The objective of this study was to examine the influence of hypoxia exposure time, metabolic rate, and water flow rate on the O2 concentration in the boundary layer outside and inside the chorion of rainbow trout ( Oncorhynchus mykiss ) embryos. Oxygen consumption, growth, and dissolved O2 in the boundary layer were measured at 15, 22, and 29 days post fertilization (dpf) from embryos reared in normoxia (O2 concentration at 100% saturation) and chronic hypoxia (>24 h, 50% saturation) and exposed to acute hypoxia (30 min, 50% saturation). Chronic and acute hypoxia exposure decreased the dissolved O2 in the boundary layer to the same extent at 15 and 22 dpf; however, at 29 dpf, O2 levels were significantly lower in acute relative to chronic hypoxia. At 29 dpf, O2 uptake per individual was significantly lower in embryos exposed to chronic relative to acute hypoxia. In addition, mass-specific O2 uptake in chronic hypoxia-exposed embryos was ~40% less than that of controls but the same as that of acutely exposed embryos. This correlates with reduced growth in embryos exposed to chronic hypoxia. We conclude that boundary layer O2 is lower after 30 min of hypoxia compared with 2 weeks of hypoxia simply because embryos exposed to chronic hypoxia grow slower and consume less O2.

SUMMARYSalmonid embryos develop in cool waters over relatively long periods of time. Interestingly, hypoxic conditions have been found to be relatively common in some nesting sites (redds). The goals of this study were to determine the ontogeny of cardiac regulation in rainbow trout early life stages and how this is influenced by chronic hypoxia. The heart rate response to cholinergic and adrenergic receptor stimulation or inhibition was measured in individuals reared in normoxic (100% O 2 saturation) or hypoxic (30% O 2 saturation) conditions from fertilization to embryonic stages 22, 26 and 29, and larval stages 30 and 32. In normoxia, heart rate increased in response to -adrenergic receptor stimulation (isoproterenol) as early as embryonic stage 22, and decreased with the antagonist propranolol after this stage. Cholinergic stimulation (acetylcholine) was ineffective at all stages, but atropine (acetylcholine antagonist) increased heart rate at larval stage 32. This demonstrates that cardiac -adrenergic receptors are functional at early life stages, while cholinergic receptors are not responsive until after hatching. Collectively, embryos had cardioacceleration control mechanisms in place just after the heartbeat stage, while cardio-inhibitory control was not functional until after hatching. Chronic hypoxia exposure triggered bradycardia, increased the response to adrenergic stimulation in embryos and larvae, and delayed the onset of cholinergic control in larvae. In non-motile stages, therefore, survival in chronic low oxygen may depend on the ability to alter the cardiac ontogenic program to meet the physiological requirements of the developing fish.