The intracellular pH (pHi) of barnacle muscle fibers was measured with microelectrodes while the fibers were exposed to the weak acids, propionic acid (98 mM), or 5,5-dimethyloxazolidine-2,4-dione (DMO) (100 mM), at extracellular pH (pH0) 7.8. Both propionate and DMO caused an initial drop in pHi, followed by a partial recovery to the final steady pHi of 7.16. In the presence of 6 mM HCO3(-) (pH0 7.8), the final pHi was 7.31 for either weak acid. In other experiments, pHi was initially lowered by temporarily exposing the fiber to NH4Cl-containing solution. The rate of subsequent pHi recovery at pHi 6.84 was expressed as an H+ equivalent flux. In the absence of HCO3(-), the H+ equivalent flux was stimulated (two- to threefold) by both propionate and DMO. Part of this stimulation was due to the reduced Cl- concentration in the external solution when the anion of the weak acid is substituted for Cl-. Another part of the stimulation may have been due to the increased buffering in the intracellular unstirred layer. HCO3(-) greatly stimulated (ninefold) the H+ equivalent flux, but in the presence of HCO3(-), propionate and DMO had no additional effect. There is no evidence from the present work indicating that either propionate or DMO anions acted as substrates for operation of the anion exchange mechanism (Cl-/Cl- and HCO3(-)/Cl-). Since exposure of the cell to either of the weak acids lowered pHi and since the rate of anion exchange fluxes is known to increase when pHi is lowered, propionate most likely stimulated anion fluxes indirectly by lowering pHi.