Arterial and central venous pressures (AP and CVP), cardiac output (CO) and heart rate (HR) were recorded, and stroke volume (SV) computed, in awake ducks before, during and after submersion, special attention being paid to the time course and extent of the induced changes. During rest CO was 1509 ml/min (S.D. 245), HR 244/min (S.D. 83) and SV 6.6 ml (S.D. 1.6). Immediately upon submersion CO and HR fell slightly and then showed a more gradual, up to twenty fold reduction within 1–2 min; SV decreased moderately despite a 10–20 mm Hg increase in CVP. During the immediate 1–2 sec postdive period HR increased to 300–500/min, with a sharp rise in AP while CVP fell. Within 10–15 sec a profound vasodilatation was established, AP and CVP returning towards normal. CO now reached 2500–4000 ml/min and SV increased beyond resting level. Thus, at the shift from submersion to emersion CO could increase up to fiftyfold within 10–15 sec; CO then returned towards control in 6–8 min. Results with vagal and sympathetic blocking agents suggest the following neurogenic events: During submersion inhibited sympathetic activity to the heart is coupled with a greatly intensified vagal discharge. reducing also ventricular contractility; the sympathetic vasoconstrictor fibre discharge is sharply increased. On emersion a complete reversal of this intense and differentiated pattern takes place within 1–2 sec. The receptors and central mechansims involved are briefly discussed.