Constraints on cardiac pumping capacity and blood oxygen extraction limit the hypoxia tolerance of Atlantic salmon (Salmo salar) at warm temperatures.

Salmon acclimated to 10 °C were surgically implanted with Doppler® probes around the ventral aorta for the measurement of cardiac output (Q·), stroke volume (SV) and heart rate (fH), and placed into respirometers for the measurement of oxygen consumption (M·O2). Then, they were exposed to progressive hypoxia [5% reduction in air saturation (air sat.) every 15 min] at 10 °C, or after overnight warming to 14 or 18 °C. At 10 °C, bradycardia was initiated at 41.8% air sat., but no clear critical oxygen tension (Pcrit) was identified. In contrast, at 14 and 18 °C, bradycardia began at 57.3 and 74.3% air sat., and Pcrit values were 47.0 and 57.3% air sat., respectively. Loss of equilibrium (LOE) occurred at 21.0% air sat. at 10 °C, this value increasing to 26.6% air sat. at 14 °C and to 41.9% air sat. at 18 °C. The oxygen level at LOE was positively related to heart rate (i.e., fH at LOE was 32.1, 37.3 and 42.8 beats min-1 at 10, 14 and 18 °C, respectively), and thus, other factors determined the salmon's hypoxic limit. These were: 1) an inability to increase SV further as fH declined; and 2) a reduced capacity to elevate blood oxygen extraction (EO2; M·O2/Q·) due to higher baseline (normoxic) values at the higher temperatures. These findings align with recent research suggesting that high fH's may be detrimental to cardiac function during hypoxia, and that both the heart's pumping capacity and the ability to increase EO2 are key determinants of a fish's tolerance to the combined stressors of hypoxia and increased temperature.