Gas exchange and cardiovascular responses during breath-holding in divers: Author names and affiliations.

• Blood pressure response to apnoea overlaps in air and in O 2. • In O 2 , apnoeas show a milder response in heart rate and peripheral resistances. • CO 2 rise may trigger the pressure increase in phase III. To check whether the evolution of alveolar pressures of O 2 (P A O 2) and CO 2 (P A CO 2) explains the cardiovascular responses to apnoea, eight divers performed resting apnoeas of increasing duration in air and in O 2. We measured heart rate (f H), arterial pressure (AP), and peripheral resistances (TPR) beat-by-beat, P A O 2 and P A CO 2 at the end of each apnoea. The three phases of the cardiovascular response to apnoea were observed. In O 2 , TPR increase (9 ± 4 mmHg min l−1) and f H 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, P A O 2 and P A CO 2 were 50 ± 9 and 48 ± 5 mmHg, respectively; corresponding values in O 2 were 653 ± 8 mmHg and 55 ± 5 mmHg. At end of phase II, P A O 2 and P A CO 2 in air were 90 ± 13 mmHg and 42 ± 4 mmHg respectively; corresponding values in O 2 were 669 ± 7 mmHg and 47 ± 6 mmHg. The P A CO 2 increase may trigger the AP rise in phase III. [ABSTRACT FROM AUTHOR]