Thoughts on how to develop bodies ability to use fat as fuel more efficiently

That's what you were taught way back when? So was I, but you should be aware that research over the last 50 years has shown no evidence to support that old (Mayerhoff 1920) hypothesis. Rather, a huge amount of empirical evidence shows that Lactate is the end producto of glycolysis and glycogenolysis.

I can give you much more info if required?

LACARPETRON DOOKMARRIOT wrote:

everything you have said is wrong and yes you can very well have glycolysis without lactate

Wrong, see post above.

Why is everyone training for the "high-fat" running events now. Why not just eat like a normal person and run like a normal person?

biochemistry wrote:

That's what you were taught way back when? So was I, but you should be aware that research over the last 50 years has shown no evidence to support that old (Mayerhoff 1920) hypothesis. Rather, a huge amount of empirical evidence shows that Lactate is the end producto of glycolysis and glycogenolysis.

I can give you much more info if required?

No it's not what I was taught "way back when" as I've only come to this subject relatively recently and am going by the definitions as they appear to stand at the time being. What I have seen to date defines glycolysis as the process that converts glucose to pyruvate. Having a look at the wiki 'talk' page I cannot see any suggestion that the model is being revised.

By all means provide more info. I'm interested.

Oh wait, are you referring to the fact that glycolysis requires oxidising power and hence necessarily involves additional steps not shown in the standard diagram? If so I understand where you are coming from. Cheers.

You seem interested, so I'm happy to provide more info. The diagram you showed, is indeed the pathway proposed by Meyerhoff in 1920 for which he jointly won the Nobel prize for Chemistry in 1922:

http://www.nobelprize.org/nobel_prizes/medicine/laureates/1922/

Research over the last 50 years have pretty much conclusively shown that the end product of glycolysis which is the breakdown of blood glucose and glycogenolysis which is the breakdown of muslce glycogen is in fact Lactate, not Pyruvate. Perhaps the most convincing evidence is that people who can't produce muscle lactate, are incapable of running or similar exercize.

Regarding the point of this thread, I think that people have the wrong idea about 'using fat more efficiently' because all runners can do this naturally, since it is a general survival strategy. What we really need to run faster is better fuel economy of both glycogen and fats which is gained by the ability to maintain just the right level of muscle stiffness for the full race. This gives you more power and endurance for the same effort. I did long fast runs up to 18 miles, long medium paced runs up to 22 miles and long slow runs up to 31 miles. But I always ran the last few miles of all these runs faster.

biochemistry wrote:

Regarding the point of this thread

Good stuff. Thanks for the reply.

You're one of the very few people I've encountered who have broached the subject of muscle stiffness; Steve Magness being about the only other I have seen discuss it in any significant depth. I'm very interested in any insight you can offer. Steve Magness' blog seemed to treat muscle stiffness as a neuromuscular component that needed to be primed in the leadup to a race but I get the feeling from your post that you feel it is a metabolic issue? My first question is, is that the case? I've encountered so little on the subject that I genuinely have no idea.

This thread was opened with the question of developing the "ability to use fat as fuel more efficiently". With my admittedly somewhat schoolboy understanding of 'biochem 101' it appears to me that building the machinery to produce ATP from fat means building larger and more numerous mitochondria, which I believe has been accepted to happen through observing muscle biopsies (please speak up if you disagree there as that's a key point). However, the krebs/ETC model tells us that increasing mitochondrial density and aerobic fat-burning power means that we have an increased aerobic glucose-burning power since it is the same machine doing the work. Hence as you say it's better to think in terms of "better fuel economy" rather than "using fat more efficiently" as the goal is minimising the proportion of glucose sent down the fermentation route. Fat only has the one route to go down.

Translating this to practical training means that what I've read from many coaches about "pushing up" rather than "pulling up" the lactate threshold is key since we want to stress the aerobic systems to stimulate more mitochondrial development rather than stress the body's ability to process lactate since the former leads to better fuel economy whereas the latter does not.

Does that sound about right? Appreciate your responses. Cheers.

Actually scratch half the crap I wrote above. Mulling over what you said about muscle stiffness whilst out on my run it occurred to me that you're talking about improved economy via improved elastic return. This makes sense to me and ties in with Steve Magness' writings on priming muscle stiffness prior to a race, and also the studies I've seen on tapering which appear to demonstrate that the best performances seem to come from focusing on race pace work in the preceeding week/couple of weeks.

Of course thinking about it race pace work features throughout the entire schedule and gradually increases prior to the taper. The 'good' tapers then maintain some race pace work but drop the other stuff to get the stiffness right.

I haven't read Magness' blog on the subject, but I agree with him that it is a neuromuscular component that need to be enhanced prior to a race. Actually prior to any fast training also otherwise you are working too hard metabolically and not maximizing training efficiency/racing efficiency. Yes this is the same concept as improved elastic return and fuel economy, getting more pace per unit of energy used.

I don't agree with the conventional wisdom about increasing mitochondrial density, I think it is mythology. If you have good basic fitness, you will naturally have your maximum mitochondrial density that you are genetically pre-disposed to have.

In a Marathon, you are probably using about 70% carbs and 30% fats, but of course you have to pace yourself well to make sure that you are not using too much glycogen in the first few miles. Perhaps the best marathon runners are using 80% in the first mile and non elits somewhat more?

Are you running London?

biochemistry wrote:

Glycogen/blood glucose metabolism (lactate production and respiration) produces heat during the LDH reaction equivalent to 7-8% of the energy in the glucose molecule. Fat metabolism doesn't produce heat.

.

Evidence? The long article you provided discusses the heat production of fat metabolism.

"When fatty acids are the principle substrate oxidized, the RER is 0.70 (palm oil oxidation = 16 CO2: 23 O2) and one liter of oxygen uptake estimates heat production at 19.6 kilojoules (1 l O2 = 19.6 kJ)....

The conversion of one liter of carbon dioxide into an estimate of heat production for glucose and fat oxidation reveals larger discrepancy in energy expenditure at 21.1 and 27.6 kJ, respectively...

In this regard, differences in heat production per unit of oxygen among fat and carbohydrate oxidation are better interpreted by bioenergetic explanations of energy transfer as opposed to gas exchange stoichiometry.

The slight 1.5 kJ increase in heat production per oxygen equivalent when carbohydrate is oxidized compared to fat (at 21.1 kJ vs.19.6 kJ) may be better attributed to the small but requisite energy transfer production of heat and entropy during anaerobic substrate level phosphorylation

Mitochondrial heat production has been traced largely to the flow of protons down this gradient. "

at what point does it state as you do: NO heat production occurs with metabolism of fat?? It doesn't.

biochemistry wrote:

That's what you were taught way back when? So was I, but you should be aware that research over the last 50 years has shown no evidence to support that old (Mayerhoff 1920) hypothesis. Rather, a huge amount of empirical evidence shows that Lactate is the end producto of glycolysis and glycogenolysis.

I can give you much more info if required?

If this is true, that "Lactate is the end product of glycolysis and glycogenolysis", always and without exception as you state, then why is it that almost any biochem textbook you'll find and journal articles written in 2013 clearly state that "pyruvate is the end product of glycolysis" ??

"Pyruvate is the end product of cytosolic glycolysis and has a variety of possible fates, the major one being mitochondrial oxidation."

(see first paragraph)

Do they need to be educated by you?

Are you stating that pyruvate ALWAYS is converted to lactate first and never to acetyl co a by PDH ? Again, this is not accurate. If so, show us, don't just tell us.

biochemistry wrote:

Are you running London?

Not really a marathoner but I'd like the experience of running London at least once in my life. I'm running Edinburgh in May which will hopefully bag me a good-for-age time that will allow me entry to London 2015; as long as I don't f**k it up.

Thanks for asking.

Gosh I hope I don't produce pyruvate or lactate in the wrong order today when I do my glycolysis workout

fatty acid man wrote:

Gosh I hope I don't produce pyruvate or lactate in the wrong order today when I do my glycolysis workout

look, I know you are mocking, and sure, it doesn't matter to a runner exactly what steps are occurring or what is the order of a pathway in metabolism, it just happens.

However, I was simply inquiring why he states that 'lactate', and not pyruvate, is the end product of glycolysis. I've seen this stated before, but much more often see pyruvate listed. Is this due to simply an issue of definitions? Is "glycolysis" considered, by some, to only mean the glycolytic pathway that involves pyruvate to lactate conversion? I believe that glycolysis is more routinely considered the pathway that results in pyruvate, and the next step, to lactate or acetyl CoA as further steps (then being defined as either anaerobic glycolysis, or aerobic glycolysis[the pyruvate to acetyl CoA step as the first step towards the latter).

Simply looking for clarification.

Tyrannosaurus Rexing wrote:Simply looking for clarification.

Me too to be honest. After quite some time digging around I have not come across any (certainly prominent) definitions of glycolysis showing lactate as the end product, nor any literature saying the Meyerhof definition is outright incorrect (details have been refined of course).

The concession I can see is that glycolysis cannot be viewed as an isolated process and is always working concurrently with other processes.

"It is only when the exercise intensity increases beyond steady state that there is a need for greater reliance on ATP regeneration from glycolysis and the phosphagen system.

...

Lactate production increases under these cellular conditions to prevent pyruvate accumulation and supply the NAD+ needed for phase 2 of glycolysis."

Would appreciate it if anyone can help explain the claim that lactate is the end product of glycolysis. I don't expect it to affect my training much but dagnammit I'm interested in this sh*t now.

Edinburgh in May? Hopefully you will have some decent weather to train for it? I don't think I would have liked to do a marathon before mid April, because training in a British winter can be tough.

The lactate dehydrogenase reaction releases heat into the cytosol before the lactate is metabolised, this doesn't happen with fat metabolism.

Yes most books show the Meyerhof pathway of 1920. In Meyerhof day, electron transfer was unkown. The guy who discovered it in the 1950's, Rudolf Marcus was actually born a year after Meyerhof was awarded his nobel prize for Chemistry, and Marcus himself also received the Nobel prize for Chemistry for that work 70 years after Meyerhof.

Applying electron transfer theory to glycogenolysis and glycolysis (redox reactions) reveals the lactate will be the end product and not pyruvate. But don't expect the text books to be updated any time soon, even though this theory has been around for 50 years due to the work of George Brooks.

biochemistry wrote:

The lactate dehydrogenase reaction releases heat into the cytosol before the lactate is metabolised, this doesn't happen with fat metabolism.

ok, not trying to be rude, but just as I figured, you didn't exactly answer/address my question.

You provided a link. SEVERAL times it references heat production with fat metabolism (albeit best estimates). Nowhere does it state that NO heat is produced during fat metabolism (which is what you wrote). As I said earlier, if this this the case, you should easily be able to reproduce a quote from an online text book or journal article that states this explicitly. Can you? I am doubting you, but will be happy to learn and say, "ok, now I know."