To check whether the evolution of alveolar pressures of O2 (PAO2) and CO2 (PACO2) explains the cardiovascular responses to apnoea, eight divers performed resting apnoeas of increasing duration in air and in O2. We measured heart rate (fH), arterial pressure (AP), and peripheral resistances (TPR) beat-by-beat, PAO2 and PACO2 at the end of each apnoea. The three phases of the cardiovascular response to apnoea were observed. In O2, TPR increase (9 ± 4 mmHg min l−1) and fH decrease (-11 ± 8 bpm) were lower than in air (15 ± 5 mmHg min l−1 and -28 ± 13 bpm, respectively). At end of maximal apnoeas in air, PAO2 and PACO2 were 50 ± 9 and 48 ± 5 mmHg, respectively; corresponding values in O2 were 653 ± 8 mmHg and 55 ± 5 mmHg. At end of phase II, PAO2 and PACO2 in air were 90 ± 13 mmHg and 42 ± 4 mmHg respectively; corresponding values in O2 were 669 ± 7 mmHg and 47 ± 6 mmHg. The PACO2 increase may trigger the AP rise in phase III.