In order to evaluate iron balance in the human body, we studied the effects of exercise on iron excretion in urine, sweat and feces. The subjects were five healthy male, college athletes. The daily intake of nutrients by the subjects was regulated by a prescribed diet (Calorie Mate, Ohtsuka), and the control measurements and the exercise measurements were performed within seven days. Excretion of iron in the urine during the exercise period was significantly higher than in the control period. The excretion of iron in the sweat was 1.076±0.118 mg, i. e, , about 70% of total iron physiologically excreted from the human body. The excretion of iron in the feces during the exercise period was significantly lower than during control period. Feces volume was positively correlated with energy expenditure and negatively correlated with the excretion of iron in the feces. Iron absorption during the exercise period was significantly higher than during the control period. These findings suggest that exercise stimulates not only iron excretion via urine and sweat, but iron absorption, and that iron balance remains positive in healthy male subjects who have normal iron status.

We investigated the effect of the difference of exercise intensity on the changes in ammonia and oxypurines (hypoxanthine·xanthine) . The subjects were 7 male university students who belonged to the Judo club. By using a bicycle ergometer with the same total work load (kpm), they performed following exercise : light exercise (27.1±0.8% HRmax), moderate exercise (72.6±2.5% HRmax) and exhaustive exercise. After light exercise, blood ammonia, serum oxypurines and urinary oxypurines excretion did not increase. Urinary uric acid excertion increased significantly, but serum uric acid decreased slightly. After moderate exercise, the significant increase was observed with blood ammonia (+ 35.3±5.9μmol/l) . Urinary oxypurines excretion also increased significantly, while serum oxypurines did not change. Also, serum uric acid rose slightly. After exhaustive exercise, the significant increase was observed with blood ammonia, serum oxypurines and serum uric acid. Each peak level and appearance time were +67.2±15.1μmol/l after 3 min, +31.4±7.6μmol/l after 30 min, 155.7±39.9μmol/l after 1 hr of exercise, respectively. These results suggest that AMP deamination occur during moderate intensity, while remarkable production of oxypurines which lead the increase of serum uric acid occur in higher exercise intensity.

In order to prevent sports anemia, caused especially by iron deficiency or shortage, a special type of food supplementation was designed. This was called“iron-food”and contained 510% of the therapeutic iron dose. According to hemoglobin (Hb) values, female subjects who had been performing hard daily training were divided into two groups ; an anemia group (A group, Hb≤11.9 g/dl, n=4) and a potential anemia group (PA group, 12.0≤Hb≤12.9g/dl, n=4) . Then the iron-food was administered for six weeks following placebo treatment. Iron status, hematological profiles and aerobic work capacity of the two groups were examined before and after the two periods to investigate the effect of the iron-food. Serum iron, iron saturation and ferritin were significantly increased in the PA group. Serum iron tended to be increased in the A group, but not significantly. Red blood cell count, Hb and hematocrit were significantly increased in the PA group, and the reticulocyte count was also increased in the A group. These results suggest that iron-food helped to increase daily iron intake in the anemic subjects, but not to a sufficient extent to aid recovery from anemia. However the ironfood was effective for improving iron status in subjects with potential anemia (latent iron deficiency) .

This study examined the effects of physical training on exercise hyperpnea (EH) in patients on hemodialysis (HD) . In baseline, 17 (trained group) and 12 (control group) patients on HD performed symptom limited exercise test using a treadmill. Trained group, but not control group, exercised 2 to 3 times weekly on non-dialysis days under medical supervision. Exercise testing was repeated 20 weeks after the baseline. Ventilatory response to exercise was evaluated using the regression slope relating minute ventilation (VE) to carbon dioxide output (VCO₂ ) during incremental exercise (VE/VCO₂ slope) below the point of respiratory compensation. In trained group, VE, oxygen uptake ( VO₂) and VCO₂ at peak exercise increased and VE/VO₂ and VE/VCO₂ decreased after physical training, respectively. No change was observed in control group. VO₂ at the anaerobic threshold increased in trained group, but not in control group. The post training VE/VCO₂ slope (33.9±5.0) was significantly (p<0.05) lower than the pre-training slope (38.0± 4.8) and remained constant in control group. In trained group, changes in the VE/VCO₂ slope correlated with those in peak VO₂ (p<0.05) . These results suggest that physical training decreases EH in patients on HD and that it correlates with changes in exercise tolerance.