Well given that the NIH now requires Open Access after a certain point for any funded work (which you should know based on all your claims about your grant writing success), one could argue that ethically all of this research should be publicly available. That, and the predatory nature of pretty much all journals at this point...
NIH requires open access for the studies that it funds. The vast majority of biomedical research, however, is privately funded, mostly by pharmaceutical companies. Do you believe that you should automatically have access to those data as well? If so, why?
NIH requires open access for the studies that it funds. The vast majority of biomedical research, however, is privately funded, mostly by pharmaceutical companies. Do you believe that you should automatically have access to those data as well? If so, why?
I steal Seiler papers all the time. Well worth it for the great PRACTICAL use he provides to athletes. Opposed to you. Obsessed with stuff literally nobody cares about. Which is why I leave all yours in the digital vault that I've just broken into.
Congrats to sirpoc and others for creating a fascinating view on how one can adapt the Norwegian method for lower mileage runners.
The stories are truly inspiring.
I'm not interested in the underlying physiology, TBH I couldn't care less. If it works it works.
It's not like sirpoc invented something new, he just copied a way of training that is very effective for cyclists and he used the same principles in running - this turned out to be a very effective and sustainable training method.
The only thing that could be argued is that is was inevitable that a very good (sub-elite) TT cyclist would eventually become a very good (sub-elite) runner, regardless of the training method. But he did one year of Daniels training and this resulted in overtraining and a disappointing 18:xx 5k.
So with this method he apparently found a sweet spot (pun intended) between training load and sustainability.
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Reason provided:
Fixed spelling and grammar.
It's not like sirpoc invented something new, he just copied a way of training that is very effective for cyclists and he used the same principles in running - this turned out to be a very effective and sustainable training method.
The only thing that could be argued is that is was inevitable that a very good (sub-elite) TT cyclist would eventually become a very good (sub-elite) runner, regardless of the training method.
I wouldn't say that it is inevitable, because that presupposes that all cyclists have or can develop their running economy well enough to convert a high sustained rate of energy production into a reasonable speed. Furthermore, there are lots of cyclists who are fast (on the flats) largely because they are big, not because they are aerobically gifted.
But, yeah, endurance training works, at least if you let it. It's when folks want to progress too rapidly or coaches get involved and make things more complicated than they should be (especially for a sport as simple as distance running) that problems arise.
TL,DR: Do as much training of the right type at the highest intensity that is sustainable, but no more.
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NIH requires open access for the studies that it funds. The vast majority of biomedical research, however, is privately funded, mostly by pharmaceutical companies. Do you believe that you should automatically have access to those data as well? If so, why?
Yes because pharmaceutical companies make money from *checks notes* people paying money to predatory publishing companies who have done sweet FA in the research process. The publishing companies have absolutely pillaged the time, resources and goodwill of academics across the globe for far too long. Absolute racket.
But let's turn the clock back, shall we, before open access publishing (which just shifts the costs to people like me, who have to somehow come up with another $2-4k to publish a study, on top of the $10-100s of k it costs to conduct it) and before people realized that the profit margin of non-society journals was so high, that significant money could be made. Back then (and still to this day), the best science was found in society journals, supported in part by subscribers (again, people like me). Do you think it is right to steal from those publications, thus driving up the costs for more ethical individuals who do pay for access?
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. The specific stimulus of keeping a long easy effort helps develop metabolic flexibility and general capacity in the mitochondria that only faster running probably doesn't accomplish.
This is common thinking, but it isn't correct.
The studies showing the largest improvements in muscle mitochondria in humans have had people training more intensely, not longer.
As far as longitudinal studies go, this early one by Gollnick remains the all-time champion:
After just 5 mo of training for only 4 h/wk, SDH activity increased by 95%, thus essentially equaling that found in elite runners who have trained much for much longer.
Your linked study resulted in a mean SDH activity of 9.06 mmol/g/min and 38% area ST fibers post intervention.
If disco and bell bottom jeans are the vibe… David Costill, Jack Daniels, et al. have a 1976 study where they sampled higher level athletes from a variety of disciplines. I’ll speak specifically to the male data in the study, sprinters (100m) had a mean SDH of 12.9 and 24% area ST fibers, mid-distance runners (800m) had mean SDH of 14.8 and 47% area ST fibers, and distance runners (5000m+) had a mean SDH of 16.6 and 62% area ST fibers. For reference, the untrained subjects in their study had an SDH of 7.4 and 56% area ST fibers. So, saying the study you linked resulted in the participants reaching near elite runner status, seems a misrepresentation of elite. Or to draw from one of your earlier comments, it would be akin to equating a sport scientist to an exercise physiologist.
Regardless, for every 6 person study that exists to draw overarching conclusions in exercise physiology, there is usually an equally underrepresented population sample to show the opposite, or at least question the aesthetic sense of anyone who thinks 1970’s avocado green paired with floral patterns should remain the preferred kitchen design of the 2020’s…
David Bishop has research that shows mitochondrial content (i.e. volume) may be more influenced by duration, where as mitochondrial function (i.e. respiratory capacity) may be more influenced by intensity. And that inferring increases in mitochondrial function from increases in certain mitochondrial enzyme activity, may not be as valid as previously thought. I think the aforementioned is what John Whelan had in mind when suggesting a longer run still has a place in the training plan.
P.S. I can assure any of those actually interested, it won't cost you $25 to access this paper... just a waste of your Saturday haha
How does this study clearly demonstrate that large volumes of low to moderate intensity exercise are neither required nor most time-efficient for increasing muscle respiratory capacity outside of the context of poorly trained people? How can you clearly demonstrate something with no comparison to an alternative method? It seems obvious to me that the main factor in the magnitude of increase between untrained and trained states there is that these participants were in terrible shape to start with.
If high volume of easy running is so unnecessary why are all basically all the best runners at basically all levels HS-elite, 1500m-marathon doing high volumes of fairly easy running as the majority of their training? I don't care about making average unfit people slightly less average, I'm interested in what optimizes performance at a high level.
If I wasn't clear enough at first, let me be more clear now, I don't claim that lower intensity is a greater stimulus, rather that it's a different stimulus. Both are important.
You say I'm reinforcing misconceptions by making false statements but have not provided any good evidence about why my statements are false. Since you have not responded to many of my points I'll repeat some of them here:
How can you say the results of this study aren't all/mostly due to the participants starting out seriously undertrained?
How reliably can we correlate something like SDH to an actual measure of performance?
What can we infer from the results of this study, or any similar study, about the development of metabolic flexibility in response to higher intensity (I'll clarify this to be anything faster than LT1), vs lower intensity (below LT1)
1. Not on my end. (Logged in from home, not signed in to my university or society accounts.)
2. Because the study reported the largest ever increase in mitochondrial marker enzyme activities ever observed in a longitudinal study (minimizing genetic advantages), to match the two-fold higher values found in elite athletes, despite the fact that the participants only trained 4 h/wk. (Apparently you've never encountered the classic 1964 paper in *Science* on "strong inference", one major point of which is that scientific progress is most rapid when you focus on *disproving* hypotheses.)
3. No one has said that larger volumes aren't necessary/beneficial - it is just to the extent that they are, *it's not because of some unique ability of "zone 2" training to alter muscle respiratory capacity" as you have claimed*.
4. *Of course* the results are partially because the individuals were initially untrained. But, that's the whole point, because that is the reference condition when evaluating the muscle respiratory capacity of highly trained individuals.
5. There are numerous studies in the literature of both rats and humans showing a high correlation between mitochondrial enzyme activities and performance, mostly dating back to the late 1960s to early 1980s. For rats, see studies from Holloszy's lab. For humans, see Sjodin's work with marathoners.
*However, this is really just a red herring. You claimed (and continue to claim) that when it comes to mitochondria/metabolism, there is something special about lower intensity, "zone 2" training. As that classic study by Gollnick et al. so aptly demonstrates, there isn't. You therefore need to find another way of rationalizing your belief system with respect to optimal training, because your hypothesis about being about mitochondria is flat-out wrong *
6. There is no LT1 or LT2, or really even an LT - lactate increases continually albeit not linearly as a function of intensity. The way to shift that curve is obviously to train with some combination of intensity and vi, but science can't tell you what is optimal, especially for any given individual.
More importantly, focusing on attempting to improve physiological responses/adaptations is a mistake. What you should focus upon is improving actual *performance*, and just let the physiology sort itself out. Otherwise, you will find yourself going down stupid rabbit holes, like doing "over-unders" to try to improve lactate clearance (which is irrelevant), or obsessively measuring lactate concentrations during almost every workout, in the mistaken belief that "intensity control" is critical to improvement.
I'm going to reiterate one final time the main aspect of my original point that you continue to not address, then will stop. You vs Lexel is a much more entertaining matchup and I don't want to distract from that anymore, and my apologizes to both you and Lexel for the accusation that you are the same person.
If the the cell metabolism is shifted at lower intensities, why wouldn't the training signals at this level be shifted as well? Why wouldn't there be unique benefits to these different signals, particularly with how they pertain to general health and the ability to adapt to training in general? If nothing else I would think there would be some specific benefit of working at lower intensity for developing the capacity to transport fatty acyl-CoA into the mitochondria. More access to fat metabolism should provide more energy for training and recovery. Even if any "uniqueness" of benefit is purely due to volume/duration isn't that practically the same because the volume/duration is only achievable with lower intensity? I'm under the impression that we still don't have a super clear concept about if and what different stimuli increase the surface area of mitochondria vs the enzymes in them, but that long and easy has been shown to be good for expanding that surface area, while shorter and harder is best for increasing the enzymes.
It obviously was a mistake to have worded my original point as a statement rather than the question/hypothesis that it really is, but I'll stand by that it's a reasonable concept. If it's not a reasonable concept certainly someone as knowledgable as yourself would have a much easier time explaining why not.
Gollnick et al. aren't really concerned about fat metabolism in that study or anything related to metabolic flexibility. They're just looking at fiber types, glycogen, aerobic capacity vis SDH, and anaerobic capacity using PFK. SDH activity is obviously important for metabolic flexibility, but since it's a few steps downstream of where the fuel is coming into the TCA cycle it doesn't seem like a good enough proxy to me. They also don't measure mitochondria volume.
When it comes to SDH they explain that they made deliberate choices to try to get the biggest effect on SDH activity -the VL muscle and an activity (cycling) that demands extensive use of this muscle. They explain that the SDH activity in the subjects is greater than what they measured in runners because cycling demands more from the VL, yet the VO2max/kg is still greater with the runners -to me this seems like they're saying it was deliberately meant to just be a small snapshot of whats going so that they could get a very large effect. It's proof of concept demonstration, but nowhere a full measure of whats going on in the mitochondria or any sort of sport-specific metabolic output. I feel you are exaggerating what this demonstrates, particularly in a comparison to runners, when the authors themselves seem to say that isn't a fair comparison.
With this I of course do have to eat some sci-hub crow -I probably don't have higher SDH activity in my VL muscle than the participants in the study. I seem to be in alight company there, as from another Gollnick study we can see that Dan Murphy (4th at 1971 NCAA XC) had a lower VL SDH than the average of those six guys at the end of their bike erg training. Like you said we should focus on performance rather than physiological responses.
I know that LT1 and LT2 (or any other way to slice up intensities) are not really true physiological anchor points/events/whatever, but they are still useful estimates for how metabolism is changing in response to intensity.
Your linked study resulted in a mean SDH activity of 9.06 mmol/g/min and 38% area ST fibers post intervention.
If disco and bell bottom jeans are the vibe… David Costill, Jack Daniels, et al. have a 1976 study where they sampled higher level athletes from a variety of disciplines. I’ll speak specifically to the male data in the study, sprinters (100m) had a mean SDH of 12.9 and 24% area ST fibers, mid-distance runners (800m) had mean SDH of 14.8 and 47% area ST fibers, and distance runners (5000m+) had a mean SDH of 16.6 and 62% area ST fibers. For reference, the untrained subjects in their study had an SDH of 7.4 and 56% area ST fibers. So, saying the study you linked resulted in the participants reaching near elite runner status, seems a misrepresentation of elite. Or to draw from one of your earlier comments, it would be akin to equating a sport scientist to an exercise physiologist.
Regardless, for every 6 person study that exists to draw overarching conclusions in exercise physiology, there is usually an equally underrepresented population sample to show the opposite, or at least question the aesthetic sense of anyone who thinks 1970’s avocado green paired with floral patterns should remain the preferred kitchen design of the 2020’s…
David Bishop has research that shows mitochondrial content (i.e. volume) may be more influenced by duration, where as mitochondrial function (i.e. respiratory capacity) may be more influenced by intensity. And that inferring increases in mitochondrial function from increases in certain mitochondrial enzyme activity, may not be as valid as previously thought. I think the aforementioned is what John Whelan had in mind when suggesting a longer run still has a place in the training plan.
P.S. I can assure any of those actually interested, it won't cost you $25 to access this paper... just a waste of your Saturday haha
Clearly you also need to improve your ability to understand and interpret the scientific literature...
The measured activity of an enzyme is obviously dependent on numerous factors, e.g., the concentrations of substrates and co-factors, pH, temperature, etc. You therefore really can't compare absolute values across studies/laboratories as you have done - indeed, even within a laboratory there can be "drift" in the measurements over time, due to, e.g., different individuals preparing standards with vary technique/accuracy. (This is why we use NIST-traceable standards when measuring nitrate and nitrite concentrations via HPLC.)
Because of the above, you should really only compare relative values/changes. In that regard, even the distance runners in Costill et al.'s classic study had an SDH activity only slightly more than twice that of the untrained controls, similar to the magnitude of the increase observed in Gollnick's study. This, despite large differences in training volume and, of course, genetics (including fiber type differences).
As for Bishop, what he has is a(n) hypothesis...others such as Martin Gibala would obviously disagree.
If the the cell metabolism is shifted at lower intensities, why wouldn't the training signals at this level be shifted as well? Why wouldn't there be unique benefits to these different signals, particularly with how they pertain to general health and the ability to adapt to training in general? If nothing else I would think there would be some specific benefit of working at lower intensity for developing the capacity to transport fatty acyl-CoA into the mitochondria. More access to fat metabolism should provide more energy for training and recovery. Even if any "uniqueness" of benefit is purely due to volume/duration isn't that practically the same because the volume/duration is only achievable with lower intensity? I'm under the impression that we still don't have a super clear concept about if and what different stimuli increase the surface area of mitochondria vs the enzymes in them, but that long and easy has been shown to be good for expanding that surface area, while shorter and harder is best for increasing the enzymes.
There you go again, repeating/reinforcing myths/hypotheses as if they are established facts...
Re. intensity: the first thing that you have to realize is that the word doesn't mean much at the level of an individual motor units/single muscle fiber. That is, by and large that motor unit is either recruited and those muscle fibers are activated, or they aren't. (Obviously rate-coding can layered on top of this, although that is a motor control strategy that seems to reserved for only short bursts of activity, not sustained exercise.) Furthermore, since the primary signals driving the muscular adaptations to training (i.e., cellular energetics, calcium, and *perhaps* glycogen availability) are all intracellular, a given muscle fiber really doesn't know or care what its neighbors are doing, or what the humoral/hormonal milleu might be). If this were *not* true, then you would find adaptations in muscle fibers/motor units and even muscles not engaged in the exercise - yet you don't, i.e., the adaptations are local. Furthermore, you can eliminate the influence of hormones using surgical approaches, drugs to block receptors, etc., yet the muscle still adapts as expected.
As for fat metabolism, it is a red herring. That is, you don't have to oxidize fat to get better at oxidizing fat, and increased rates of fat oxidation are not responsible for the training induced increase in muscle mitochondria.
Finally , the whole "train long for mitochondrial quantity, train hard for mitochondrial quality" idea is belief by the dynamic nature of the mitochondrial reticulum, as I described previously.
Clearly you also need to improve your ability to understand and interpret the scientific literature...
The measured activity of an enzyme is obviously dependent on numerous factors, e.g., the concentrations of substrates and co-factors, pH, temperature, etc. You therefore really can't compare absolute values across studies/laboratories as you have done - indeed, even within a laboratory there can be "drift" in the measurements over time, due to, e.g., different individuals preparing standards with vary technique/accuracy. (This is why we use NIST-traceable standards when measuring nitrate and nitrite concentrations via HPLC.)
Because of the above, you should really only compare relative values/changes. In that regard, even the distance runners in Costill et al.'s classic study had an SDH activity only slightly more than twice that of the untrained controls, similar to the magnitude of the increase observed in Gollnick's study. This, despite large differences in training volume and, of course, genetics (including fiber type differences).
As for Bishop, what he has is a(n) hypothesis...others such as Martin Gibala would obviously disagree.
Absolutely bizarre you would take a shot at Hard2find like that, when he's actually contributed massively to the thread. Actually quite shocked how much of a rude, obnoxious quite frankly flat track bully you are. Literally brought nothing to the table but your ego and hot air. You are the the perfect definition of an online troll which I find absolutely extraordinary given your academic background and career. You make our very own JS look mentally stable with your incoherent ramblings. Shows how easy it is to pull the wool over people's eyes, not just for a minute but clearly you have made a career out of it!
Absolutely bizarre you would take a shot at Hard2find like that, when he's actually contributed massively to the thread. Actually quite shocked how much of a rude, obnoxious quite frankly flat track bully you are. Literally brought nothing to the table but your ego and hot air. You are the the perfect definition of an online troll which I find absolutely extraordinary given your academic background and career. You make our very own JS look mentally stable with your incoherent ramblings. Shows how easy it is to pull the wool over people's eyes, not just for a minute but clearly you have made a career out of it!
I genuinely didn't know anyone could come across make idiotic, stubborn, stuck to a position they would die for more than lexel. Even better more downvoted by the fans. But Coggan, I salute you. You've taken all those things to a new level my man. Well played sir, gg. I will have to revoke my Drexel fan club card and move over to the great AC. aka. Pandy Andy "I've had papers published you know" , "did you hear about my latest research grant?" "You're wrong of course" "I've got an IQ of 87!" Coggan.
But let's turn the clock back, shall we, before open access publishing (which just shifts the costs to people like me, who have to somehow come up with another $2-4k to publish a study, on top of the $10-100s of k it costs to conduct it) and before people realized that the profit margin of non-society journals was so high, that significant money could be made. Back then (and still to this day), the best science was found in society journals, supported in part by subscribers (again, people like me). Do you think it is right to steal from those publications, thus driving up the costs for more ethical individuals who do pay for access?
Why on earth have this discussion here and not in its own thread? No one clicks on this thread to discuss open publishing, or read about open publishing.
And yet...and yet, I would be the first to tell people to stop confusing/distracting themselves by worrying about physiological minutiae, putative mechanisms, etc., and just get on with their friggin' training. Exactly what you do during a single workout means almost nothing in the big scheme of things - instead, the key to forward progress lies in cogent application of principles such as specificity and overload in the context of the overall training plan. Instead of constantly biting off more than one can chew, jumping from one plan to another, obsessing over just how hard you do your long runs, etc., just ignore the noise, keep the faith, be consistent, and (for runners) avoid injury. Beyond that, there's really not anything more that you can do.
TL,DR: There is no such thing as the perfect training plan (wisdom from a brilliant - and beautiful - former national champion in the IP).
This is a great summary of exactly what the training method described in this thread is attempting to do -- to attempt to apply this philosophy in a way that is feasible for runners (who will have different limitations to consistency/progress due to risk of injury than will cyclists)
Yes, I noticed that, too. I didn't want to brag.
"I would be the first to tell people to stop confusing/distracting themselves by worrying about physiological minutiae, putative mechanisms, etc., and just get on with their friggin' training." --Andrew Coggan
Does the average recreational endurance runner’s muscle type (%ST/%FT) differ much from an elite endurance runner. Is the average recreational runner more FT?
Absolutely bizarre you would take a shot at Hard2find like that, when he's actually contributed massively to the thread. Actually quite shocked how much of a rude, obnoxious quite frankly flat track bully you are. Literally brought nothing to the table but your ego and hot air. You are the the perfect definition of an online troll which I find absolutely extraordinary given your academic background and career. You make our very own JS look mentally stable with your incoherent ramblings. Shows how easy it is to pull the wool over people's eyes, not just for a minute but clearly you have made a career out of it!
I will "take a shot" at anyone who posts misleading information/incorrect conclusions. Simply put, egos don't matter - facts do.
Welcome to the Internet, where thread drift is a fact of life.
Well, any thread you pop up in….drifts. Same here as just about every forum you’ve been a part of…and booted from. And now you’re resorted to LR…since most other forums have asked you to go away.
Love your scientific rigor. Your personality (especially academically) is a dime a dozen tho. Ugh.