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ration, the meal, ready-to-eat (MRE), as their only food. Although the average zinc intake during the field exercise was lower than zinc intakes in a sedentary control group of soldiers who were fed the same food, intakes by both groups were considered adequate. Urinary zinc concentrations in the active soldiers increased from an average basal level of 400 µg per day to about 700 µg per day during the study. Sweat mineral losses were not assessed.

This finding shows that there are short-term effects of exercise on zinc metabolism; however, the immediate physiological consequences of these effects are not known. Dressendorfer and Sockolov (1980) have suggested that a high level of constant exercise can have long-lasting effects on zinc metabolism. This suggestion was based on the observation that a significant number of endurance runners were characterized by low serum zinc concentrations even when tested prior to an exercise bout. This hypozincemia in endurance runners has since been reported by other laboratories (Couzy et al., 1990; Deuster et al., 1986; Dressendorfer et al., 1982; Hackman and Keen, 1986; Haralambie, 1981).

The mechanisms underlying the development of exercise-induced hypozincemia are presumably multifactorial and may include impaired absorption of zinc, excessive sweat and urinary loss of the element, and an altered metabolism of zinc (Anderson et al., 1984; Deuster et al., 1989; Miyamura et al., 1987). Although there is considerable debate about the value of plasma zinc in diagnosing zinc deficiency, most investigators agree that prolonged low plasma zinc concentrations are indicative of suboptimal zinc status. Given that the consequences of a suboptimal zinc status can include behavioral abnormalities, impaired immunocompetence, and reduced rate of recovery from injury (Hambidge, 1989; Keen and Gershwin 1990), it is evident that the functional significance of exercise-induced hypozincemia needs to be defined in future studies. In addition, the interactive effect of prolonged exposure to high temperatures and intense exercise needs to be defined. Exposure to extremes in temperature by itself can result in a stimulation of the acute-phase response with subsequent changes in zinc metabolism (Sugawara et al., 1983; Uhari et al., 1983); sweat losses of zinc can range from 0.5 to 1 mg per liter (Aruoma et al., 1988; Van Rij et al., 1986). Thus a strong synergistic effect of prolonged exposure to exercise and heat would be predicted. To illustrate the above scenario, the following calculations can be made. First, assume a dietary zinc intake of 15 mg, with a typical absorption of 20 percent (King and Turnlund, 1989), resulting in an uptake of 3 mg of zinc. By assuming a sweat zinc concentration of 0.5 mg per liter, it is evident that sweat losses in excess of 8 liters can present a significant problem. In addition, typical urinary zinc losses under conditions of stress will average 0.5 to 0.8 mg per day. Zinc absorption may also be reduced under conditions of stress. Given the above calculations, sus-



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