BUOYANCY REGULATION DURING HYPOXIC STRESS IN STICKLEBACKS (CULAEA-INCONSTANS, PUNGITIUS-PUNGITIUS) AND THE MINNOW (PIMEPHALES-PROMELAS)

This study shows that differences exist among three species on exposure to hypoxia in their pattern of change in swim-bladder lift, in mechanisms used to regulate such lift, and ultimately in their buoyancy-related adaptations to hypoxia. Fathead minnows (Pimephales promelas), which are physostomes, maintained swim-bladder lift during a rapid decline in dissolved O2 (100%-5% O2 saturation in 90 min). Air gulping was used to offset gas loss from diffusion with surface access present, but, when this access was denied, fish used gas secretion. Physoclist brook sticklebacks (Culaea inconstans) increased swim-bladder lift during both gradual (100%-5% O2 saturation in 6 h) and abrupt (direct transfer from 100% to 5% O2 saturation) exposure to hypoxia by reducing internal pressure of swim-bladder gas allowing the bladder to expand compensating for initial gas loss and also by secreting gas into the bladder. On asphyxiation there was loss of swim-bladder gas (O2) resulting in a decline of swimbladder lift. Ninespine sticklebacks (Pungitius pungitius), also physoclist, lost 5%-7% of swim-bladder lift during both gradual and abrupt exposure to hypoxia at 10% O2 saturation and required several hours to regain lift. The brook stickleback has more superior buoyancy-related adaptations to hypoxia than does the ninespine stickleback. It can regulate lift more precisely with its ability to alter internal pressure, faster rate of increase of lift, and greater resistance to gas loss in hypoxia. Control of swim-bladder lift in hypoxia is critical to the efficient performance of aquatic surface respiration.