Thanks for the link!

Good info! I just got my VO2 max, AT and LT tested this week and its certainly good to know more about it all. Thanks for sharing!

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http://www.MattRussellTri.com -Pro Triathlete -Tri Coach

I wrote the link about thresholds referred to above. If anyone has questions about the material, I will try to answer them as best as possible.

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Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom

Jerry,

Thank you for putting great time and energy into that article. It has been incredibly helpful to me, and my understanding of the physiology of sport!

Thanks.

Nice job carving through a very meaty topic!
For me, the great debate on AT was among Brian Whipp (rip), James Davis, and George Brooks in the 70's.

Jerry, one question i have that I did not see mentioned in the article. First, I apologize in advance for using confusing/wrong terminology, but here it goes:

I have read a lot of recent research about the acidosis that occurs in the muscles during higher intensity exercise (above the MLSS) that states it is more likely is due to H+ ion accumulation from ATP hydrolysis and not because of the lactate accumulation in the muscle. If anything, I was under the impression that lactate works to decrease metabolic acidosis. I find it difficult to make sense of the entire situation since current scholarly articles seem to be split about 50-50%, with half asserting the newer above ideas and the other half holding onto the premise that lactic acid accumulation in the muscles slow down glycolysis and/or other ATP re-synthesizing systems.


Hopefully my rambling makes some sense and you (or anyone) can clear this up for me!?


(I do understand that in practice the lactate accumulation curve does trend right directly with increased endurance performance and have a full grasp of how this all practically applies... I'm more interested in trying to figure out more as to what is going on at the biochemical level).

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http://cyclussports.com/ - #ZeroPositive #CyclusSports
http://app.strava.com/athletes/355549
https://twitter.com/ryanAjoyce

It seems clear that a deydrated athlete will have a reduced capacity to buffer lactic acid, but is there much data out there regarding what level of dehydration actually produces a noticeable difference. Obviously a multi-hour race can reduce blood volume quite a bit, but what about normal day-to-day fluctuations? If I drink too much coffee the day before a 10k am I dooming my chance of a PR? Or is the difference rather negligible at that level?

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Tri Me.
Work Me.

I have all the articles but haven't read them in years. Brooks has done a lot of work on lactate metabolism and is frequently on a panel when it is discussed at ACSM. As i remember they do not get into the dynamics behind the threshold. This is best explained by the work of Alois Mader.

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Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom

Whipp and Davis argued about whether the "gas exhange anaerobic threshold" occurs at a fixed blood lactate level.

I believe you are referring to the articles published by Roberg several years ago. I am not sure it was really anything new though it did cause a stir. Lactate is formed from pyruvate by adding two hydrogen ions. I believe one is a free floating H+ while the other comes from NADH. I could be wrong on the specifics of the chemistry since I do not have a background in chemistry, biology or exercise science. So Roberg said the formation of lactate removed an hydrogen ion and thus helps lower the acidity of the muscles. There was at least one discussion amongst several researchers in the Journal of Applied Physiology a few years ago on Roberg's iideas.

But I believe that in the process of producing pyruvate which precedes the formation of lactate, hydrogen ions are produced by glycolysis. This is the source of the hydrogen ions. So when lactate is formed there are still a lot of hydrogen ions still left in the muscle from the glycolysis process after lactate is formed. And lactic acid does not enter the process at all even though all over the world people associate lactic acid with problem. There may be a biochemical expert here who could clarify this.

Since we have been involved with lactate (17 years now) it was always our understanding that lactate was not the culprit for the burning feeling or the inhibition of contraction but that hydrogen ions were the metabolite that caused the problem. There are some who point to other metabolites such as potassium as the cause for the cessation of contraction. Like anything it is getting clarified over time.

The one thing that is clear is that fatigue is associated with lactate build-up though few believe lactate is the actual cause. So a good marker of the underlying problem is lactate accumulation even though it is not the actual problem.

The real value of lactate is not the threshold, though that is important. Its real value is that the measure of lactate enables one to assess both the aerobic and anaerobic systems. The energy systems are probably the most important thing one is trying to affect with training though certainly not the only thing. The measurement of lactate in the right context lets one assess these energy systems. And over time it can tell you if desired changes have taken place. I have to thank Jan Olbrecht for the insight that it is mainly about energy systems.

I hope that helps but as I said I may not be the best one to answer specific chemistry questions.

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Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom

cool, that explanation goes a long way to untangling all of the "i read a bit of this here but then i read a bit of that there" information I had bouncing around in my head. Thanks much

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http://cyclussports.com/ - #ZeroPositive #CyclusSports
http://app.strava.com/athletes/355549
https://twitter.com/ryanAjoyce

Got mine tested this year, was one of the most valuable tests to date. Made it a very enjoyable base training cycle.

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Jerry,

Thanks for the article. Coupla questions:

--Does the "training to train" system explain and/or quantify the semi-apocryphal gains that Mark Allen achieved under the Maffetone running system and the early-season "patience" phase?

--Is it accurate that, as an AG endurance athlete racing regional events of 2-5 hours, the object of my training should be to increase my LT as a %age of VO2 max? And that the main physiological way to do that is by increasing mitochondrial mass in muscle cells? Trying to connect a few dots here but it's a lot of info for my peanut brain.

--Can the lay reader extrapolate useful tri training info from Olbrecht's swimming book?

I appreciate your time.

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_____________________________________
What are you people, on dope?

—Mr. Hand

I am not knowledgeable on what Mark Allen did or the Maffetone running system so I cannot answer that. When I wrote this I was quoting a top coach in the US. He mainly trained runners but also advised some swimming coaches. After working with Olbrecht for several years I believe the best way to interpret this is that aerobic capacity slowly increases over years and certainly increases during a season. So a lot of the training is building this aerobic capacity so that one can then train harder later on. These harder workouts will not be at a higher percentage of VO2 max and therefore no more stressful. But one has to be careful that aerobic capacity has truly increased. For a discussion of aerobic capacity or VO2 max see this on our site.

http://www.lactate.com/vo2max.html

For example, Olbrecht once told me that a 50 m swimmer uses almost none of his or her aerobic system for energy during a race. But that a strong aerobic base is necessary for tolerating the training at higher levels even for pure sprinters. Someone like Pieter van den Hoogenband who held the 100 m freestyle record for nearly 8 years had a very high aerobic capacity which allowed him to workout at much higher levels even though most of the energy for his race would be provided by anaerobic systems. And one of the swimmers he advised for the London Olympics (Ranomi Kromowidjojo) set the Olympic records in the 50 and 100 m freestyle. She has and needs an extremely high aerobic capacity to tolerate the hard training regimen and also to recover faster.

For endurance athletes such as triathletes the aerobic system is the main source of energy but it has to be slowly built so that even harder workouts can be tolerated later on. One of the problems with endurance athletes is that they can get faster by lowering their anaerobic capacity and this lulls the athlete into thinking he or she is now more fit and will then train harder. This often has negative results.

I am sure there will be many who will disagree but it is food for thought. That is why it is important to know if any improvements are from an increase in aerobic capacity or due to a decrease in anaerobic capacity.



Increasing the LT is highly desirable but one has to understand just how it is being done. Some ways have long term benefits while others are only of temporal value.

Here is a chart with some accompanying text from our website on the triathlon

http://www.lactate.com/...bic_controlling.html

Implications for Training

Since training can affect both of these capacities in ways not always expected, it is useful to continually monitor an athlete to assess whether training is having the desired effects. The following chart indicates what can happen to lactate levels when aerobic and anaerobic capacity changes.



The chart can be read as follows. In the upper left hand box where anaerobic capacity rises and aerobic capacity also rises, lactate production could go up or down at a specific effort level. An increase in anaerobic capacity will tend to increase lactate production while and an increase in aerobic capacity will tend to lower it. So when both of these capacities increase, the net effect could be either higher or lower lactate production. It could go up or down depending upon which change had a greater effect.

When aerobic capacity goes up and anaerobic capacity goes down, the amount of lactate produced is often dramatically less. This is a situation quite common with swimmers and many other athletes during base training. However, when a swimmer increases anaerobic capacity training later in the training cycle it is quite common to see lactate levels rise because aerobic capacity has essentially topped out for the training period. Thus, the athlete is in the middle box on the left hand side. For an athlete such as a swimmer who is competing in short events (1-2 minutes) this is an indication that they are getting faster as their anaerobic system will be producing energy more quickly during these short events.

For triathletes they should know which box they fit in or else they can not accurately assess their training.
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This is getting long so I will stop here. As far as the Olbrecht book helping triathlon training, all the principles are applicable to any form of training though the book is focused on competitive swimming which are mainly anaerobic events. One of the athletes he advised won the 10 k swimming event in Beijing. He also used them with Luc van Lierde and other triathletes.

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Jerry Cosgrove

Sports Resource Group
http://www.lactate.com
https://twitter.com/@LactatedotCom

"One of the problems with endurance athletes is that they can get faster by lowering their anaerobic capacity and this lulls the athlete into thinking he or she is now more fit and will then train harder."


Maybe most of ST knows this but it's news to me. Brilliant! thanks x2

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_____________________________________
What are you people, on dope?

—Mr. Hand

Yes, the biochemists have worked out the stoichiometry (sort of like biochemical math) and there is no net hydrogen ion accumulation from the production of lactate. However, you have a good perspective on this. Lactate tells us something about the metabolic fitness of the muscles, so it is important to measure. It helps to paing a more complete picture of an athlete. Thank goodness for products like the lactate scout. I used to do this the hard way with the full biochemical assay and a spectrophotometer. It was a long, laborious process. Now it is easy. Back then I had to think long and hard about doing lactates, now the decision is easy.