Influence Of Lung Volume On Circulatory Function And Arterial Blood Gases During Prolonged Breath Holding In Elite Apnea Divers

Abstract

Maximal apnea in elite breath hold divers involves the suppression of involuntary breathing movements (IBMs). During apnea at total lung capacity (TLC), stroke volume (SV) is reduced due to compression of the vena cava; however, IBMs are thought to improve apnea time by elevating cardiac output (Q[Combining Dot Above]) and cerebral oxygen delivery (CDO2) via increased venous return. Although not experimentally investigated, this suggests CDO2 is limited by the reduced Q[Combining Dot Above] secondary to lung inflation. The purpose of this study was to investigate whether a higher Q[Combining Dot Above] during apnea at functional residual capacity (FRC) facilitates CDO2 and determine whether IBM onset and apnea end are linked to PaO2, oxygen content (CaO2) or CDO2. Fifteen elite divers (1F; 185 ± 7 cm, 82 ± 12 kg, 29 ± 7 years) completed two maximal apneas at TLC and FRC. Cardiovascular responses were assessed continuously via photoplethysmography. Global extra-cerebral blood flow (gCBF) and intra-cranial velocities were measured via extracranial and transcranial ultrasound, respectively. Arterial blood gases were assessed at IBM onset and apnea end. Maximal apnea was 38% longer at TLC vs. FRC (304 ± 71 vs. 188 ± 44 sec, P<0.001) and IBM onset occurred later (150 ± 44 vs. 113 ± 36 sec, P <0.001). At FRC, SV and Q[Combining Dot Above] did not change from baseline (P>0.05). In contrast, during the TLC trial SV and Q[Combining Dot Above] were decreased until 80% and 40% of apnea duration, respectively, (P<0.05). Consistent with Q[Combining Dot Above], gCBF was significantly lower at 20% apnea during the TLC trial but recovered for the remainder of the apnea. Mean arterial pressure rose progressively in both trials but to a greater extent at TLC. At apnea end, although PaO2 was lower (30 ± 8 vs. 35 ± 11 mmHg, P=0.004) in the FRC trial, CaO2 was the same due to a higher PaCO2 in the TLC trial. IBM onset occurred at the same PaCO2 (43 ± 5 vs. 43 ± 5 mmHg, P=0.60) but a lower PaO2 (46 ± 14 vs. 71 ± 18 mmHg, p<<0.001) during the FRC trial. Lung volume has a profound effect on SV, Q[Combining Dot Above] and gCBF during the early stages of apnea. However, at apnea end, Q[Combining Dot Above], gCBF and CDO2 are the same irrespective of lung volume. A comparable CaO2 despite a lower PaO2 at FRC apnea end highlights the importance of acidosis on the oxygen dissociation curve. In addition, IBMs appear to be governed by PaCO2 rather than PaO2 suggesting any beneficial effect of IBMs on CDO2 to be indirect and secondary to hypercapnia.