Responses of Swimming Skipjack (Katsuwonus pelamis) and Yellowfin (Thunnus albacares) Tunas to Acute Hypoxia, and a Model of Their Cardiorespiratory Function

Abstract

Heart rate and swimming-speed responses to acute hypoxia were measured in skipjack (Katsuwonus pelamis) and yellowfin tunas (Thunnus albacares). Swimming speeds began to increase in both species when O2 tension (Po2) reached approximately 124 mmHg. Bradycardia became significant in both species when Po2 reached approximately 130 mmHg. Heart rate fell with Po2 in yellowfin tuna, but, in skipjack tuna, it increased at the lowest O2 levels reached (89–70 mmHg). Bradycardia occurred in both species despite concomitant increases in swimming speed. A continuous infusion dye dilution system was used to monitor changes in ventilation volume (V̇g) during hypoxia in yellowfin tuna. As Po2 fell, V̇g increased. At the lowest O2 levels (109–90 mmHg), V̇g was 45% higher than during normoxia. Ventilation volume increased despite no concomitant increases in swimming speed. Data from these experiments were used to develop a model capable of predicting O2 demand and delivery, maximum sustainable (i.e., aerobic) swimming speeds, and minimum survivable O2 levels for yellowfin and skipjack tunas. Results from the model indicate that the cardiorespiratory system of tunas is capable of maximum rates of O2 delivery, even at low swimming speeds, that are approximately three times those of other active teleosts. We believe that, because the pelagic environment provides no place to hide and rest following exhaustive activity, the ability of the cardiorespiratory system of tunas to deliver O2 to the tissues at high rates evolved for the rapid repayment of O2 debts rather than to permit exceptionally high sustained swimming speeds.