Boils down to what’s already been stated: low intensity (effective) exercise increases the number of mitochondria and high intensity (efficient) exercise increases the function of mitochondria – we need both to be awesome. 
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No, this is only the view of Bishop et al. The other group around Gibala disagrees with this view. This disagreement is what this series of papers is all about.
I think before thinking about what increases mitochondrial function we need to have defined what function it is we want. They do many different things. Do we want them to be able to use Fatty Acids as energy source or is it just something specific to anaerobic metabolism etc. I don’t know. My guess is what we want is to increase the ability to use fat.
Thanks for providing the opposing views. While I the find original research has its holes (Stephen Seiler’s work on 80/20 looks like Swiss cheese trying to replace the Hoover Dam for holding back water along the Colorado River in Nevada), I found the rebuttals unconvincing. However, I think the real indicators as to whether the rebuttals “hold water” (pun intended 
) will be whether the world tour teams (who have access to exercise physiologists that can read the same stuff we have access to) change their team training protocols as a result of their research papers.
When considering these kinds of endeavours, we always need to remember that pro athletes are different than amateur athletes. Not only in the amount of time they have to train but also their physiology, meaning they most likely are high responders to both volume and intensity vs non-pro athletes. So while a lab protocol may be of benefit to them, it may be next to useless for the weekend warrior.
(As well, without access to measurement, the amateur rider, unlike the pro, has no idea if what they are doing is creating the desired effect, i.e. mitochondrial biogenesis.)
That said, long Z2 rides are a great opportunity to grow lots of other abilities.
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A few months back on NPR I heard an interview with a researcher who was studying muscle memory and why many athletes who test positive and are sidelined for a year or two come back relatively strongly when they return to competition. He said that the use of anabolic steroids drives the production of mitochondria in muscle cells and that these elevated levels of mitochondria remain in the cells for up to 15 years after stopping the steroids. If I remember correctly, he said some body builders had hundreds of mitochondria in some muscle cells. He added that these artificially high counts of mitochondria would be especially beneficial to endurance athletes, essentially giving them an advantage throughout their competitive careers. He also said the anabolic steroids would be most effective in producing mitochondria if taken at the age at which an individual’s natural testosterone level is highest. The interviewer seemed to want to close that conversation path and went in another direction.
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This fact has been previously mentioned, sourly, on the AACC podcast. Juice up during those training months, then go clean during race season and enjoy the full natty boost!
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I think the key finding was not necessarily the production of the mitochondria but that training (and anabolic steroids) develops many nuclei per muscle cell, and that these nuclei linger for many years, almost indefinitely. When you stop training, the cell shrinks and the muscle fibers atrophy, but the nuclei remain: Muscle memory discovery ends ‘use it or lose it’ dogma - Science & research news | Frontiers
There may also be another similar study talking about mitochondria, and if there is my apologies! This is the study that was posted on this forum and some others earlier this year so I thought it might be the one you were thinking of.
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Which brings up a good point that other factors can influence mito, not just exercise. A mito supportive diet is also a must to get the biggest bang for your buck.
I must admit as research scientist myself I find most sport science papers intellectually interesting but of minor value for deriving any practical advise. And I agree so much with your take on Seiler/80/20. I was really shocked when I looked up the original papers and compared them to what is floating around the internet. Really shocked.
However, w/r to those crosstalk papers, really the main deficiency is the fact, the most cited studies in there are with sedentary or only healthy participants.This chart here from Bishop (which is probably what 95% of all reader will only look at … and draw their conclusions):
not a a single data point is from a study with somehow trained subjects. Still, many people will see this and miss this important fact. Gains are easy in the beginning, but what about later. Do you need intensity to push mitochondrial biogenesis further. We don’t get this anwser from the papers.
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Alex Hutchinson on this “debate” … however, while I really like his final remarks no word on the lack of data on actually trained people.
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Do more squats!
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