Acid-base regulation is one of the most tightly regulated physiological processes in animals20. Changes in blood and cellular pH impact protein charge, and the consequences to protein function can impair everything from enzyme function, cellular ion transport, muscle contractility and metabolism through to survival21. While the mechanisms and capacity for acid-base regulation via the teleost gill have been reasonably well studied, much less is known about the hagfish gill22. Given the intimate association between ion and acid equivalent exchange during acid-base compensation at the teleost gill1 and that hagfish are ionoconformers9, one might expect limited acid-base compensatory capacity. Contrastingly, aspects of hagfish life history suggest otherwise: hagfish burrow in soft sediments and use their toothed tongue to enter dead animal carcasses while feeding where they may remain for extended periods23. These conditions promote aquatic hypoxia (low environmental O2) and hypercarbia (elevated environmental CO2), both of which can severely disrupt acid-base status. Indeed, Pacific hagfish, Eptatretus stoutii, are supremely tolerant of hypoxia and anoxia13. However, hypercarbia tolerance in hagfishes is unknown14, and while elevated CO2 is an environmentally relevant challenge, hypercarbia exposure can also be used as a tool to quantify acid-base regulatory capacity. Here we exposed hagfish to sustained hypercarbia to induce a rapid acidosis. Subsequent recovery was used to quantify the rate and degree of blood acid-base compensation for direct comparison with other aquatic craniates, which has not been previously investigated.