The Myth of Permanent Keto in Sports: Understanding True Muscle Physiology

The Myth of “Keto 24/7” in Sports: When Some YouTube Narratives Clash with Muscle Physiology

by Laurent Glatz – for Athletic Carnivore

There’s a notion that some pro-keto influencers repeat so often it starts to sound like scientific fact: the longer you stay in ketosis, the better you perform.

Whether in endurance, bodybuilding, CrossFit, marathons, or even high-intensity efforts, the message remains the same. Your body would be “fat-adapted,” producing the necessary glucose through gluconeogenesis, so all you need is to stay in ketosis permanently.

It’s appealing.

It’s simple.

But biologically, it’s far too simplistic.

The problem isn’t that the body can’t produce glucose. It does so very well.

The problem lies in the speed at which it can supply glucose compared to how fast the muscle can consume it when power output rises.

And this difference changes everything.

A Muscle Doesn’t Consume Theories. It Consumes ATP.

When you increase exercise intensity, the first thing that rises isn’t “calorie needs.”

It’s the ATP demand per second.

A muscle fiber must continuously regenerate ATP to enable the actin-myosin cycle, operate ion pumps, return calcium to the sarcoplasmic reticulum, and maintain membrane excitability.

The more frequent or powerful the contractions, the higher the ATP flow required.

Not all energy substrates can produce ATP at the same rate.

Fatty acids are remarkable for producing large amounts of energy over time.

But they require multiple steps: mobilization, transport, mitochondrial entry, β-oxidation, acetyl-CoA production, Krebs cycle, and respiratory chain.

Muscle glycogen, on the other hand, is already inside the cell.

Glycogen → glucose-1-phosphate → glucose-6-phosphate → glycolysis.

The muscle literally has its fast fuel on site.

This is precisely why glycogen becomes critical as intensity increases.

Fat Produces Lots of Energy. It Doesn’t Always Produce It Fast Enough.

This is the central error in many pro-keto arguments.

They confuse total energy capacity with metabolic power.

An athlete may have tens of thousands of kilocalories stored as fat.

True.

But that doesn’t mean they can extract those kilocalories at the rate needed to sustain any intensity.

It’s like having a 1,000-liter tank with a pipe that’s too narrow.

The problem isn’t quantity available.

It’s flow rate.

As intensity rises, the body increasingly depends on muscle glycogen and circulating glucose.

This isn’t an anti-keto opinion.

It’s bioenergetics.

“Gluconeogenesis will produce the necessary glucose”: Yes, but that’s not the right question.

The liver can produce glucose from lactate, glycerol, alanine, and other gluconeogenic substrates.

The kidney can also contribute more in certain situations.

But again, simply saying:

“the body makes its own glucose”

doesn’t address the athletic challenge.

The real question is:

At what speed?

Gluconeogenesis isn’t an instantly mobilizable muscle reserve.

It’s a continuous metabolic process regulated by hormonal status, precursor availability, hepatic blood flow, energy availability, and the body’s needs.

Meanwhile, a muscle fiber that suddenly shifts from easy effort to high power output can ramp up glycogenolysis almost immediately.

When intracellular calcium rises with contractions and AMP, adrenaline, and other metabolic signals activate relevant enzymes, glycogen is locally mobilized.

The liver doesn’t even get a chance to weigh in.

Glycogen Isn’t Just for Sprinters.

Another common shortcut: glycogen is mainly useful for sprinting or CrossFit, while endurance athletes can function almost exclusively on fat.

This is false once you look at what endurance competition really entails.

A marathoner doesn’t run in a metabolic chamber at a perfectly constant speed.

They accelerate.

They slow down.

They attack a hill.

They surge after a turn.

They reposition.

They respond to a competitor.

They face headwinds.

They finish faster.

With every power increase, muscle recruitment changes and glycogen use rises.

Endurance is never just slow, steady fat burning.

It’s a constant blend whose relative contribution shifts second by second.

The FASTER Study by Volek Shatters the Idea That Fat Adaptation Makes Glycogen Secondary.

Jeff Volek’s FASTER study is probably one of the most cited by proponents of sports keto.

And for good reason: the fat oxidation results are impressive.

In ultra-endurance athletes adapted long-term to very low-carb diets, peak fat oxidation reached 1.54 g/min, compared to only 0.67 g/min in athletes consuming more carbs.

The peak even occurred around 70% of VO₂max in low-carb athletes.

It’s a remarkable metabolic adaptation.

But here’s the part often missing from enthusiastic videos on the topic.

After three hours of running, both groups had depleted about 64% of their muscle glycogen.

Yes: 64%.

Even the athletes extremely adapted to fat.

Even those capable of oxidizing more than twice as much fat.

Their glycogen use during exercise and replenishment afterward were similar to the control group.

In other words:

Exceptional fat-burning capacity doesn’t eliminate massive glycogen use.

This is probably one of the most important findings in this entire discussion.

Burke Showed What Happens When Fat Adaptation Is Taken Too Far.

Louise Burke and her team studied international-level walkers on a ketogenic diet for several weeks.

As expected, their fat oxidation skyrocketed.

In the 2017 study, some reached about 1.57 g/min of fat oxidized during exercise.

Seen only from a “fat burning” perspective, the result is spectacular.

But their locomotion economy worsened.

At comparable speeds, they consumed more oxygen.

While groups with high or periodized carbohydrate availability improved performance after training, the keto group did not regain this benefit.

The experiment was repeated.

Same result: impressive fat oxidation increase but worsened exercise economy and performance.

A more recent publication on similar athletes also showed lower training quality on LCHF diets: slower speeds during intervals and tempo sessions despite higher heart rates.

The message becomes hard to ignore:

Burning more fat doesn’t mean producing more performance.

Why? Because one oxygen molecule doesn’t yield the same power depending on the fuel used.

This is especially important in endurance.

Fat oxidation produces a lot of ATP per substrate molecule.

But it requires more oxygen to produce a given amount of ATP than glucose oxidation.

As you approach your aerobic limits, oxygen becomes a precious resource.

If producing the same mechanical power demands more oxygen, your economy decreases.

That’s exactly what Burke observed: LCHF adaptation greatly increased fat oxidation but also raised oxygen cost at competition-relevant speeds.

Again, the problem isn’t that fat is a bad fuel.

The problem is trying to make it the optimal fuel for all intensities.

And when you demand high power, the problem becomes even clearer.

When Effort Becomes Highly Glycolytic, Keto Shows Even More Limits.

In a randomized crossover study with trained individuals, only four days of ketogenic diet caused about a 7% drop in peak power and 6% in mean power during a Wingate test.

Distance covered in a Yo-Yo intermittent test was also about 15% lower.

This study involved short adaptation and can’t be directly applied to athletes keto-adapted for months.

But it reminds us of something essential:

The higher the glycolytic demand, the less credible it is to claim fat and gluconeogenesis will always suffice.

And This Is Exactly Where Targeted Dextrose Makes Perfect Sense.

At Athletic Carnivore, we’re not talking about adding sugary products all day long.

We’re talking about targeted fuel when physiology justifies it.

Dextrose is simply D-glucose.

It doesn’t need conversion from another monosaccharide.

After intestinal absorption, it quickly enters circulation.

During exercise, the active muscle has a particularly interesting mechanism: muscle contraction stimulates GLUT4 transporter translocation to the cell membrane.

This means a working muscle increases its capacity to uptake circulating glucose without relying solely on a large insulin spike.

This is fundamental.

So we’re not talking about consuming dextrose while sitting in front of Netflix.

We’re talking about providing glucose when muscle tissue is precisely increasing its ability to use it.

It’s a completely different metabolic logic.

However, Dextrose Isn’t Meant to Replace Glycogen Already Stored in the Fiber.

We must also avoid the opposite shortcut.

When you start a sprint or heavy set, the dextrose you just consumed won’t instantly reach the sarcoplasm and replace muscle glycogen.

Local glycogen retains a major advantage: it’s already stored inside the cell.

The benefit of dextrose during sufficiently long effort is to support blood glucose, provide an immediately oxidizable exogenous substrate after absorption, and gradually reduce exclusive dependence on endogenous stores.

The reasoning becomes much more coherent:

- Muscle glycogen for immediate availability;
- Circulating glucose to sustain effort;
- Fat to supply huge energy amounts when intensity allows oxidation;
- Gluconeogenesis to help maintain blood glucose and homeostasis.

All these work together.

This is precisely what the “stay in ketosis at all costs” narrative completely crushes.

Ketosis Is Not a Performance Medal.

It’s important to correct a major misconception.

Having ketone bodies in the blood during exercise doesn’t mean the body isn’t using a lot of glucose.

You can have measurable ketonemia and simultaneously use large amounts of muscle glycogen.

That’s why using β-hydroxybutyrate levels as an absolute marker of sports performance makes little sense.

The real issue is energy flux.

How many ATP molecules per second must your muscle supply?

What portion can fat oxidation cover?

What portion requires glycolysis acceleration?

What is your glycogen level?

How long is the effort?

What is the actual intensity?

These are the right questions.

True Metabolic Flexibility Is Not About Staying Keto.

This is probably where some pro-keto YouTubers’ messages become most paradoxical.

They constantly talk about metabolic flexibility while presenting the ideal goal as maintaining the same metabolic state all day long.

But flexibility, by definition, is exactly the opposite.

It’s being able to strongly oxidize fat when power demand allows.

Then rapidly increase glycogen and glucose use when intensity rises.

Then switch back to fat when intensity drops.

A flexible engine isn’t locked onto a single fuel.

Volek’s work shows you can become exceptionally good at fat oxidation without stopping massive glycogen use.

Burke’s work shows pushing fat dependence further can worsen exercise economy and reduce the ability to efficiently use glucose at high intensities.

Recent data continue to show ketogenic LCHF diets aren’t a universal solution for endurance performance, especially when events require high intensity or pace changes.

Here’s the point that must stop being hidden behind phrases like:

“I burn fat, so I no longer need glucose.”

Physiology doesn’t show that.

Your muscle doesn’t pick a fuel to defend your diet.

It chooses metabolic pathways capable of supplying the ATP needed at the requested rate.

And when you demand more power, glycogen and glucose naturally regain importance.

At Athletic Carnivore, that’s exactly why we don’t treat carnivore, low-carb, or ketosis as dogmas to maintain at all costs. Our editorial line places performance in a logic of fuel adapted to effort, recovery, individual context, and metabolic flexibility.

The question to ask those who say an athlete must absolutely stay in ketosis 24/7 is very simple:

If your muscle instantly demands an energy flow that fat oxidation and gluconeogenesis can’t supply fast enough, what will you use to produce the missing ATP?

And that’s where slogans usually become much less convincing.

Understanding My Metabolic and Athletic Terrain

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