environment where chromium losses in sweat would be predicted to be high. Studies on the functional consequences of activity-induced changes in chromium metabolism are needed.
It is well recognized that iron-deficiency anemia can be associated with a diminished performance in maximal and submaximal physical exercise (Andersen and Barkve, 1970; Edgerton et al., 1981; Gardner et al., 1977; McDonald and Keen, 1988 and references cited therein). However, there is considerable controversy about the extent to which exercise contributes to the development of iron deficiency. Although there is a common perception that athletes as a group tend to have a high incidence of anemia compared to sedentary populations, hematological surveys of elite athletes have typically not supported this idea (Brotherhood et al., 1975; de Wijn et al., 1971; Stewart et al., 1972). Thus, overt iron-deficiency anemia does not appear to be a common complication of chronic intense exercise.
High levels of physical activity have been suggested to cause ''sports anemia'' (typically defined as a drop in hemoglobin concentration, hematocrit, and red blood cell count; Balaban et al., 1989; Yoshimura, 1970). The phenomenon of sports anemia has been associated with increased erythrocyte destruction, depressed iron absorption, increased sweat loss of iron, and gastrointestinal blood loss (Dressendorfer et al., 1991; Ehn et al., 1980; Frederickson et al., 1983; Paulev et al., 1983; Puhl et al., 1981; Stewart et al., 1984). Although most investigators agree that sports anemia is common in athletes who initiate rigorous training programs, this "anemia" is typically transitory in nature with hematological values often returning to pretraining values within 3 weeks despite continued training (Frederickson et al., 1983). Based on these findings, it has been suggested by some that sports anemia may be in part a consequence of plasma volume expansion and a functional dilution of the red blood cell count because blood volume can increase by as much as 20 percent during training (Brotherhood et al., 1975; Hegenauer et al., 1983).
In recent years there has been interest in the idea that exercise training can result in reduced tissue iron stores. Ehn at al. (1980) reported low bone marrow iron stores and evidence of increased iron absorption in elite distance runners who were characterized by normal hemoglobin and serum iron levels. Low serum ferritin concentrations have been reported by numerous investigators to be a consequence of prolonged, strenuous exercise (primarily when the subject is involved in weight-bearing sports) (Magazanik et al., 1988; Nickerson et al., 1985; Parr et al., 1984; Roberts and Smith, 1990; Snyder et al., 1989). Although there is considerable debate about the extent to which iron supplements may prevent exercise-induced reductions in tis-