Gill ventilation, blood gas and acid-base values, Mo,, Mc.02 and the gas exchange ratio have been measured before, during, and after exposure to hypoxia in the channel catfish, Zctalurus punctatus. Z.punctatus maintains M,,, at control levels to a PI,, as low as 60 mm Hg, through a profound branchial hyperventilation. Concomitantly, however, a lactic acidosis usually develops, indicating a significant anaerobic glycolysis. Both a metabolic acidosis and respiratory alkalosis occur inzctalurus during hypoxic exposure, with the former usually predominating. MCo, doubles and the gas exchange ratio (R,) increases from 0.8 at control levels to 2.0 at hypoxic levels, indicating that, in addition to anaerobic glycolysis, nonglycolytic pathways producing CO, also oper- ate during hypoxic exposure. Analysis reveals that at least half of the increased MCo2 during hypoxic exposure is due strictly to lactate acidification of the tissue HCO,- pool, rather than from metabolic production of molecular CO,. Thus, the actual respiratory quotient (RQ) only rises to 1.5 during hypoxic exposure. Within one hour of a return to air saturated water, a large lactate "flush" and severe plasma acidosis occur, and control levels for these and other values are not reachieved for 2-6 hours after hypoxic exposure. Complete analysis of 0, and CO, exchange in the catfish exposed to short-term hypoxia thus must consider both the time course of acid-base disturbance and the evolution of CO, from the acidified tissue bicarbonate pool. Limitation of oxygen delivery to the tissues, whether due to the increased demands of exer- cise or the reduced supply during envi- ronmental hypoxia, is a physiological problem encountered at some time by almost every fish species. While extensive investigation has cen- tered on adjustments and adaptations evoked to maintain oxygen delivery in the face of po- tential 0, limitations, it is also generally ac- knowledged that various tissues of many fishes can sustain considerable levels of anaerobic metabolism by which the minimum energy re- quirements of the animal are alternatively satisfied. Evidence for anaerobiosis is often presented in the form of increased blood, tissue, or urine levels of lactate, one of the major metabolic end-products of vertebrate anaerobic gly- colosis. Thus, elevations in lactate during or following environmental hypoxia have been at- tributed to a progressive shift towards anaerobic glycolysis in many fresh water and marine fishes (Leifestad et al., '57; Heath and Pritchard, '65; Holeton and Randall, '67; Ban- durski et al., '68; Caillouet, '68; Wittenberger, '68; Hunn, '69; Burton, '70a, b; Burton, '71; Bur- ton and Spehar, '7 l; Hughes and Johnston, '78). However, nonglycolytic anaerobic pathways resulting in the evolution of CO, and end- products other than lactate, apparently also operate during hypoxic or anoxic exposure in fishes (see Blazka, '58; Burton and Spehar, '71; Hochachka and Somero, '73). Increases in lactate and other anaerobic end-products in fish offer an indication that anaerobic metabolism is occurring-they can- not, however, provide quantitative information on the time course of development of anaerobiosis or on the anaerobiclaerobic met- abolic balance during acute hypoxic expo