Changes in vascular pressures, blood respiratory properties and blood gas transport induced by swimming were investigated in the leopard shark Triakis semifasciata (Girard). In resting sharks, the mean ventral and dorsal aortic pressures (systolic/diastolic) were 6.8/5.6 kPa and 4.5/3.9 kPa, respectively, and only the former were increased significantly during swimming. Swimming also caused a significant decline in venous Po2 (1.6 to 0.9kPa), O2 content (0.9 to 0.4mmoill−1) and percentage O2 saturation {SO2, 39 to 18%) but the arterial variables were not affected. A significant decline in venous pH and an increase in venous Po2 also occurred during swimming but lactate concentration did not increase during or after swimming. An in vivo dissociation curve compiled from blood Po2 and So2 data for sharks in the resting, swimming and post-swimming recovery phases shows a mean P50 of 2.04 kPa, as determined by Hill transformation. The pH-bicarbonate plot for this fish shows a weak blood buffer capacity of 9.3mmoll−11pHunit−1 and during swimming the average blood pH and bicarbonateconcentration follow the buffer line which was not compensated in recovery. Neither oxygenated nor deoxygenated blood pH values were affected by CO2 equilibration, suggesting the absence of a Haldane effect. Thus, at the expense of respiratory acidosis, Triakis can aerobically sustain long (up to 60min) and moderately intense (0.45 Ls−1, where L is body length) periods of swimming by increasing cardiac output and tapping its venous reserve. Introduction Most vertebrate circulatory

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