple formula for anearobic respiration that produces lactate, and another one for one type of aerobic respiration that consumes it, what else would one expect?

- Doug

This is a cute article for those new to athletics. Reality is that scientists have known for many years that lactic acid was a source of energy. Problem is that the general media/fitness industry can make more money by propogating myths, and does so. Wait a few more years and you will see this article again, I remember reading it back around 2000; just in another newspaper.

Hmm now im confused. I remember in BIO last semester that glucose, C6H12O6 was given to the mitocondria where it was put through a staircase of gradual energy release(of ATP) where the final product is CO2 and H20.

And it also was that anarobic activity (alcoholic production or lactic acid) only happened in the absence of oxygen.

They say in this article that the glucose is turned into lactic acid and then given to the mitocondria...

What do i believe? textbook or article?

csabour wrote:Hmm now im confused.
What do i believe? textbook or article?

You and me both. This is a pretty good link

http://home.hia.no/~stephens/lacthres.htm

that seems to contradict lactic acid as fuel. In any case, it doesn't matter to us exercising. Lots of long rows will make you faster and there's plenty of reason to throw in a few fast workouts now and then. Hey, sounds like Mike's Wolverine Plan.

Would be interested, however, if lactic acid is really a fuel or a by-product that needs to be flushed.

The key part of the above link, which is Copyright 1996 Stephen Seiler, is:

"There is a critical metabolic fork in the road at the end of this chemical pathway. At this fork, glucose has been converted from one 6 carbon molecule to two, 3 carbon molecules called pyruvic acid, or pyruvate. This pyruvate can either be shuttled into the mitochondria via the enzyme pyruvate dehydrogenase, or be converted to lactic acid via the enzyme lactate dehydrogenase. Entry into the mitochondria exposes the pyruvate to further enzymatic breakdown, oxidation, and a high ATP yield per glucose. Conversion to lactate means a temporary dead end in the energy yielding process, and the potential for contractile fatigue due to decreasing cellular pH if lactic acid accumulation proceeds unchecked."

I have added the emphasis. Maybe this is being proven incorrect now? Anyway it seems at odds with the NY Times article, as I read it.

Evidently it is being proven wrong. It's been known for a long time that lactate could be reoxidized. The trouble was that this seemed to take place primarily in the liver (although heart muscle apparently loves lactate), too slowly to prevent debilitating lactate buildup in intensely working muscles. If Brooks is right -- and he's state-of-the-art when it comes to this stuff -- it turns out that muscle-cell mitochondria also are capable of processing lactate, more or less on the spot. For endurance-strength sports like rowing, it follows that training that tends to build these mitochondria will trump training that doesn't. Other things equal.

Here's a link to an earlier version of the story that is more illuminating than Kolata's rehash in the Times: http://www.sciencedaily.com/releases/20 ... 235214.htm

I haven't looked at Brooks' paper yet, but may try to get round to it one of these days. Among other reactions: I suspect that whereas cells may actually be able to process lactate, with elite athletes better at it than novices, too much lactate accumulation is almost certainly still a bad thing.

NavigationHazard wrote: Here's a link to an earlier version of the story that is more illuminating than Kolata's rehash in the Times: http://www.sciencedaily.com/releases/20 ... 235214.htm

Thanks for the link. Interesting reading. Both sources, the older 1996 and Brooks, favor endurance training to either increase "the number of lactate transporter molecules in mitochondria" or synthesize additional mitochondria and construct new capillaies.

Sounds exactly the same for a training regimen.

I’ve copied your comment from another thread: “I, and I think others, would be interested in your thoughts on any implications of Brooks' work. See the NY Times thread under training.” Well, I can say that when I began my graduate work in Kinesiology, the textbook Exercise Physiology: Human Bioenergetics and Its Applications by George Brooks and Thomas Fahey had a tremendous influence on me and shaped my whole approach to the understanding of physiology and human performance. Since then I have read dozens of papers by Brooks and they tend to be clear and bring a different perspective to concepts that students of exercise science have been conditioned to accept without question, such as “oxygen debt”. For example, “Anaerobic Threshold: Review Of the Concept and Directions For Future Research” (Medicine & Science In Sports & Exercise, vol. 17, pp. 22-31, 1985) notes that “the [AT] hypothesis fails on the bases of theory and prediction”, and discusses lactate kinetics during exercise.

In 2004, a couple of researchers named Allen & Westerblad published a paper called “Lactic Acid – The Latest Performance-Enhancing Drug” (Science, vol. 305, pp. 1112-1113). It described how lactate can actually have ergogenic properties – at least for skinned, isolated animal fibers artificially stimulated in a laboratory setting. You would think scientists would know better than to make wholesale conclusions about the effects of lactate extrapolated to whole-body human beings during exercise, but the paper caused some ripples in the scientific literature. A couple of recent summaries regarding lactate & exercise are a point-counterpoint debate called “Lactic Acid Accumulation Is An Advantage/Disadvantage During Muscle Activity” (Journal of Applied Physiology, vol. 100, pp. 1410-1414, 2006) and “Lactic Acid and Exercise Performance: Culprit Or Friend?” by Cairns (Sports Medicine, vol. 36, pp. 279-291, 2006). So not only in the popular literature, but also in the scientific literature, has there been confusion about the effects of lactate on performance. (The whole “its bad – no, its good” thing reminds me of the Woody Allen movie “Sleepers” where the doctors of the future laugh at how it was once thought smoking was bad for you!)

In my experience, virtually everyone (scientists, coaches, athletes, laypeople, the media, etc.) has had a tendency to oversimplify muscular fatigue during exercise. For years past and probably for years to come, “Hard exercise causes lactic acid to form and that in turn causes fatigue/pain” is about as far as people take it. While it’s not completely clear exactly why muscles fatigue during short-term/high-intensity events like a 2K (as opposed to marathon-type events where glycogen depletion or dehydration are most likely to be the dominant factors), accumulation of various metabolites that interfere with the ability of muscle fibers to properly contract are probably the dominant factor (as opposed to effects on the central & peripheral nervous systems). Probably the biggest fatigue factor is the increase in intracellular Na+ and the increase in extracellular K+ that occurs with intense muscular contractions, altering the sarcolemma’s membrane potential and the fibers’ ability to respond to stimulation. (An excellent review is “Na+-K+ Pump Regulation and Skeletal Muscle Contractility”, by Clausen, Physiological Reviews, vol. 83, pp.1269-1324, 2003.) Other probable factors include Ca++ ions leaving the sarcoplasmic reticulum and entering the mitochondria and interfering with oxidative phosphorylation, and the toxic effects of ammonia that accumulates as the result of breakdown of amino acids as well as IMP (from AMP resulting from the myokinase reaction: ADP + ADP = AMP + ATP). And of course lactic acid, whose accumulation is associated with a decrease in pH (rise in acidity) of the muscle environment, which is known to inhibit enzymes that regulate the glycolytic process. I guess its no surprise that many researchers (and coaches, etc.) would focus on lactate since it is the easiest to measure. But it is one of only several factors that are involved in the fatigue process in what appears to be a complex and perhaps synergistic way. Clearly large accumulation of lactate is correlated with muscle fatigue in many (but not all) cases, though correlation is not causation. Also implicating lactate in the fatigue process is the fairly consistent research finding that artificial buffering (such as by consuming baking soda prior to exercise) can raise muscle pH and enhance performance. (Before anyone asks, I’m not eager to try this myself, since common side effects to bicarbonate loading include severe stomach cramps and diarrhea.)

The answer to the question of “Lactate – Friend or Foe?” is simple: it’s both. Brooks himself has noted that lactate “sits at a metabolic crossroads” and is a “two-edged sword”. Rapid glycolysis produces the necessary ATP that oxidative metabolism alone can’t provide, with lactate as a byproduct. This probably contributes to fatigue. You can’t make an omelet without breaking some eggs. But lactate is not simply a “waste product”; it’s a tremendously useful fuel and raw material for resynthesizing glycogen or amino acids. Some tissues thrive on lactate and are very efficient at oxidizing it for energy – tissues like the heart & Type I muscle fibers. (Modest amounts of lactate injected into the circulation would be and excellent ergogenic aid for marathon runners.) During exercise, lactate produced by glycolytic fibers can enter the bloodstream and circulate to oxidative fibers for consumption – an ideal means of efficiently distributing fuel to all working fibers while keeping tissue pH within tolerable limits. More energy production and reduced fatigue. Win, win. So, yes, lactate is a fuel – as has been known for decades. I can sympathize with Dr.Brooks’ frustration that some people can’t see the obvious (such as the proper way to pace a 2K…)

As I have been saying from the beginning, training for 2K racing needs to include the proper combination of high-intensity intervals and prolonged, low-moderate intensity workouts (“distance training”). Intense intervals maximize energy production, both aerobically and anaerobically (well-trained athletes produce more lactate than lesser trained counterparts). Distance work increases endurance and enhances the ability to resist fatigue; adaptations include increased lactate transporters in glycolytic fibers to help lactate enter the bloodstream, and increased mitochondria in oxidative fibers so they will be better able to utilize lactate as fuel. The whole lactate discussion illustrates why I subscribe to the “black box” approach to training & performance. Training goes in, and as long as the right performance comes out, we don’t really have to know what happens in-between. Some people feel compelled to assign causes without sufficient justification, which can actually cloud the issues and cause people to train inefficiently or incorrectly. (I could go off on a tangent about HR-based training, but I don’t have the energy.)

Mike Caviston

Thanks Mike,

A interesting read as usual. And thanks for not going off on that tangent about HR based training. Like Fox Mulder, I want to believe.

Rick

Thanks, Mike!
Joan

dougsurf wrote:This is old news to Xeno's fans

Old news to all sorts of people. I'm wondering what the Times was thinking.

Mike - Good stuff, thank you. I think I remember that you have been reluctant (or too busy) to discuss the physiological underpinnings of the WP, but it looks like this goes a long way to doing just that. Excellent.

Now I really -do- wish that you would take us on that "tangent". There is sooo much brain power and ink being spent promoting HR based training that it is hard to ignore. Give us some ammunition!

Regards,
MM

Being entirely new to training of any sort whatever, when I began to erg 18 months back, I took a copy of the UK C2 Training manual as my guide.
One must begin somewhere.
I suspect that it would be considered HR based.

It would be a great help for me if some one with the writing skills and apparent knowledge of the previous posters would either shed some light or at least post some links.

So far this thread is balanced and informative - let us pray it ascends, rather than falling into the . . . well, let us hope.

Thank you, and please consider enlightening us all - not merely with the alternatives, but with the reasoning.