I think you should substantiate your statements with exact references from the scientific literature because to be honest and do not take this wrongly, but if I had to chose who to trust, between ISM who has a PhD, is Assistant Professor and is trainer of the UAE Emirates World Tour team and a random guy (who I accept is more knowledgeable than me) who has a very entretaining and interesting podcast on the internet, I (with all due respect) would chose ISM.
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Refinement of La curve: this went better this time. You really need a proprer drop of blood, especially with an analyzer which requires only a small amunt of blood.
Now I have a clear baseline. First rise above baseline at ~250W. Nice move compared to 4 years ago. Baseline at 0.9-1.1 mmol/L.
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Found that self testing took a couple rounds to get sorted. Once you have your materials arranged and a process defined it goes pretty well.
I keep different size lancets on hand. Some guys need bigger pokes that others to get that good blood drop out.
Given your background, will be curious to see your analytic approach to the data 
@sryke I have yet to be about to do a full max test (of any kind) without needing assistance with lactate. I’ll see if I can find the trick Steve Neal suggests, but it’s a pain even if you get it.
However, I rarely do full max tests. No need. I can get that info some other way and save strips.
One thing I know Arild does is to “spot check” his athletes. I have started to do this. It’s easy enough (on trainer) to let your intensity stabilize a bit (be it tempo, near LT1, whatever), reach over for the analyzer and get a quick peak of where you are.
Because it’s sub-threshold intensities, the needle doesn’t move that quickly. So no need to assess very often. I have started to like the spot checking, though.
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Can you refer me to a longer explanation on this? Also yes, I know his relationship with Brooks, who is also not infallible. There are a few things from his papers I want to argue with as well but they’re not germane to this conversation.
@empiricalcycling is factually correct in stating that training reduces blood lactate by decreasing lactate production. Here’s some of Brooks’ very own data on the topic.
(Note how net lactate release tends to be lower after training even when the subjects were tested at the same %VO2max, and therefore a higher absolute power.)
He is also correct in stating that MHC expression and muscle respiratory capacity don’t always change in parallel, such that the latter can be similar in type IIa and type I fibers in highly trained athletes.
He is also correct in stating that if you have a lot of type I motor units, you’re going to have to ride really hard or really long to recruit anything else.
As for ISM, he seems to be far more of a coach than an academic, having published only two or three original studies of humans (and 11 papers total) in his career.
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We can’t use the frequency of publication to determine effectiveness as a scientist. He’s done some very good work where aside from the constant use of “lactate clearance”, like: Metabolomics of Endurance Capacity in World Tour Professional Cyclists - PMC
It’s a cold day in hell where we agree on so much 
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yep, went through quite a few strips. Really haven’t dialed in the “drop generation”.
Wouldn’t know what to do with apart from simply plotting it.
Same here. With the La test I don’t see myself doing much above “comfort level intensity” . The information provided so far is already sufficient. For anything else you would do better with someone else. However, the data is nice enough to extrapolate. Perfect exponential growth. For an MLSS test, I don’t know yet.
And just what novel and important insights have been gained by applying this expensive but mostly just shotgun approach to blood samples?
Side project, can you find a function to fit it, and a more mathematical description of ‘first rise above baseline’ and ‘steeper rise point here’?
(Not having a pop at you, I just find this talk of ‘baseline’ in what is clearly some sort of power function confusing and wish someone would come up with a better definition.)
Sometimes just looking at data is sufficient, no need for fancy algorithms. Look at the grey-dash line in Figure 2
Though my data series looks nicer, points line up nicely.
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just adding this observation, not saying Maffeton is right, this may just be coincidence, but heart rate at my 250W (the last point on baseline) is identical with this MAF heart rate. Exactly.
An exponential function usually fits well. In part that’s why it has been argued that there is no such things as LT.
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I know, mine is one beat off. Drives me nuts. 
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Just Dr. Ferrari’s Medio training zone (80-90% AT4) to improve what he has been calling “lipid power” for decades. Search his article “lipid power” on 53x12.
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Yes - great forum.
Shame he does not comment any more.
He suggests 2-4 hours of medio per week as a good starting point.
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Indeed this guy had it all figured at least two decades ago.
It just seems like everyone has been reinventing the wheel ever since
https://www.53x12.com/the-lipid-power
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Including how much EPO to give people.
Hey, somebody had to say it, right?
(BTW, did anybody else notice how ISM’s PowerPoint featured at least two dopers?)
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This is an interesting one @old_but_not_dead_yet. Thank you for sharing this paper. I have unpacked this a bit more and I find it fascinating that it is in reference to Endurance training. This is my understanding of why this occurred - feel free to agree with or correct the below summary.
Because this training was Endurance based, the subjects increased their VO2 and decreased their VLaMax. Therefore, the lower the anaerobic capacity and the higher the aerobic capacity, the greater the propensity to produce energy away from glycolysis e.g using fat as the preferred substrate rather then glucose. Thus, if less energy is being created via glycolysis, then less lactate is being produced as a by product. This would indicate that the subjects had shifted their LT1 and LT2 to the right.
In a nut shell - increase your aerobic capabilities through VO2 (central factors such as increased stroke volume = more blood pumped to working muscles etc.) and Endurance (peripheral factors through long slow steady rides to increase mitochondrial function and biogenesis, capillarization etc. = more MCT1 to clear any lactate that is produced, more oxygen sites etc.)
It does seem that Anaerobic Capacity and Aerobic Capacity are in direct competition as to who wins as an energy source. I guess it comes down to what sort of rider you are - a sprinter would have a higher Anaerobic Capacity at a given VO2 max, and thus, perhaps a lower LT2 as they need to process glucose quickly for their efforts, whereas a GC rider or long distance rider might have a lower anaerobic capacity but a higher LT2 as they drift away from needing glycolysis as much as the sprinter.
In any case, it seems like a delicate balance of the two systems. If you go to far aerobically, you might lack the ‘punch’ needed to sprint to the line. Alternatively, too much sprint power and your ability to process and clear lactate might be too low for the event your’re riding. Interesting. Well, atleast in my very limited n=1 understanding.