Part II

8 March, 2003.

So, if we find that our runner has little or no evidence of a relationship between his/her race performances (especially if this is so as the distance gets longer), we can be very sure the problem is in his legs.

If you waded your way through the long thread I referred you to above, you will realize that this means the mitochondria, capillaries and aerobic enzymes your training should have created in your leg muscles, did not happen. Whatever training you have done to this point has not been as effective as it could have been. Usually, I have found, for two reasons (as given above):

  1. You don’t run enough mileage.
  2. You train too fast.

Way back in 1973, physiologist David Costill and his coworkers introduced what they termed, the “fractional utilization” of VO2max. Which really just means, how much of their VO2max can each runner actually use in a distance event. The argument was made that those who could use the greatest fraction (percent) of their VO2max stood every chance of being among the faster runners. This “fractional utilization” we now know is basically made up of a runner’s lactate threshold (LT) and their particular economy.

As the authors state,

At all running speeds above 70% VO2max, the faster runners were found to accumulate less blood lactate than the slower runners at similar speeds and relative percentages of their aerobic capacities. The findings suggest that successful distance running is dependent on the economical utilization of a highly developed aerobic capacity and the ability to employ a large fraction of that capacity with minimal accumulation of lactic acid.

Simply put, the more you can use of your maximum aerobic potential in a race, the better you will perform.

As recently as 1997, this paper by Costill was cited by J.A. Hawley et al in a paper aimed at enhancing endurance performance.

As the authors state, “It would appear that the fraction of VO2peak or power than an athlete can sustain for prolonged periods is inversely related to the accumulation of lactate in the working musculature.” (more lactate = lower % VO2max that can be sustained = stop sooner; less lactate = higher % VO2max = maintain for longer).

They go on,

For example, in well-trained endurance athletes, there is little or no increase in blood (and presumably muscle) lactate concentration until the work rate elicits close to 85% VO2peak. Direct support for this comes from the data of Coetzer et al (1993) who reported that black African distance runners had lower blood lactate concentrations after submaximal (21km/hr) and maximal (24km/hr) exercise compared with white runners, despite similar running economies. Elite Kenyan distance runners have also been found to have lower lactate levels than top Scandinavian distance runners during both submaximal and maximal exercise.

Sooooo. Let’s sum all this up, it’s very simple.

  1. Better trained runners can maintain a higher percentage of their VO2max (85% or higher) in a marathon than lesser trained runners.
  2. They can do so because their blood lactate AT ANY PACE or any percentage of VO2max is lower than the blood lactate of less well-trained runners (ie: they are not “tougher” and just somehow putting up with more discomfort than the runners around them, they are actually more “comfortable”, under less lactate “stress”, than all other runners at the same pace/intensity).

This also agrees with a large amount of sport science studies which show a very high correlation between the lactate threshold and performance in distance events. The higher (faster) the running pace at the LT, the faster the pace in distance races.

Sjödin and Svedenhag (1985) in a review on the physiology of marathon running agreed, “the ‘threshold’ is the single best predictor of performance in long-distance running, including the marathon.” Once again, fast pace at LT = fast pace in a distance race.

As I repeatedly stressed in my long earlier thread, the training to improve your VO2max (essentially the stroke volume of your heart) is NOT the same training as that required to raise your LT (increase capillaries, mitochondria and aerobic enzymes in your muscles). The speeds required are totally different. LT training is one case in which faster is NOT better.

So. To go back to our hypothetical runner. After I find out the PR’s of the runner who has approached me, (and assuming he/she has no good relationship between performances), I lactate test him.

Now don’t be concerned, I only bring this in here to explain exactly why our young runner (and possibly yourself) cannot maintain a positive relationship across performances. In short, his LT is weak. It will NOT be necessary for you to undergo lactate testing to know how to proceed to improve your own training and your LT.

You see, I know from his poor race results that my new runner is building lactate long before he should (which is why, as I have tried to explain above, there is NO relationship). Remember, high lactate = poor long distance race ability.

So, somewhere along the way as he increases his running pace, his blood lactate is climbing (earlier than it should and at slower paces than it should). I know this. His results are telling me this, even before I test him. If I can determine when that happens, at what pace/effort that is happening, I will then know exactly how to train him to make the lactate at that pace begin to stay low, and not climb until he runs at a faster pace. And then a faster pace… and a faster pace…

Think of it like this. If your LT is low (at slow pace relative to VO2max), you are “borrowing” from your anaerobic ability to help your aerobic ability maintain the particular pace you are running at. Like having an overdraft at the bank because you cannot live within your monthly wage. But as the race distance gets longer, you cannot borrow more and more, but can only borrow less and less. Until at the marathon, which is 99% aerobic, you cannot borrow at all and your poor aerobic ability is exposed and you are left wondering why the pace is so slow compared to (eg) your 10k.

Now here I would have liked to explain the mechanics of how to test, because although you will not need to be lactate tested, the knowledge of how to do so will be important further down the line. However, for you to understand it fully, you would need to see some charts, which I am unable to post. Fortunately I am able to refer you to a website that does a very good job of explaining the rationale and the lactate testing procedure in a very clear manner. If you would genuinely like to improve your training (and race performances), spend some time and go and read the information on the linked site. It is only a single page of text and charts (although there are other links that some of you might like to explore, although doing so is not necessary). I expect to have to refer to the knowledge the single page contains in later parts.

Lactate Testing - Some Basics

Final summation: if you cannot maintain a good relationship across race performances it is because your LT is not good enough (not a high enough percentage of your personal VO2max). Your LT is dependent on adaptations in your leg muscles caused by training. If you have a poor LT, your adaptations have not occurred well enough (despite even years of training). As will be better explained later, these adaptations are intensity dependent (train too fast, they won’t happen).

My apologies if this appears long-winded, but it is a long-held belief of mine that runners train better if they understand WHY they are doing such-and-such training.

Addendum To Part II

9 March, 2003.

Let’s look at some major negative effects of “borrowing” from your anaerobic ability in a distance event (anything from 5k upwards). (For those of you who do not think you are doing this, just note that if you have a poor(er) pace relationship as the distances increase, you are.)

  1. When the muscle cells in your legs build up too much acidity (caused by running anaerobically), those cells shut down since the acidity inhibits enzymatic action and contractibility in the cell and energy breakdown can no longer continue. So, the more you are trying to stoke the boilers, pour on the speed, and fire on all cylinders, the more some of those cylinders are shutting down. This is not so if you use those self-same cells/fibres aerobically.

  2. Breaking a molecule of glucose down into energy anaerobically is horrendously wasteful of fuel. It will result in fuel economy the equivalent of “2 miles per gallon”. Breaking that exact same glucose molecule down into fuel aerobically results in “36 miles per gallon”. If you are going far enough (HM or marathon), you better be as economical as possible and get as many miles as possible per gallon because otherwise you are going to run out of fuel and crash long before the finish line. Note that the muscle cells that are operating anaerobically will be unable to access your huge store of fat as a fuel (which would give you wayyy better than even 36 mpg). Fuel which would ensure you get to the 20 mile mark and still find you can pour it on.

Think of it like this. Put the smallest compact car you can think of, and a Ferrari, side by side. Empty both fuel tanks, give both of them one gallon of fuel and tell them to go as far as possible. Which is gonna win?

Since your LT measures at what pace you change over from aerobic to (increasingly more) anaerobically-fueled running, it is also a measure of when you stop being economical and become more and more uneconomical. So, we can also say that a low (poor) LT also means poor fuel economy.

Many of you will be able to give examples of guys (I know at least two) who can crank out 20 mile long runs at 6.00m/m and yet not finish a marathon at that pace. Why? Because, due to their precise fuel economy (or lack thereof) they cannot store enough CHO to get them through the final 6.2 miles. Their fuel economy, and therefore their LT, is too low.


On to Part III

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