ing a role as a scavenger of free radicals and a
modulator of the inflammatory response as an
acute phase protein. Copper is also part of super-
oxide dismutase, the enzyme that converts the
harmful superoxide radical into the less harmful
hydrogen peroxide. As part of cytochrome c
oxidase, copper functions in the electron trans-
port chain of the mitochondria. Copper is also
needed for haemoglobin formation. A complete
review of copper containing enzymes and pro-
teins can be found elsewhere (Linder 1996).
There is not sufficient information to establish
an RDA, so the Food and Nutrition Board recom-
mended an estimated safe and adequate daily
dietary intake (ESADDI) of between 1.5 and
3.0 mg · day–1. Copper is found in organ meats
(especially liver), seafoods (especially oysters),
nuts and seeds (Food and Nutrition Board 1989).
Many diets in the general population contain less
than 1.6 mg · day–1but this value may underesti-
mate intake (Food and Nutrition Board 1989).
Most studies reported that athletes ingest ade-
quate amounts of copper (Deuster et al. 1986;
Worme et al. 1990; Bazzarre et al. 1993; Singh et al.
1993). However, in many of these studies, there
was a small fraction of athletes ingesting less
than two thirds of the ESADDI for copper. For
example, about 5% of Navy Seals did not ingest
two thirds the ESADDI (Singh et al. 1989).
Copper status and effects of exercise
Blood levels of copper are most commonly used
to assess status. Several studies have found that
athletes had similar or higher levels than controls
(Dressendorfer & Sockolov 1980; Olha et al. 1982;
Lukaskiet al. 1983, 1990; Weight et al. 1988; Singh
et al. 1989; Bazzarre et al. 1993; Wang et al. 1995;
Tuya et al. 1996). One study reported that male
distance runners had lower plasma copper levels
than controls (Resina et al. 1990). However, the
weight of the data suggests that copper defi-
ciency, as assessed by blood copper levels, is rare
in trained athletes.
Wang et al. (1995) reported that female orien-
teers had higher serum copper concentrations
than male orienteers, which they suggested may
342 nutrition and exercise
be due to the use of oestrogen-containing oral
contraceptives. Newhouse et al. (1993) found that
the mean copper values for females on oral con-
traceptives was 30.1mmol · l–1vs. 18.8mmol · l–1for
women not on oral contraceptives. The reason
for high circulating copper in women on oral
contraceptives is not known but could be due to
higher plasma ceruloplasmin levels from altered
liver function and/or increased absorption of
dietary copper with no change in urine loss
(Newhouseet al. 1993). This effect is related to
oestrogen use because oestrogen replacement
therapy by postmenopausal women also signifi-
cantly increased serum copper levels.
Results of training on blood copper levels are
equivocal. Dressendorfer et al. (1982) reported an
increase in plasma copper over the first 8 days
of a 20-day road race which remained elevated
throughout the duration of the race. These
authors suggested that the elevation in plasma
copper may be due to an increase in the liver’s
production of ceruloplasmin in response to exer-
cise stress. In contrast, Hübner-Woz ́niaket al.
(1996) found that bodybuilders who began a
strength training programme for 10 weeks
showed no pre- to posttraining change in blood
copper levels. Anderson et al. (1995) reported that
an acute bout of strenuous exercise increased
blood copper levels in both moderately trained
runners and untrained men, demonstrating that
the release of copper into the circulation was
independent of the degree of training. However,
Olhaet al. (1982) found that trained runners had a
significantly greater increase in serum copper
after exercise than untrained subjects.
Several studies reported that an acute bout of
exercise results in an increase in plasma copper
levels immediately after exercise which returned
to baseline within a couple of hours (Olha et al.
1982; Ohno et al. 1984). In contrast, Anderson
et al. (1984) found no increase in serum copper
immediately or 2 h after a 9.6-km run, Marrella
et al. (1990) found a slight but significant decrease
in plasma copper after a 1-h cycling test, and
Bordin et al. (1993) found a decrease in plasma
copper after approximately 30 min of a run-to-
exhaustion test. The reason for these discrepant