Additional studies are needed that define the mechanisms underlying exercise-induced increases in plasma copper concentrations.
It is important to point out that the occurrence of high plasma copper concentrations does not necessarily translate into high tissue copper concentrations; indeed, high plasma copper concentrations in some disease states have been correlated to low soft tissue copper concentrations (Clegg et al., 1987; Dubick et al., 1987). Although the interpretation of normal to high plasma copper concentrations with regard to assessing an individual's copper status can be difficult, there is general agreement that low plasma copper concentrations typically reflect a compromised copper status. Thus the report of low plasma copper concentrations in some endurance athletes (see above) is of concern. Although loss of basal copper via sweat is typically considered negligible (Gutteridge et al., 1985; Jacob et al., 1981), Consolazio et al. (1964) reported that the amount of copper lost via sweat can be considerable; men who were maintained at 37.8°C and 50 percent relative humidity lost as much as 1 mg per day in sweat. This value should be contrasted to typical dietary copper intakes, which are on the order of 1 to 2 mg (Pennington et al., 1989). Thus prolonged, excessive loss of copper via sweat during strenuous exercise could result in a marginal copper status. The simultaneous exposure to hot temperatures would be expected to accelerate the development of a marginal copper condition.
Prolonged strenuous exercise can result in marked changes in chromium, copper, iron, magnesium, and zinc metabolism. Evidence of these changes can persist for several days after the exercise is discontinued. Some of the observed changes in plasma mineral concentrations may be attributed in part to an acute-phase response, which occurs as a result of tissue trauma or stress. Reductions in plasma mineral concentrations may also in part reflect an increased loss of these minerals from the body via urine and sweat. The increased rate of mineral loss that occurs in sweat with exercise is amplified by the simultaneous exposure to hot temperatures.
Given the above observations, the following questions emerge: Do endurance-associated changes in mineral metabolism result in some or all of the following:
a compromised endurance capacity?
a compromised immune defense system?
a compromised antioxidant defense system?
a slower rate of recovery from injury?
Additional work on the influence of prolonged exposure to strenuous exercise and heat is urgently needed. The influence of diet on the above