Kang Derwent and Linsenmeier (2000) reported that the a- and b-waves of the cat electroretinogram (ERG) are resistant to hypoxemia, at least for PaO2 above 40 mm Hg. The a-wave may be resistant because the photoreceptor can increase glycolysis during hypoxemia. This hypothesis was tested by making the animal hypoglycemic, which should minimize the ability of the photoreceptor to switch to glycolysis. The ERG of dark-adapted anesthetized cats was recorded between an Ag/AgCl electrode in the vitreous humor and a reference electrode near the eye. Responses to bright flashes of diffuse white light were recorded at 3-min intervals during hypoxic episodes at three levels of blood glucose. The moderate hypoglycemia (50 to 70 mg/dl) had a relatively small effect on the a-wave amplitude. Furthermore, the a-wave amplitude increased transiently by 16 ± 7% within 30–40 min of the start of severe hypoglycemia (20 to 40 mg/dl), before recovering to near normal. Severe hypoglycemia alone decreased the b-wave amplitude by 15 ± 13%. Combined hypoxemia and hypoglycemia decreased the b-wave amplitude more than the a-wave amplitude. At all levels of blood glucose, b-wave decreases began at a higher PaO2 than the a-wave changes. For both the a- and b-waves, hypoxemic effects began at higher PaO2 when the animal was hypoglycemic. The increased sensitivity to hypoxemia during severe hypoglycemia suggests that a switch from oxidative to glycolytic metabolism ordinarily protects the retina from moderate hypoxemia. Because the a- and b-waves were affected to different degrees and at different PaO2s, it is unlikely that inner retinal changes are caused completely by changes in the photoreceptor.