“…These studies described the cardiovascular response to apnoea as consisting of three distinct phases: (i) a short dynamic phase ( 1), that lasts less than 30 s, characterised by rapid changes in blood Abbreviation: DBP, diastolic blood pressure; fH, heart rate; FIO2, inspired oxygen fraction; MBP, mean blood pressure;Q , cardiac output; SaO2, arterial oxygen saturation; SBP, systolic blood pressure; SV, stroke volume; TPR, total peripheral resistance;V O2, oxygen uptake; 1, first, dynamic phase of the cardiovascular response to apnoea; 2, second, steady-state phase of the cardiovascular response to apnoea; 3, third, dynamic phase of the cardiovascular response to apnoea.pressure and f H ; (ii) a steady state phase ( 2), of about 2 min, in which the values attained by each variable at the end of 1 are maintained invariant; and (iii) a further subsequent dynamic phase ( 3), lasting about 1.5 min, characterised by a continuous decrease in f H and increase in blood pressure, until the volitional breaking point was reached. According to Perini et al (2008Perini et al ( , 2010, the end of 2 might occur at the attainment of the physiological breaking point of apnoea (Hong et al, 1971), which is characterised by a specific alveolar PO 2 and PCO 2 composition possibly capable of inducing the first diaphragmatic contraction (Agostoni, 1963;Cross et al, 2013;Lin et al, 1974;Whitelaw et al, 1981): the higher is the alveolar PO 2 , the higher must be the concomitant PCO 2 eliciting diaphragmatic contractions, and vice versa. Ceteris paribus, the time necessary to reach that alveolar gas composition is directly proportional to the body oxygen stores at the beginning of the apnoea and inversely proportional to the body metabolic rate during apnoea.…”