Recent investigations have demonstrated that rainbow trout cope with acute high pH (pH > 9.0) exposure (lasting 3–8 days) through their ability to counteract high‐pH‐induced disturbances to ammonia excretion (JAmm), acid‐base homeostasis, and electrolyte balance. In the present investigation our goal was to establish how these physiological processes were modulated during chronic (28‐day) high pH (pH = 9.5) exposure. Chronic high pH led to minimal mortality, and there were no long‐term changes in stress indicators levels, such as cortisol or glucose. JAmm was initially reduced by 40% at high pH but rapidly recovered and fluctuated around control rates, thereafter. Decreased JAmm was associated with an initial 2.5‐fold increase in plasma ammonin concentrations (TAmm), followed by a return toward pre‐exposure levels after 3 days. Overall, plasma TAmm was slightly higher (40–80%) in the treatment fish, and this likely led to plasma PNH3s that were sufficient to sustain JAmm at high pH. White muscle TAmm stores were also chronically elevated, by 50–100%. There was a transient, twofold elevation of JUrea immediately following high‐pH exposure, but by 3 days JUrea had returned to control rates and stabilized thereafter. Plasma ion balance was well maintained at high pH, despite a chronic depression of Na+ influx. Even though there was a persistent respiratory alkalosis at alkaline pH, blood pH was effectively regulated by a simultaneous metabolic acid load, which was not associated with increased lactic acid production. White muscle intracellular pH (pHi) was unaltered during high pH exposure. We conclude that the long‐term survival of rainbow trout in alkaline environments is facilitated by higher steady‐state internal ammonia concentrations, the development of a sustained, compensatory metabolic acidosis which offsets decreased plasma PCO2, and the effective regulation of plasma electrolyte balance. © 1996 Wiley‐Liss, Inc.