Nazzareno Fagoni1, Andrea Sivieri2, Guglielmo Antonutto3, Christian Moia4, Anna Taboni2, Aurélién Bringard4, Guido Ferretti5. 1. Dipartimento di Scienze Cliniche e Sperimentali, Università di Brescia, Italy; Dipartimento di Specialità Medico-Chirurgiche, Scienze Radiologiche e Sanità Pubblica, Università di Brescia, Italy. Electronic address: nazzarenofagoni@gmail.com. 2. Dipartimento di Scienze Cliniche e Sperimentali, Università di Brescia, Italy. 3. Dipartimento di Scienze Mediche e Biologiche, Università di Udine, Italy. 4. Département des Neurosciences Fondamentales, Université de Genève, Switzerland. 5. Dipartimento di Scienze Cliniche e Sperimentali, Università di Brescia, Italy; Département des Neurosciences Fondamentales, Université de Genève, Switzerland.
Abstract
PURPOSE: We hypothesized that the third dynamic phase (ϕ3) of the cardiovascular response to apnoea requires attainment of the physiological breaking point, so that the duration of the second steady phase (ϕ2) of the classical cardiovascular response to apnoea, though appearing in both air and oxygen, is longer in oxygen. METHODS: Nineteen divers performed maximal apnoeas in air and oxygen. We measured beat-by-beat arterial pressure, heart rate (fH), stroke volume (SV), cardiac output (Q˙). RESULTS: The fH, SV and Q˙ changes during apnoea followed the same patterns in oxygen as in air. Duration of steady ϕ2 was 105 ± 37 and 185 ± 36 s, in air and oxygen (p<0.05), respectively. At end of apnoea, arterial oxygen saturation was 1.00 ± 0.00 in oxygen and 0.75 ± 0.10 in air. CONCLUSIONS: The results support the tested hypothesis. Lack of hypoxaemia during oxygen apnoeas suggests that, if chemoreflexes determine ϕ3, the increase in CO2 stores might play a central role in eliciting their activation.
PURPOSE: We hypothesized that the third dynamic phase (ϕ3) of the cardiovascular response to apnoea requires attainment of the physiological breaking point, so that the duration of the second steady phase (ϕ2) of the classical cardiovascular response to apnoea, though appearing in both air and oxygen, is longer in oxygen. METHODS: Nineteen divers performed maximal apnoeas in air and oxygen. We measured beat-by-beat arterial pressure, heart rate (fH), stroke volume (SV), cardiac output (Q˙). RESULTS: The fH, SV and Q˙ changes during apnoea followed the same patterns in oxygen as in air. Duration of steady ϕ2 was 105 ± 37 and 185 ± 36 s, in air and oxygen (p<0.05), respectively. At end of apnoea, arterial oxygen saturation was 1.00 ± 0.00 in oxygen and 0.75 ± 0.10 in air. CONCLUSIONS: The results support the tested hypothesis. Lack of hypoxaemia during oxygenapnoeas suggests that, if chemoreflexes determine ϕ3, the increase in CO2 stores might play a central role in eliciting their activation.
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