than 20mg·l–1(vs. only one of 112 controls). In
eight of the runners, faecal iron (gastrointestinal
blood) loss was gauged by radiolabelling haem
iron and testing stool samples. When the runners
were not training, average gastrointestinal blood
loss was 1–2 ml · day–1. With training or racing,
average loss increased to 5–6 ml · day–1. In
general, gastrointestinal blood loss correlated
with intensity of running, not distance
(Nachtigallet al. 1996).
Iron loss in sweat
Controversy continues on whether athletes can
lose enough iron in sweat to cause iron deficiency
(Haymes & LaManca 1989). The most meticulous
study in resting subjects, one that minimized iron
loss in desquamated cells and iron contamina-
tion of skin, found a very low sweat iron loss,
averaging 23mg·l–1, compared with much higher
values in previous studies. The authors con-
cluded that variations in sweating have only
marginal effects on body iron loss (Brune et al.
1986).
The most recent study in athletes also suggests
that sweat iron loss is modest (Waller & Haymes
1996). It shows that sweat iron level drops over
time, at least during the first hour of exercise. It
finds that exercising men have about twice the
sweat iron loss as women, because of higher
sweat rates in men and likely also because of
greater iron stores in men. The authors estimate
that 6–11% of the iron typically absorbed per day
is lost in sweat during 1 h of exercise. They con-
clude that sweat iron losses would likely not
deplete iron stores in men but might do so in
female athletes whose diets are low in iron.
Iron loss in urine
Some iron is lost in urine (Haymes & Lamanca
1989), but the amounts are negligible (Nachtigall
et al. 1996). Athletes can develop haematuria
from diverse causes, but not enough haematuria
to drain iron stores (Eichner 1990a, 1990b). Exer-
tional haemolytis rarely depletes haptoglobin
and so does not increase urinary iron loss
(Eichner 1985; O’Toole et al. 1988). Urinary iron
loss in athletes is negligible.Shift of iron to liver
The ‘liver shift’ hypothesis sought to explain
why some runners had low ferritins (and low
bone marrow iron scores) yet seemed notiron
deficient by other criteria (Magnusson et al.
1984). The notion was that ‘footstrike haemo-
lysis’ shifted iron from normal storage sites
(macrophages) to hepatocytes, and that iron in
hepatocytes was not readily available for reuse
and not registered by the serum ferritin. This
hypothesis lacked experimental support and
should be put to rest by the finding in elite dis-
tance runners that when ferritin is low, hepatic
iron is also low (Nachtigall et al. 1996).Iron status and athletic performance
Anaemia and athleticism
It is well known that anaemia, even mild
anaemia, impairs all-out athletic performance
(Dallman 1982; Cook 1994); this needs no review.
In my experience with runners, even a 1–2 g · dl–1
decrement in haemoglobin from baseline slows
race performance. Coaches, trainers and sports
medicine physicians, then, need to be alert for
mild anaemia in athletes. When anaemia is mild
and serum ferritin is marginal, it is difficult to
distinguish pseudoanaemia from iron deficiency
anaemia; indeed, they may coexist. When in
doubt, a therapeutic trial of oral iron is wise; a
rise in haemoglobin of 1–2 g · dl–1is the ‘gold
standard’ for diagnosing iron deficiency anaemia
(Eichner 1990a).Low ferritin without anaemia
About two decades ago, a myth arose that low
ferritin alone, without anaemia, impairs athletic
performance. This led to monitoring ferritin as a
marker of performance potential. When runners
without anaemia were told that their ferritin was
30 mg·l–1 and ‘should be much higher’, they