Five days of a high fat diet changed what the muscle was built to burn

What FAT/CD36 is

Fat does not cross into a muscle fibre in useful quantities on its own. It is carried by transporter proteins, and FAT/CD36 is the main one in human skeletal muscle, so counting it asks what the muscle is equipped to do rather than what it happened to burn.

Drawn from background physiology, not from this paper.

Why they ran it

Dietary fatty acids were already suspected of regulating gene expression, but almost nothing was known about whether changing the fat in a person's diet changes gene regulation inside human skeletal muscle. So the authors measured the genes for fatty acid transport and beta oxidation, in trained people rather than in cells.

Drawn from the paper's stated objective.

Fourteen well trained male cyclists and triathletes ate either a high fat diet, more than 65 percent of energy as lipid, or an isoenergetic high carbohydrate diet at 70 to 75 percent of energy as carbohydrate, for five days each in a crossover. Muscle and blood were sampled at rest on day 1 and again after the five days.

After the high fat diet the muscle carried more messenger RNA for FAT/CD36, the fatty acid transporter, and more messenger RNA for beta hydroxyacyl CoA dehydrogenase, an enzyme of fat oxidation. Both differences were at P less than 0.05. The abundance of the FAT/CD36 protein was also greater.

Three of the five transcripts measured did not move. Plasma membrane fatty acid binding protein, carnitine palmitoyltransferase I and uncoupling protein 3 showed no significant change on either diet.

The numbers

Diet duration, each arm	5 days
High fat arm, energy from lipid	more than 65 percent
High carbohydrate arm, energy from carbohydrate	70 to 75 percent
FAT/CD36 messenger RNA, high fat versus high carbohydrate	greater after high fat, P less than 0.05
Beta hydroxyacyl CoA dehydrogenase messenger RNA	greater after high fat, P less than 0.05
FAT/CD36 protein abundance	greater after high fat
Transcripts that did not change	FABPpm, CPT I, UCP3
Mean peak oxygen uptake	67.0 ml/kg/min

Why this might happen

Shown in this study The study measured this step directly.

Their conclusion is that changing the fatty acids available in the diet rapidly and markedly modulates the expression of the messenger RNA encoding the proteins needed for fatty acid transport and oxidative metabolism, which they frame as nutrient and gene interaction inside human muscle.

In that reading the diet is not only supplying a fuel. It is acting as a signal about which proteins to build.

Drawn from the paper's stated conclusion. The full discussion was not openly reachable.

What this does not show

More transporter is not more fat burned. Everything here was measured in resting muscle. The study shows the machinery for taking up and oxidising fat was built up, and says nothing about how much fat was actually oxidised during exercise, because no exercise trial was run.
Two of five transcripts moved, not all of them. Carnitine palmitoyltransferase I sits at the step where fatty acids enter the mitochondrion, and it did not change. A coordinated rebuild of the whole pathway is not what was observed.
Five days is the tested window, not a general rate. This says a five day exposure is enough to move these transcripts. It cannot say how much of the change happened on day one, or whether it keeps going past day five.
Fourteen trained men. All male, all endurance trained, mean peak oxygen uptake 67 millilitres per kilogram per minute. Nothing here reaches women, untrained people, or anyone with a metabolic condition.

Where this leaves us

It is now more likely that a change in the fat in a diet is registered by muscle as an instruction rather than only as a supply. This confirms in trained humans what had been shown in cells and animals, and it sets the five day timescale that the rest of this literature works with.

Fourteen well trained male cyclists and triathletes, sampled at rest after five days on each diet.

The same design with an exercise trial and substrate measurement attached, so that the built machinery could be checked against the fuel actually used.

Caveats worth holding

The abstract reports the direction of change and the P values but not the fold changes, so the size of the effect on each transcript cannot be stated here.
All sampling was at rest. There is no exercise trial and no performance outcome in this study.
The two diets differed in both fat and carbohydrate at once, so the design cannot separate an effect of more fat from an effect of less carbohydrate.
The full discussion was not openly reachable, so the mechanism section rests on the paper's stated conclusion rather than on its own explanatory text.
Fourteen trained men, no women.