EVIDENCE of a form of metabolism in which less oxygen per unit of energy is used in the fetus and newborn than in older animals has been recognized for some time. An "anaerobic" metabolism leading to the traditional "oxygen deficit" in muscle activity is well established. The purpose of this preliminary communication is to review published observations bearing on this point and to add some of our own that indicate the existence of a similar metabolism in human young, and to discuss its practical significance. In subsequent reports we hope to follow up these studies. The discussion will be concerned with three general topics: (1) Direct observation of resistance of newborn animals to anoxia. (2) Studies of acidosis in normal premature and full term infants. (3) Observations of the effect of oxygen on the respiratory pattern of premature infants. RESISTANCE OF NEWBORN ANIMALS TO ANOXIA Selle and Witten, and Thoms and Hiestand, have shown that survival of the primitive respiratory center in decapitated rats and mice is retained much longer by the anoxic newborn than by the older animal. The heads of young rats under five to six weeks of age showed a persistence of gasping for 20 to 40 minutes in anaerobic conditions while those older than five to six weeks had lost this ability. Fazekas, Alexander, and Himwich studied adults, infants, and fetuses in utero of various animal species under conditions of oxygen lack. Nitrogen, helium, and other gases were used to produce partial or complete displacement of oxygen from the respired atmosphere. Their observations reveal that mature animals survive after breathing undiluted nitrogen for approximately three minutes, while the average survival time for a newborn animal was as follows:[see table in source pdf]. They conclude, first, that there is a greater tolerance to oxygen lack in the young than in the adult of the same species, and second, that the difference in survival time between newborn of different species is due to their difference in maturity at birth. These workers used sodium fluoride and sodium iodoacetate as enzyme poisons to interrupt the carbohydrate breakdown series, presumably at the phosphoglyceric acid and triosephosphate levels. Table I shows the results of their experiments on the survival time of newborn rats under various conditions.