Cardiovascular responses to dry resting apnoeas in elite divers while breathing pure oxygen

Highlights

• We investigated the effects of oxygen breathing on the cardiovascular responses to apnoea.

• In oxygen as in air, the three phases of the cardiovascular responses to apnoea were observed.

• The values of investigated variables were the same in the two conditions, but the duration of steady phase II and unsteady phase III was longer in oxygen than in air, as hypothesized.

• These results support the concept that the end of phase II may correspond to the physiological breaking point of apnoea.

• The lack of hypoxaemia in oxygen apnoeas suggests that, if indeed chemoreflexes determine phase III, increasing CO₂ stores might play a key role in eliciting chemoreflex activation.

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 (f_H), stroke volume (SV), cardiac output (${\displaystyle \dot{Q}}$).

Results

The f_H, SV and ${\displaystyle \dot{Q}}$ 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.

Introduction

In recent years, changes in blood pressure, heart rate (f_H), stroke volume (SV), cardiac output (${\displaystyle \dot{Q}}$) and total peripheral resistance (TPR) in response to apnoea (cardiovascular response to apnoea) were determined beat-by-beat on elite divers during apnoeas prolonged to the volitional breaking point (Costalat et al., 2013, Lemaître et al., 2008, Perini et al., 2008, Perini et al., 2010, Sivieri et al., 2015). These studies described the cardiovascular response to apnoea as consisting of three distinct phases: (i) a short dynamic phase (ϕ1), that lasts less than 30 s, characterised by rapid changes in blood pressure and f_H; (ii) a steady state phase (ϕ2), of about 2 min, in which the values attained by each variable at the end of ϕ1 are maintained invariant; and (iii) a further subsequent dynamic phase (ϕ3), 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., 2008, Perini et al., 2010, the end of ϕ2 might occur at the attainment of the physiological breaking point of apnoea (Hong et al., 1971), which is characterised by a specific alveolar PO₂ and PCO₂ 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 PO₂, the higher must be the concomitant PCO₂ 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. In fact, a beat-by-beat analysis of the cardiovascular responses to apnoeas carried out during light exercise demonstrated not only a reduction, but even a disappearance of ϕ2, with remarkable shortening of ϕ3 (Sivieri et al., 2015).

On the opposite side, an increase in oxygen stores would postpone the attainment of the condition determining the onset of ϕ3. The largest increase in oxygen stores before breath-holding is attained by having subjects breathe pure oxygen (inspired oxygen fraction, FIO₂, of 1) before the performance of maximal breath-holds. The investigations of breath-holding in hyperoxia are scanty and rarely using pure oxygen (Bjurström and Schoene, 1987, Breskovic et al., 2012, Klocke and Rahn, 1959, Lin, 1987, Otis et al., 1948). None of them studied the cardiovascular responses to apnoea on a beat-by-beat basis.

The general hypothesis of this study is that the onset of ϕ3 is related to the onset of diaphragmatic contractions, requiring the attainment of a specific alveolar gas composition and representing the so-called physiological breaking point of apnoea, as proposed by Perini et al., 2008, Perini et al., 2010. In the context of this hypothesis, we postulated that the three phases of the cardiovascular response to apnoea would be present both at FIO₂ = 1 and at FIO₂ = 0.21, but the duration of ϕ2 and ϕ3 would be longer in the former than in the latter condition. To this aim, we investigated the effects of breathing pure oxygen before the performance of maximal breath-holds on the cardiovascular response to apnoea.