put into the plasma as a result of exercise may have long-lasting effects, as suggested by the observation that plasma copper levels at rest tend to be higher in athletes than in untrained individuals (Haralambie, 1975; Lukaski et al., 1983; Olha et al., 1982).
Given the putative antioxidant properties of ceruloplasmin (Goldstein et al., 1979; Gutteridge, 1986), one explanation for the exercise-induced increase in the concentration of this plasma protein is as a response to tissue injury associated with oxidative damage or to the presence of an increased concentration of free radicals (Alessio et al., 1988; Davies et al., 1982; Jenkins, 1988; Kanter et al., 1986). An additional possibility is that the increased ceruloplasmin output from the liver, and hence increased levels in the plasma, is an adaptive response by the body to an increased requirement for extrahepatic copper. It is known that the higher values of maximal oxygen uptake in trained individuals are correlated to an increase in oxidative enzymes within the cell. One of the enzymes increased is the copper-containing protein, cytochrome oxidase (Terjung et al., 1973). It has been shown that ceruloplasmin copper can be incorporated into cytochrome oxidase, and cell receptor sites for ceruloplasmin have been identified (Stevens et al., 1984). Ceruloplasmin copper has also been demonstrated to be transferred to apo-copper, zinc superoxide dismutase (Percival and Harris, 1991). An increase in cellular copper, zinc superoxide dismutase activity could represent an adaptive response to exercise-induced intracellular oxidative stress (Jenkins, 1988; Lukaski et al., 1990).
In contrast to reports of increased plasma copper concentrations, Anderson et al. (1984) reported that plasma copper concentrations were similar in men prior to and after completing a 6-mile run; Lukaski et al. (1990) reported no influence of training on plasma copper concentrations in elite swimmers, and Singh et al. (1991) observed no change in plasma copper concentrations in men engaged in intense physical activity over a 5-day period. Resina et al. (1990) reported that plasma copper concentrations were lower in long-distance runners than in sedentary controls, and Dowdy and Burt (1980) reported that plasma copper concentrations and ceruloplasmin activity decreased in competitive swimmers over a 6-month period. Uhari et al. (1983) reported that plasma copper concentrations decreased in male and female subjects following exposure to hot temperatures in a sauna bath.
Reasons for the above differences in reported effects of exercise on plasma copper concentrations are various, including differences in copper status of the subjects; type, intensity, and duration of the exercise; physical condition of the individual; and extent of exercise-induced tissue trauma. Presumably, increases in plasma copper occur primarily when there is tissue damage that triggers an acute-phase response. However, note that in the study by Singh et al. (1991), despite evidence of significant tissue damage (see zinc section above), plasma copper concentrations were not elevated.