Cardiac preload (central venous; pressure, Pcv), mean circulatory filling pressure (MCFP), dorsal aortic blood pressure (P-DA) and relative cardiac output (Q) were measured in sea bass (Dicentrarchus labrax) at rest and while swimming at 1 and 2 BL s(-1). MCFP, an index of venous capacitance and the upstream venous pressure driving the return of venous blood to the heart, was measured as the plateau in Pcv during ventral aortic occlusion. Compared with resting values, swimming at 1 and 2BL s(-1) increased Q (by 15 +/- 1.5 and 38 +/- 6.5%, respectively), Pcv (from 0.11 +/- 0.01 kPa to 0.12 +/- 0.01 and 0.16 +/- 0.02 kPa, respectively), MCFP (from 0.27 +/- 0.02 kPa to 0.31 +/- 0.02 and 0.40 +/- 0.04 kPa, respectively) and the calculated pressure gradient for venous return (Delta Pv, from 0.16 +/- 0.01 kPa to 0.18 +/- 0.02 and 0.24 +/- 0.02 kPa, respectively), but not PDA. In spite of an increased preload, the increase in 0 was exclusively mediated by an increased heart rate (fH, from 80 +/- 4 beats min(-1) to 88 +/- 4 and 103 +/- 3 beats min(-1), respectively), and stroke volume (V-s) remained unchanged. Prazosin treatment (1 mg kg(-1) M-b) abolished pressure and flow changes during swimming at 1 BL s(-1), but not 2 BL s(-1), indicating that other control systems besides an alpha-adrenoceptor control are involved. This study is the first to address the control of venous capacitance in swimming fish. It questions the generality that increased Q during swimming is regulated primarily through V-s and shows that an increased cardiac filling pressure does not necessarily lead to an increased V-s in fish, but may instead compensate for a reduced cardiac filling time.