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The marked increase of pulmonary ventilation during exercise is caused primarily by the more rapid formation of carbon dioxide, which causes an increased tension of this gas in the blood and alveolar air. Douglas and Haldane (1) showed that if the exercise were not too strenuous the increase in pulmonary ventilation and the increase in alveolar carbon dioxide tension bore approximately the same relation to each other as when the ventilation was increased by the addition of carbon dioxide to the respired air. Thus, according to Haldane (2) the hyperpnea of mild or moderate exercise can be attributed solely to the increased tension of carbon dioxide. When the exercise is more strenuous, the pulmonary ventilation increases out of proportion to the increase of alveolar carbon dioxide tension. Under these circumstances some factor, or factors, additional to the carbon dioxide tension contributes to produce the hyperpnea. One of these contributory factors is the excessive formation of lactic acid in the exercising muscles. Its accumulation produces a lactic acid acidosis; and during strenuous exercise lactic acid salts escape into the blood and urine. A second cause of excessive hyperpnea during moderate and strenuous exercise is oxygen want, for Briggs (3) showed that oxygen inhalations lessen the hyperpnea, at least in individuals who are not in excellent physical condition. Since removal of the lactic acid formed during exercise is an oxidative process, the inhalation of oxygen during exercise might influence the pulmonary ventilation through lessening the accumulation of lactic acid in the muscles and in the body at large. In the following

THE EFFECT OF BREATHING OXYGEN-ENRICHED AIR DURING EXERCISE UPON PULMONARY VENTILATION AND UPON THE LACTIC ACID CONTENT OF BLOOD AND URINE