Oxygen transport and cardiovascular responses to exercise in the yellowfin tuna Thunnus albacares.

Yellowfin tuna Thunnus albacares (1400-2175 g) instrumented with electrocardiogram electrodes and pre- and post-branchial catheters were subjected to incremental swimming velocity tests. Increasing velocity, from a minimal speed of 1.0 FLs-1, where FL is fork length, resulted in a 1.4-fold increase in heart rate (from 61.4 to 84.6 beats min-1), an elevated ventral-aortic blood pressure (from 10.8 to 12.2 kPa) and a decreased systemic vascular resistance. Relative branchial vascular resistance at minimal speed ranged from 24.4 to 40.0% of total vascular resistance and tended to increase with velocity. Yellowfin blood has a high oxygen-carrying capacity (16-18 ml O2 dl-1), and a low in vivo oxygen affinity (P50 = 5.3 kPa). Exercise caused a rise in arterial saturation (from 74 to 88%) and a decline in venous saturation (from 48 to 44%), resulting in a 1.3-fold increase in tissue oxygen extraction from the blood (arterial-venous oxygen content difference). Whereas arterial oxygen partial pressure (PO2) tended to increase with exercise, venous PO2 remained unchanged (approximately 5.3 kPa). The observed decrease in venous oxygen content was brought about by a lowered blood pH (from 7.80 to 7.76) and a large Bohr shift. Cardiac output and the increased blood oxygen extraction are estimated to have contributed nearly equally to the increased oxygen consumption during exercise. The large venous oxygen reserve still available to yellowfin tuna at maximal prolonged velocities suggests that the maximal oxygen delivery potential of the cardiovascular system in this species is not fully utilized during aerobic swimming. This reserve may serve other aerobic metabolic processes in addition to continuous swimming.

Heart rate and stroke volume contribution to cardiac output in swimming yellowfin tuna: response to exercise and temperature.

Cardiac performance in the yellowfin tuna (Thunnus albacares, 673-2470 g, 33-53 cm fork length, FL) was examined in unanesthetized fish swimming in a large water tunnel. Yellowfin tuna were fitted with either electrocardiogram electrodes or a transcutaneous Doppler blood-flow probe over the ventral aorta and exposed to changes in swimming velocity (range 0.8-2.9 FLs-1) or to an acute change in temperature (18-28 degrees C). Heart rates (fH) at +/-1 degree C (30-130 beats min-1) were lower on average than previous measurements with non-swimming (restrained) tunas and comparable with those for other active teleosts at similar relative swimming velocities. Although highly variable among individuals, fH increased with velocity (U, in FLs-1) in all fish (fH = 17.93U + 49.93, r2 = 0.14, P < 0.0001). Heart rate was rapidly and strongly affected by temperature (Q10 = 2.37). Blood flow measurements revealed a mean increase in relative cardiac output of 13.6 +/- 3.0% with exercise (mean velocities 1.23-2.10 FLs-1) caused by an 18.8 +/- 5.4% increase in fH and a 3.9 +/- 2.3% decrease in stroke volume. These results indicate that, unlike most other fishes, cardiac output in yellowfin tuna is regulated primarily through increases in fH. Acute reductions in ambient temperature at slow swimming velocities resulted in decreases in cardiac output (Q10 = 1.52) and fH (Q10 = 2.16), but increases in stroke volume (Q10 = 0.78). This observation suggests that the lack of an increase in stroke volume during exercise is not due to the tuna heart operating at maximal anatomical limits.