"Salmon migrating from freshwater (FW) to saltwater (SW) must maintain a constant internal osmotic environment to survive their external salinity transition. Up to 40% of SW introduced coho become stunted and eventually die. With the exceptions of growth hormone (GH), hypocalcin, and possibly epinephrine, stunts maintain a hypoendocrine status. Nine hundred yearling coho salmon were raised in SW for five months; 100 salmon were reared in FW for the same duration. After five months in SW 12% of the population developed into stunts as defined morphologically by low body weight and the retention of parr marks. Early stunts hypoosmoregulated more effectively than their smelt counterparts (significantly higher gill chloride cell activity, higher mean intestinal water/ion transport, significantly lower blood osmotic pressures), but over a period of several days displayed fatal osmoregulatory failure (significantly decreased gill chloride cell activity, decreased mean intestinal water/ion transport, significantly increased blood osmotic pressures). Increased liver potassium in stunts correlated positively with blood osmotic pressure and may be a causal agent of osmoregulatory dysfunction. Elevated liver potassium was found to be a probable function of stress (possibly epinephrine mediated), but not of blood osmotic pressure. Muscle potassium concentrations appear to be a direct function of the protein to fat ratio in the muscle, with healthy smelts possessing low muscle K+ and stunts higher muscle K+. Stunt muscle K+ was not influenced by elevated blood osmotic pressure. Fish allowed to smelt in FW (after four months) appear to revert back to the physiological form of a parr. Coho which smoltified in SW, and were then reacclimated to FW for one month retained elevated intestinal water transport rates (J[subscript v]) characteristic of a SW fish, but otherwise resembled the FW reared smelts. After FW reacclimation and hormone level normalization, stunts and smelts were exposed to 67% SW for 12 hours. During this time stunts maintained lower blood osmotic pressures than the smelts; this can be attributed to a reduced stunt intestinal J[subscript v] which was lacking in the smelts. Salmon growth hormone (sGH) injected intramuscularly for three weeks increased gill chloride cell activity, reduced blood osmotic pressure, and raised mean intestinal J[subscript v] rates in stunts and smelts placed in 67% SW for 12 hours. These characteristics resemble early SW stunt physiology, and thus may help implicate naturally increased GH in SW stunts as an osmoregulatory crutch to an otherwise hypoendocrine condition. Finally, after studying the relationship of fish size to migratory behavior within several different species, it seems that stunt distributions could potentially divide certain species with moderate degrees of anadromy into separate migratory and non-migratory populations. Considering the high amount of energy required to sustain anadromous behavior, a more efficient non- migratory population could be selected for (given adequate food availability). Viewed in this way stunts might be considered a population in transition to full FW residency, rather than just fish with a hypoosmoregulatory dysfunction"--Document.