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The misunderstanding of endurance adaptation and how to train all muscle types together

There are plenty of articles that explain much more in detail the different muscle fiber types and how to train for endurance or how to build muscle so I won’t go into those details. What I do want to address is the issue with getting both trained at the same time.

First, the problem with muscle fiber types and training type

The main difference between type I and type II is in the way they generate power and for how long they can do this. Type I is low in fiber growth but dense in mitochondria. Its strength comes from longer sustaining ATP production. This makes them very well suited for endurance. Type II is the opposite, it responds easier with growth but is lower in mitochondria. Because it can grow larger in size more easier, its strength comes from the total capacity of the fiber contraction. Although it has fast ATP production, this is limited in time because the production capacity is limited.

They are essentially each others opposite:

Muscles are a mix of both fiber types. In some muscles, the mix will dominate towards type I while in others it is more balanced or goes towards type II predominantly. And then there is of course your genetics which may shift the balance further towards one or the other.

In a simplified way, this result in the following situation:

So what is the problem?

1) One type of exercise trains one type of fiber.

In order for the fiber type to adapt to a training stimulus, the muscle cell must run out of energy. Type II responds to weight lifting because the heavy weight is carried by type II. They can generate the power to lift the weight (assisted by type I) but once they are fatigued and have reached the stimulus, you cannot lift anymore. But the type I fiber didn’t reach fatigue yet, it is just not strong enough to continue by itself with the same weight.

Endurance training on the other hand is relying on type I fiber and then we have on top of that the complexity of type IIa fiber which can shift its profile between the two extremes depending on the type of training you do.

2) Endurance training inhibits mTOR (muscle growth)

The following is an often visualized picture of training adaptation:

It shows how endurance activates AMPK and that cascades down to blocking mTOR which runs the protein synthesis. Although this is correct, I’ll show why this is also wrong and leads to misunderstanding.

Mitochondrial biogenesis

In order to explain what is wrong with that picture, we need to understand what creates more mitochondrial mass. This is where the increase in strength is coming from for endurance.

PGC-1α is the factor that opens up the transcription of the genes for mitochondrial protein production. AMPK phosphorylation (activation) induces PGC-1α and this AMPK activation in turn is driven by low levels of ATP.

This paper shows that by inhibition of nitric oxide, the activation of PGC-1α fails by AMPK alone.

“Nitric oxide and AMPK cooperatively regulate PGC-1α in skeletal muscle cells”

Although not entirely comparable to skeletal muscle, the heart muscle type, which is the most important endurance muscle, shows us that insulin is involved in mitochondrial fusion, to make them bigger and produce more ATP.

But a study in humans looking at skeletal muscle also showed that insulin itself can stimulate mitochondrial biogenesis. These results were obtained together with leucine infusion to maintain plasma levels.

“Insulin Stimulates Mitochondrial Fusion and Function in Cardiomyocytes via the Akt-mTOR-NFκB-Opa-1 Signaling Pathway”“Effect of insulin on human skeletal muscle mitochondrial ATP production, protein synthesis, and mRNA transcripts”

Putting both together, it is critical to understand that nitric oxide production is stimulated by insulin. This is important for insulin to get across from the blood circulation into the muscle cells.

“Insulin-stimulated activation of eNOS is independent of Ca2+ but requires phosphorylation by Akt at Ser(1179)” – “Insulin-mediated skeletal muscle vasodilation is nitric oxide dependent. A novel action of insulin to increase nitric oxide release”“Nitric oxide release accounts for insulin’s vascular effects in humans”

“Nitric Oxide Directly Promotes Vascular Endothelial Insulin Transport”

What stimulates insulin release? Leucine in your food (or protein shake) triggers the release of insulin from the pancreatic beta cells.

“Leucine metabolism in regulation of insulin secretion from pancreatic beta cells”

So, AMPK inhibits mTOR but this is only until food comes in that allows the cell to adapt and build the necessary protein to become more resistant. This food will activate mTOR. AMPK will split (fission) the existing mitochondria and influences the type of protein that are produced so that when mitochondrial protein are produced, they are assembled into those fragments created by AMPK.

Blood Flow Restriction (BFR)

BFR is special because by its reduction in oxygen availability, it affects all fiber types at the same time. The reason is that hypoxia will limit the ATP production in mitochondria so that the glycogen will become the main source of ATP production via glycolysis instead of glucose or fat via the mitochondria.

Type II fibers already have reduced mitochondria so they are already more prone to glycolysis. Type I fibers are more resistant so they may still require a bit more prolonged exposure to BFR.

Below is a schematic of how BFR will trigger training in both fiber types, covering the info provided above.

So go and lift your weights but apply BFR to stimulate endurance adaptation simultaneously in your type I fiber while also enhancing the effect on type II fiber if that is what you are after.

When you go running, cycling.. apply BFR so that it enhances the endurance training effect and stimulates muscle growth in those type II fibers.


In order to adapt to the training stimulus, new protein must be build. The fiber type will determine how the response is made. Type I will push for mitochondrial protein to increase endurance capacity while type II will push for muscle protein synthesis in order to grow new muscle cells aka proliferation aka hyperplasia.

As discussed above, insulin alone will not do the job, it needs to be combined with sufficient leucine so make sure to have a protein source that contains enough leucine.

AMPK, via PGC-1a activates the transcription to build mitochondrial protein which are assembled by mTOR. This is why type I muscle fiber do not grow in size so easily. It first inhibits mTOR and then changes the program to make sure that, when mTOR gets activated again, it concentrates on mitochondrial protein construction instead of muscle protein.


Just as an example to show the effect. Because metformin stimulates AMPK it was thought that it would result in a benefit for endurance adaptation. Rather the opposite is true and it blunts the adaptation. Although this was not tested yet in the literature, to my knowledge, I suspect that the chronic stimulation of AMPK also causes a chronic downregulation of mTOR which could explain why there is no buildup of mitochondria and thereby lack of increased endurance.

“Metformin Improves Mitochondrial Respiratory Activity through Activation of AMPK”

“Metformin inhibits mitochondrial adaptations to aerobic exercise training in older adults”

Probably the reason why they thought it would enhance exercise is because they made the same mistake as I did and didn’t understand that the mTOR inhibition needs to be lifted in order to build those mitochondrial protein.

You actually need mTOR for mitochondrial protein synthesis just as much as any other protein synthesis.

– – – T H E – E N D – – –


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