Electrical stimulation of a trout saline-perfused trunk preparation resulted in metabolic and respiratory responses comparable to those occurring after exhaustive exercise in vivo. Recovery of intracellular acid-base status and glycogen resynthesis were faster than in vivo. Intracellular carbonic anhydrase (ICF CA) blockade elevated intracellular PCO₂ relative to untreated postexercise controls, whereas extracellular CA (ECF CA) blockade did not, in contrast to previous work with muscle at rest. ECF CA blockade had only a transient effect on postexercise CO₂ and ammonia efflux. The relatively small pool of membrane-associated CA appears to be overwhelmed by exercise-induced CO₂ production in muscle. Transmembrane ammonia efflux appears to shift from diffusion primarily as NH₃ at rest, which is facilitated by ECF CA, to movement predominantly as NH⁺₄ after exercise, which is independent of CA. The postponed recovery of intracellular pH caused by either or both ECF and ICF CA inhibition was consistent with reduced metabolic acid and lactate excretion from muscle. Creatine phosphate resynthesis was delayed by CA inhibition, whereas ATP replenishment was not affected. Delayed glycogen recovery indicates that HCO₃-dependent pathway(s) may be involved in glyconeogenesis.