The case for fat adaptation in endurance

Pointing out the obvious

It is pretty obvious by now in sports is that if the body requires something then you need to give that in order to enhance performance. Be it vitamines, minerals, energy… whatever it needs to produce that wattage, make sure it doesn’t fall short to sustain the performance. Except for one element. Even though it is right there in front of our face and of all the researchers, it is overlooked…

A presentation I recently looked at summarized it all yet somehow seems to miss it.

“IS-PM05 – High-carbohydrate or high-fat diets for optimizing training adaptation and performance?” https://www.youtube.com/watch?v=AJ1MFa2uvtA

A first thing to note is that endurance exercise such as running and cycling elicit AMPK activation. More so under a low glycogen state than under high but nonetheless the activation is there.

The reason I’m highlighting AMPK is just to give some background on what we are looking at. AMPK is responsible for setting in motion the growth of mitochondrial mass. During exercise, mitochondria get (partially) damaged. They need to be split up so that the damaged parts can get recycled and the other parts that are in good health become the seeds to multiply and grow a bigger mitochondrial mass overall.

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“AMPK: guardian of metabolism and mitochondrial homeostasis” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5780224/

What does this enhancement in mitochondrial mass result in? Indeed, increased exercise performance, higher ATP production.

In sports physiology they know very well that this results in a higher fat oxidation rate as the presentation further highlights.

The results below, in the presentation, are from a study looking at endurance training in a group of moderately overweight men. We see that there is no adaptation in the amount of carbohydrate oxidation but there is adaptation in the amount of fat oxidized. This is in the Trained group and the Diet group which were fed a reduced amount of calories.

The study also looked at a group to keep calories identical in order to exclude if the adaptation is due to weight loss. Also here the Trained-identical calories group shows the same adaptation in fat oxidation. C is the control group.

What this tells us is that both weight loss and endurance training stimulates a greater fat oxidation capacity with no change in carbohydrate oxidation.

I’ll speculate later on about why this is happening but let’s first have a look at what determines our level of fat oxidation, our maximum fat oxidation rate. The presentation continues on this topic…

As fasting is prolonged, the fat oxidation goes up and we see a correlation with the circulating free fatty acids (FFA).

Actually, the data shows us a very high correlation between the free fatty acids (FFA) and maximum fat oxidation.

Further evidence is given in the presentation from a study that looked at ultra-endurance. Normal diet, at least nothing specific to a ketogenic diet or high fat diet in general, yet we see again how the body adapts to increase fat oxidation.

Pointing out the obvious

So it should be clear by now that the body, as an adaptation to endurance, increases its fat oxidation capacity. On one hand by increasing mitochondrial mass and on the other hand by making more fat available in the circulation via FFA. Without more mitochondrial mass you cannot process more FFA and more mitochondrial mass is useless without additional fuel.

But what are these researchers missing? The type of fuel!

If the body wants to increase fat oxidation in order to sustain that demand in performance, wouldn’t it be natural to provide the body with that fat, which it is demanding for, during exercise?

Why is there not a single trial that involves ingesting fat in one way or another during exercise? If we want to go for a higher peak fat oxidation, shouldn’t we simply eat fat to get our FFA up?

Is it fair research when putting athletes on a high-fat diet, thereby having a higher reliance on their maximum fat oxidation rate, to supplement them with carbohydrates pre/during exercise which releases more insulin so that the insulin can stunt fat release thus lowering their circulating FFA and showing no performance gain, or worse, performance loss?

In the pre‐treatment trial, all subjects received a standardised CHO‐rich breakfast providing 2 g kg−1 CHO;

“Low carbohydrate, high fat diet impairs exercise economy and negates the performance benefit from intensified training in elite race walkers” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5407976/

No!

That is comparing highly optimized high-carb athletes with high-carb fueling to highly optimized high-fat athletes with stunted fueling. You might as well just put a concrete block around their legs.

A study that compared normal versus ketogenic diet in exercise monitored the FFA during the exercise. It shows how important the availability of FFA are during exercise. Being the main source of fuel and being greatly dependent on, it is only natural to supplement with fat. The mixed diet group has a much lower reliance on fat and we also see that in a much lower fluctuation during this exercise exercise.

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“The Effects of a Ketogenic Diet on Exercise Metabolism and Physical Performance in Off-Road Cyclists” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4113752/

Specifically towards the most intense part of exercise during this test we see the lowest availability of FFA. What would happen if we’re able to maintain that level of FFA from the start towards the end by ingestion or, just for the sake of experiment, infusion?

This is an area where research could see a lot of surprises and progression in understanding.

UPDATE 2020-09-29:

A point I did not address is the type of fat used. This is actually very important because long chain fatty acids (LCFA) require carnitine for transport into the mitochondria.

Carnitine content reduces to less than 30% during high intensity (100% VO2max)

“Muscle carnitine metabolism during incremental dynamic exercise in humans” https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1748-1716.1990.tb08845.x

Medium chain fatty acids (MCFA) do not require carnitine and thus are able to sustain a higher rate of appearance in mitochondria. But for that they need to be made available in circulation at a higher rate as well.

“Regulation of plasma fatty acid oxidation during low- and high-intensity exercise” https://pubmed.ncbi.nlm.nih.gov/9227453/

Why is this adaptation to fat happening?

It is of course just a hypothesis but the most obvious thing would be protein sparing. Engaging in long duration activity requires energy. If it would all have to come from glucose then our body would have to break down muscle as a source for gluconeogenesis. By relying more on fat, both the energy requirement can be met and at the same time protect our muscle from catabolism.

If you want to go more in depth on this protection mechanism then you can read a few of my previous post on the subject. You’ll see it has quite broad implications.

https://designedbynature.design.blog/2020/04/24/linking-the-hepatic-glycogen-buffer-with-protein-protection/

https://designedbynature.design.blog/2020/01/14/protein-and-fructose/

https://designedbynature.design.blog/2020/03/30/the-liver-buffers/

https://designedbynature.design.blog/2020/05/13/hyprocico-the-theory-behind-obesity/

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