nor less. The question is, which is to be master?’
So it goes today with ‘anaemia’ and ‘fatigue’ and
‘iron deficiency’ in athletes. As I will cover, these
words mean different things to different people.
First, a description of normal iron balance is in
order.
Normal iron balance
Because iron—as the core of the oxygen-
delivering haemoglobin molecule—is the most
precious metal in the body, it is recycled. Recy-
cling ensures a constant internalsupply of iron—
independent of externalsources such as diet—to
maintain an optimal red cell mass. So the bulk of
the iron needed for the daily synthesis of haemo-
globin (20–30 mg) comes from recycling the iron
in senile red cells.
Senile red cells are destroyed by macrophages
in the spleen, releasing iron that is taken up by
transferrin (the iron-transporting protein in
plasma), carried to the bone marrow, removed by
developing red cells (normoblasts), and incorpo-
rated into haemoglobin of new-born red cells
(reticulocytes).
Because of this avid recycling—a ‘closed
system’—little iron is lost from the body. Indeed,
the body has no active mechanism to excrete
unneeded iron. The average man loses only 1 mg
iron · day–1; the average woman (because of
menses), 2 mg. The small obligatory loss (other
than menses) is in sweat and in epithelial cells
shed largely from skin, intestine and genitouri-
nary tract.
Because obligatory loss of iron is small, only
small amounts must be absorbed. The normal
USA diet provides 10–20 mg of iron daily; each
1000 calories in food is usually associated with
5–6 mg of iron. To maintain iron balance, the
average man absorbs 1 mg · day–1; the average
woman, 2 mg. During times of increased iron
need—growth, pregnancy, bleeding—the intes-
tine increases its absorption of iron, up to 4 or
5 mg · day–1. When the need declines, absorption
returns to baseline.
The average total body iron of an adult man is
4000 mg. Up to three quarters of this iron is in the
‘functional compartment,’ mainly haemoglobin
and myoglobin, and about one quarter, or
1000 mg, is in storage, a bountiful buffer against
deprivation of dietary iron. In contrast, iron
stores are typically lower in adult women
(300–500 mg), marginal to absent in college-aged
women, and absent in young children and many
adolescents. Unlike most adult male athletes,
then, female and adolescent athletes need a
steady dietary supply of iron to maintain iron
balance and avoid anaemia.
Body iron is stored in parenchymal cells of the
liver and macrophages of the liver, spleen and
bone marrow. The main storage protein is fer-
ritin. Soluble ferritin is released from cells (into
plasma) in direct proportion to cellular ferritin
content. So in general, the level of ferritin in the
plasma parallels the level of storage iron in the
body (Finch & Huebers 1982; Baynes 1996).
Unfortunately, as will be covered below, the use
of serum ferritin level to gauge ‘iron deficiency’
among athletes is fraught with problems, not the
least of which is that one can have low ferritin
level (low iron stores) yet still be absorbing
enough iron from the diet to avoid anaemia. Put
another way, iron deficiency evolves through
predictable stages of severity, in which depletion
of storage iron, the first stage, precedes anaemia.
The development of iron deficiency anaemia
goes through the following stages.
1 Absent marrow iron stores; serum ferritin less
than 12mg·l–1.
2 Low serum iron; high iron-binding capa-
city; increase in level of free erythrocyte
protoporphyrin.
3 Normocytic, normochromic anaemia with
abnormal red cell distribution width.
4 Microcytic, hypochromic anaemia.Effect of training and competition
Training, especially endurance training, and
competition, especially ultramarathons or events
spanning several days or weeks, affect haemo-
globin concentration and iron profile in ways
both physiological and pathophysiological. Mis-
interpretations of these perturbations, notably