Determination of functional residual capacity, arterial gas tensions and pH, and arterial-alveolar differences was carried out in a group of nondistressed premature infants to determine if significant alterations in lung volumes or ventilation perfusion relationships sufficiently large to cause cyanosis could be detected after feeding. The only statistically significant changes observed in these parameters were immediately following feeding, a fall of .01 pH units and a fall of 6 mm Hg in arterial oxygen tension; and 15 minutes after feeding, a fall of .01 pH units and a rise in arterial PCO2 of 3 mm Hg. In addition, significant falls in peripheral blood flow were observed five minutes after feeding in association with marked elevations in peripheral vascular resistance. The mild impairment in pulmonary function in association with the more profound changes in limb blood flow are consistent with other studies in premature and full-term infants. These data suggest that cyanotic attacks following feeding may have a complex etiology and require an aggressive multisystem approach for adequate diagnosis and therapy.