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.

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