the reduction in plasma magnesium may be due in part to an increased rate of magnesium loss from the body, redistribution of magnesium from the plasma pool into other sites may also contribute to exercise-induced decreases in plasma magnesium. For example, Costill et al. (1976) reported an increased magnesium content in exercising muscle during prolonged work that paralleled the decline in plasma magnesium. Redistribution of serum magnesium into red blood cells (Abbasciano et al., 1988; Deuster et al., 1987; Lukaski et al., 1983) and into adipocytes (Franz et al., 1985) with exercise has also been reported. Researchers generally agree that prolonged exercise can result in lower than normal plasma magnesium concentrations; however, they have not agreed on the functional consequences of this reduction. Jooste et al. (1979) reported that in some cases the reduction can be severe enough to trigger epileptic-type convulsions in runners. Similarly, Liu et al. (1983) reported a case in which an exercise-induced reduction in plasma magnesium was associated with the induction of carpopedal spasms in a 24-year-old woman. Marginal magnesium deficiency has been associated with the etiology of some cardiac diseases (Rayssiguier, 1984), hypertension (Altura and Altura, 1984), and reduced work capacity (Conn et al., 1986; Keen et al., 1987; Lowney et al., 1990; Lukaski et al., 1983). Marginal magnesium status has also been implicated in a number of human psychiatric disturbances and in chronic fatigue syndrome (Cox et al., 1991).
Given the above reports, it is clear that prolonged strenuous exertion can result in reductions in plasma magnesium concentrations. These reductions can be attributed in part to an increased rate of magnesium loss via sweat, which could be significantly amplified in hot environments. Given the recognition that marginal magnesium deficiency can present a significant health risk to an individual, studies are needed that define the functional consequences of exercise-and heat-induced reductions in plasma magnesium concentrations.
Acute, strenuous exercise has been reported by several investigators to result in a marked increase in plasma copper concentrations, which has been attributed to an increase in plasma ceruloplasmin concentrations (Haralambie, 1975; Ohno et al., 1984; Olha et al., 1982). An increase in ceruloplasmin concentrations is consistent with the induction of an acute-phase response as discussed above. The effects of intense exercise on increasing plasma copper levels can continue for prolonged time periods. Dressendorfer et al. (1982) reported that men engaged in a 20-day, 500-km road race were characterized by plasma copper levels that increased constantly during the first week, after which they remained fairly constant. This increased copper out-