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So you are not actually measuring the underpinning physiological changes occurring at cellular level, but other proxy integral measures for the result of such changes, such as VO2max and BL response.
Yes, and no.
At the most basic level, one is interested in the gene expression of various proteins as a result of various exercise processes. These proteins will lead to various changes in cellular structure and chemistry.
No one yet understands this but they are studying it and learning more all the time. These changes result in changes to the energy producing capabilities of the muscle which will reflect in the ability of the person to contract the muscles in terms of speed and sustainability.
There is more than one energy producing system in the body but for most races there are only two that matter, aerobic metabolism and glycolysis. These two systems affect performance from races of 20 seconds up to ultra marathons. Thus, it would be prudent to understand just how these systems work to produce the energy necessary for contraction.
One system dominates energy production after 40 seconds and that is aerobic metabolism. There are contributions of energy from glycolysis after this time up till ultra long races. One can still contract the muscles without glycogen or a source of glucose so obviously there are examples where almost 100 % of the energy is from aerobic metabolism, nearly all of it the metabolism of fats.
Because of the small amount of energy from glycolysis in long races, exercise scientists essentially discounted it as a factor in endurance races. But there was a problem as several have pointed out, people with the same ability to produce energy by aerobic metabolism often exhibited very different abilities in long races. And one of the consistent findings was that the out put of glycolysis was causing this differential ability to utilize the aerobic metabolism. Hence the origin of the terms such as anaerobic threshold, lactate threshold, maximal lactate steady state (MLSS) and OBLA (onset of blood lactate accumulation.)
Most who study this just referred to some unknown factor or pointed to a result in the environment, not in the muscle as the cause of this difference. However, some looked for a metabolic explanation and they believe they found it. This metabolic explanation, not at the level of gene expression, but at a subsequent point in the process involved the interaction of the aerobic and glycolytic systems and the strength of each.
They named a process in the body for glycolysis similar to what exercise scientists had named for aerobic metabolism. They called it anaerobic capacity or VLA max to represent the rate of pyruvate production in the body. They also found that this capacity varied widely in people and obviously athletes. Now aerobic metabolism and glycolysis are the result of several things but rather than look specifically at each of the sub components, it became important to look at the two systems as a whole. This does not mean that there is no interest in the causes of each but for explaining muscle contraction it was easier to consider them as wholes within the cell.
They also found that two capacities interacted and affected how much of each capacity could be utilized in a race. The stronger the anaerobic capacity the more the contracting muscles used glycolysis and the more metabolites were produced which eventually limited contraction or the amount of aerobic energy that could be utilized.
So it makes sense to consider both in any athletic event. Aerobic capacity is best measured by a VO2max test but there are other ways of approximating it. One is blood lactate because the fuel for the aerobic system at VO2max is almost 100% pyruvate or lactate. Lactate is also the product of glycolysis so it can be used to assess the strength of the other system too. But any lactate test that does this is subject to the same problem that any other non VO2 max test has, it does not reflect the contribution of each system to the effort level. But lactate also reflects the output of glycolysis so can be used to try an assess anaerobic capacity.
It is not VO2 max and lactate. It is lactate as a window into both systems. Some find it easy to estimate VO2 max this way since the window into the aerobic system only requires a 4-6 minute sub-maximal test and not a one hour all out test. It is just as precise or maybe more so than a FTP test. The lactate test gets even more precise with multiple readings. Any maximal test to estimate anaerobic capacity is less than a minute so not onerous on any athlete.
Now you have offered up the MMP curve as an example of what can be done without lactate. Each point on the MMP reflects the input of the three energy systems but after 10 second it reflects just glycolysis and aerobic metabolism. The curve that Dr. Coggan provided above is a perfect example of two athletes with the same aerobic capacities but differing anaerobic capacities. The one with the greater anaerobic capacity will excel at shorter distances as the curve indicates but at some point will start to get slower at longer distances. It is an almost perfect illustration of Mader's theory which is the basis for my comments.
Go to
http://www.lactate.com/...riathlon_faster.html for examples of athletes that differ in time to exhaustion at various distances which is the basis for this curve.
I have been patiently pointing this out for a couple years but it seems to get lost in the rhetoric and the mocking. Now one can disagree with this assessment but it is something that one should carefully consider and not just reflexively dismiss it.
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Jerry Cosgrove
Sports Resource Group
http://www.lactate.com https://twitter.com/@LactatedotCom