"It is concluded that ingesting a fat-rich diet during an endurance training programme is detrimental to improvement in endurance. This is not due to a simple lack of carbohydrate fuel, but rather to suboptimal adaptations that are not remedied by short-term increased carbohydrate availability." womp womp
You don't have very good reading comprehension if you think this thread is about a high fat/low carb diet for cycling and in particular for racing. I have not advocated a ketogenic diet. Not sure anyone has in this thread. So you can take your womp womp back as it has nothing to do with this thread. A ketogenic diet is for another thread topic.
KWalker wrote:Don't understand physiology yet you are the one that somehow believes ketosis and fat adaptation is efficient despite the fact that they are an incredibly inefficient way to produce atp from oxygen. One of the most basic aspect of the krebs cycle. Anyways, you clearly have so much more passion for the interwebs and this topic so I concede.
I am not advocating a ketogenic diet. Never said such things. I have advocated for a few fasted state/glyocgen depleted state training to get the benefit of (1) shifting the crossover point of your metabolic efficiency graph, (2) increase VO2 max and (3) increase muscle glycogen storage, (4) improved whole body fat utilization. That is the point of incorporating a fasted state training into a training regimen. No one has said to only do fasted state training for all your rides. No one has said to live on a ketogenic diet. The fact that you keep bringing those up tells me you have poor reading comprehension ability, or you are trolling. Might be both.
KWalker wrote:Or here is a basic premise that is the foundation of empirical inquiry- what, of this "evidence", concludes in a statistically significant manner on a similar population that any of these modalities produce net long-term improvements in the outcomes desired by this thread? Cell signaling bullshit aside, where is that proof? That's why I called it a hack- at the end of the day the few studies that have tried to determine such an outcome show no net improvement, and in more cases net detriment.
Fascinating thread? This topic is years old in other sports, but cyclists tend to cling to ideas that have since passed. But don't trust Louise Burke, it's only been her entire career and she's only worked with hundreds of athletes from all endurance sports...
Fasted state training has been used in cycling since the 1950s/1960s and is still be used today. I have already provided way more published articles supporting the benefit of a fasted state/glycogen depleted state into a training plan. The cell signaling aspect is not bullshit. Regardless of how much you want to disregard it. Again, you will not get a research study with thousands and thousands of participants. There just isn't going to be government or private founding funding for this kind of research study of any large (i.e. expensive) type of research study. You will need to take the limited studies we already have on this topic + what current team docs for ProTour teams are saying.
Louise Burke? What about what Joe Friel, Dr. Andrew Coggan, and Dr. James Morton? If anything, I believe what Dr. Andrew Coggan and Joe Friel have done on this subject.
KWalker wrote:53x12 apparently can't read past abstracts, but if you find that approach compelling by all means do follow his advice. I guess the approach of picking a bunch of things that could be indicative then produces truth?
The reason I posted the abstracts was to refute your statement there were only 3 published studies on this subject and that Stannard was involved with all of them. You were wrong then, you are wrong now. I have read all the articles that I posted the abstracts for. The reason I posted the abstracts is that there is no easy way for me to legally post the full articles, people like you wouldn't take the time to read the whole article and for the rest of the members reading this thread the abstract provides the gist of the research article to get the point.
KWalker wrote:Take for example the study, which he doesn't link for some reason "Beneficial adaptations..." done in 1985. All it does is list possible benefits, but is not a statistically significant comparison of the benefits of multiple approaches.
That published article by Van Proeyen from 1985 is one of the abstracts that I posted. I don't need to provide the link. Go to Pubmed and enter all the data and pull it up yourself. You have the authors names, title, date of publication and more importantly I provided the DOI and PMID information. Would take you 15 seconds to pull it up yourself.
The reason I posted that Van Proeyen article was because it showed that fasted state training lead to being more effective than carbohydrate training in increasing muscular oxidative capacity and it also enhanced net intramyocellular lipid breakdown.
KWalker wrote:Or loving the AMPK-based studies, despite that they do not prove any increase in actual performance nor bodyfat reduction in the case of this thread. No studies that show a long term net increase in fat oxidation despite short term increases. So, when the OP goes to do their century ride they can either remain LCHF and limit intensity and increase PE, or resume a normal diet and gain nothing.
Again, you don't understand how research studies are funded. I have had to write and submit R01, R43, TL1...etc. grants to the NIH for funding. To get the kind of study that you want for any large amount of participants, to have a look at the signaling pathways of athlete in a fasted state training group vs. a carbohydrate rich study and then to look at long term net increase in fat oxidation or increase in performance just isn't a study that would get funded. There is no interest at the NIH level to fund something this minute and non-applicable to the general public or the general public health. That is why you have these small studies where a researcher is able to do them pretty inexpensively on the side of other projects or with limited funding from some other source. That is why you have to piece together the studies that are already published, accepted them for what they have shown and stop trying to project the kind of research that you want done onto what has already been done and shown.
The Pilegaard 2004 article that I referenced earlier showed that PDK4 expression was increased from a fasted state training. Their study wasn't looking at whether this had net impact on performance, it was looking at what PDK4 did during a fasted state.
The Civitarese 2005 article that I referenced earlier showed that glucose ingestion during exercise decreases the expression of genes involved in lipid metabolism rather than increasing genes involved in carbohydrate metabolism.
The De Bock 2005 article that I referenced earlier showed that fasted state facilitates fibre type-specific intramyocellular lipid breakdown and stimulates glycogen resynthesis.
The Schrauwen 2002 article that I referenced earlier showed that increase in uncoupling protein (UCP3) expression appears to be an effect of prolonged elevation of plasma FFA levels and/or increased fatty acid oxidation. In the fasted state, UCP3L mRNA expression was increased significantly and wasn't in the glucose group. Acute exercise on its own had no effect on UCP3 protein levels.
What those studies show is that at a biochemical and protein level, the body makes adaptations to training in a fasted state. The body becomes more efficient at this and leads to what we have already talked about. That fasted state training leads to: 1) shifting the crossover point of your metabolic efficiency graph, (2) increase VO2 max and (3) increase muscle glycogen storage, (4) improved whole body fat utilization. Even some research showing depleted state leads to increased mitochondrial biogenesis.
Just for completeness of this topic of fasted state training, I will provide more research studies supporting its use in a training program.
^ Both of those published articles showed a trained athlete, uses more fat than an untrained individual during intensive exercise (at same intensity level). Reason would dictate, that a trained athlete would want to optimize and train this system to be as efficient as possible. Don't miss this point "the better performance by the well trained group was explained by their nearly threefold higher rates of fat oxidation at high intensity."
"Marginal gains are the only gains when all that's left to gain is in the margins."