The serum copper parameters were evaluated in 41 male trained runners and in a control group of 24 male subjects engaged in normal physical activity. In the runner group lower serum copper concentrations, lower serum ceruloplasmin biological activity, and higher serum ceruloplasmin levels were found compared with the control group. Reduced serum copper levels may affect the ceruloplasmin biological activity, even if the serum ceruloplasmin levels are higher. The results suggest that more attention should be paid to serum copper and ceruloplasmin in athletes.

The aim of the present study was to compare the iron status of 19 top-level soccer players and 20 male control subjects. All players showed no impairment of physical performance and had a dietary iron intake adequate to cover the iron losses. Serum iron, TIBC, % transferrin saturation and serum ferritin were not significantly different in athletes and controls: serum haptoglobin was significantly lower in the former than in the latter, the result probably indicating an increase in resting intravascular hemolysis. Since the formed Hb-Hp complex is taken up and metabolized by hepatocytes, it has been suggested that in soccer players a redistribution of iron stores occurs among tissue compartments. A multiparametric hematological monitoring of iron metabolism, just as in runners, is therefore necessary in these athletes, too, in order to detect subjects at risk of real iron deficiency. The pharmacological iron supplementation should be limited to these subjects and only when clinical evidence of reduced tissue iron supply is present.

Twenty-two subjects with Wolff-Parkinson-White (WPW) electrocardiographic pattern performing agonistic physical activity were referred to our laboratory to assess arrhythmogenic risk (group 1). This allowed us to evaluate a less known aspect, namely that of effects of training on the electrophysiologic properties of the atrium and accessory pathway. This was done utilizing a control group of 10 WPW patients who did not perform agonistic physical activity (group 2). All subejcts were symptom free, and without signs of associated cardiopathy if we exclude 1 patient of group 1 who presented moderate mitral valve prolapse. Group 1 patients showed significantly higher mean values for basic cycle length (p < 0.001), atrial effective (p < 0.04) and functional (p < 0.02) refractory period, and anterograde effective refractory period of the accessory pathway (p < 0.02). The different behavior observed in group 1 patients could be explained considering the known influence of training on the equilibrium of the autonomic nervous system. Moreover, it is noteworthy that the two groups did not differ for inducibility of atrial fibrillation (AF). This should be taken into account considering the importance of AF in WPW. In conclusion, our study does not demonstrate any negative electrophysiologic effects of training in patients with WPW.

Physical exercise appears to affect both blood magnesium status and erythrocyte 2,3-diphosphoglycerate (2,3-DPG) concentration. Concentrations of erythrocyte and plasma magnesium (ErMg and PlMg) and erythrocyte 2,3-DPG were measured three times over a period of 2 months in a group of 11 athletes who were training for a marathon. The concentration of 2,3-DPG was found to be significantly increased at the end of the 1st month (P < 0.05) compared to its level at the beginning of the study. However, at the end of the 2nd month, it was significantly lower (P < 0.05) than at the end of the 1st month. This decrease might have been due to the reduction in the intensity of training, despite an increase in the training distance. Both ErMg and PlMg did not change significantly after the 1st and 2nd months of training. However, the decrease of total circulating magnesium, i.e., whole blood magnesium was significant, after both the 1st and 2nd months. This decrease may have been due to an increased loss of magnesium or to a shift of magnesium from the blood to other compartments. We observed a significant negative correlation between ErMg and 2,3-DPG after the 1st month: r = -0.59, P < 0.05. We hypothesized that this inverse relationship might have been due to the sympathetic stimulation secondary to physical stress. Furthermore, in view of the mechanism of binding ErMg and 2,3-DPG by haemoglobin, the negative correlation between ErMg and 2,3-DPG might have been due to the relative tissue hypoxia that accompanies aerobic exercise.