Iron and endurance

Three ways training takes iron out

The first is mechanical. Every footstrike destroys a small number of red cells in the capillaries of the sole — foot-strike haemolysis — and the iron inside them is not all recovered. On its own this is minor. Multiplied by a hundred kilometres a week, for years, it stops being minor.

The second is sweat, which carries iron in small quantities that add up over long sessions in heat.

The third is the one people miss, because it works in the opposite direction to intuition. Hard exercise raises hepcidin, the hormone that shuts down iron absorption, and it stays raised for hours afterwards. So the meal eaten after a hard session — the one an athlete is most careful about — is absorbed worse than the same meal on a rest day. The body loses iron to training and then briefly refuses to take more in.

Why a normal blood count proves nothing

Haemoglobin is the last thing to fall. The body has a store — ferritin — and it will empty that store completely before it lets the blood count drop, because carrying oxygen is more urgent than keeping a reserve.

So there is a long stretch, often many months, where the reserve is gone, the athlete feels progressively worse, and every standard blood test comes back normal. This is called iron deficiency without anaemia, and it is the state most affected athletes are actually in. Anaemia is the end of the process, not the start of it.

The test that sees it is ferritin, and it has to be asked for. It is not on a routine panel. If you take one thing from this page, it is the name of that test.

What the number means, and its one big trap

The threshold used in sports medicine is higher than the one used to diagnose anaemia in the general population, because the question is different — not "is this person ill" but "does this person have enough reserve to train hard".

The trap is that ferritin also rises with inflammation, and hard training is inflammatory. A ferritin drawn the morning after a hard session can read reassuringly high while the actual store is low. Blood taken on a rest day, ideally alongside a marker of inflammation, is worth the inconvenience of arranging.

Why not to just take some

Because the body has no way to get rid of a surplus. It regulates iron by absorbing more or less, and once it is in, it stays. Sustained supplementation in someone who was not short accumulates, and in a person carrying a haemochromatosis gene — which is common enough that you would not know — it accumulates fast.

Iron also competes with zinc and copper for the same absorption routes, so months of unnecessary iron can create a different deficiency while you are treating one you did not have.

Where a genuine shortfall is confirmed, treatment is straightforward and often dramatic. That is the argument for testing rather than against acting.

The food side is mostly about what it is eaten with

Absorption from a plant source swings by a factor of five or more depending on the rest of the plate. Vitamin C in the same meal multiplies it. Tea or coffee with the meal roughly halves it, and the athlete who has porridge and a large coffee is undoing the porridge.

The practical version of this is unglamorous: move the coffee an hour away from the iron-containing meal, and put something acidic on the plate. That is a bigger intervention than most supplements, and it is free.