Effect of Maximal Apnoea Easy-Going and Struggle Phases on Subarachnoid Width and Pial Artery Pulsation in Elite Breath-Hold Divers

Abstract

PurposeThe aim of the study was to assess changes in subarachnoid space width (sas-TQ), the marker of intracranial pressure (ICP), pial artery pulsation (cc-TQ) and cardiac contribution to blood pressure (BP), cerebral blood flow velocity (CBFV) and cc-TQ oscillations throughout the maximal breath hold in elite apnoea divers. Non-invasive assessment of sas-TQ and cc-TQ became possible due to recently developed method based on infrared radiation, called near-infrared transillumination/backscattering sounding (NIR-T/BSS).MethodsThe experimental group consisted of seven breath-hold divers (six men). During testing, each participant performed a single maximal end-inspiratory breath hold. Apnoea consisted of the easy-going and struggle phases (characterised by involuntary breathing movements (IBMs)). Heart rate (HR) was determined using a standard ECG. BP was assessed using the photoplethysmography method. SaO2 was monitored continuously with pulse oximetry. A pneumatic chest belt was used to register thoracic and abdominal movements. Cerebral blood flow velocity (CBFV) was estimated by a 2-MHz transcranial Doppler ultrasonic probe. sas-TQ and cc-TQ were measured using NIR-T/BSS. Wavelet transform analysis was performed to assess cardiac contribution to BP, CBFV and cc-TQ oscillations.ResultsMean BP and CBFV increased compared to baseline at the end of the easy phase and were further augmented by IBMs. cc-TQ increased compared to baseline at the end of the easy phase and remained stable during the IBMs. HR did not change significantly throughout the apnoea, although a trend toward a decrease during the easy phase and recovery during the IBMs was visible. Amplitudes of BP, CBFV and cc-TQ were augmented. sas-TQ and SaO2 decreased at the easy phase of apnoea and further decreased during the IBMs.ConclusionsApnoea increases intracranial pressure and pial artery pulsation. Pial artery pulsation seems to be stabilised by the IBMs. Cardiac contribution to BP, CBFV and cc-TQ oscillations does not change throughout the apnoea.

Increased inspiratory resistance affects the dynamic relationship between blood pressure changes and subarachnoid space width oscillations

“…It is also unlikely that an initial WCO decline can be attributed to diminished SaO 2 . The SaO 2 decrease was moderate and similar to those observed in maximal breath-hold, where large WCO swings were absent [12,13]. We did not measure intrathoracic pressure and sympathetic activity, but these measurements have been well-described in animals and humans and our data are consistent with previous findings.…”

“…Performing the Mueller manoeuvres in 60 s series followed by a titration procedure, better mimicked increased inspiratory resistance and high sympathetic drive characteristic of OSA, and thus may be compared to our other protocols [12,13,14]. We observed typical BP changes [30,31].…”

Competitive apnea and its effect on the human brain: focus on the redox regulation of blood‐brain barrier permeability and neuronal‐parenchymal integrity

“…Alternatively, and perhaps more likely, is that a transient increase in cerebral S100β release from the brain was missed using the single arterial‐venous measure within a minute after the apnea. That is, the small systemic increase in S100β may have resulted from minor BBB leakage, subsequent to the transient increase in intracranial pressure (evidenced by increased IJVP; Table 1) experienced exclusively during the apnea (53, 54). Importantly, intracranial pressure was normalized almost immediately after the apnea breaking point because it occurs primarily from high lung volumes in combination with involuntary breathing movements (53).…”

Physiology of static breath holding in elite apneists

“…It is speculated that intrathoracic vessel (e.g. superior vena cava) compression from high lung volumes, in combination with transient surges in intrathoracic pressure from IBMs (Cross et al., ; Winklewski et al., ) collectively increase the ICP by reducing the passive pressure gradient for cerebral venous drainage (Stembridge et al., ). Mathematelically, an increase in ICP will result in reduced cerebral perfusion pressure (CPP; i.e.…”

“…The vasoconstrictor impact of cerebral sympathoexcitation during apnoea remains speculative, but might prevent cerebral haemorrhaging associated with the large increases in cerebral blood volume(Brassard, Tymko, & Ainslie, 2017) and arterial pressure. Indeed, measures of subarachnoid width(Winklewski et al, 2015) and internal jugular venous pressure (IJVP;Figure 7;Bloomfield, Ridings, Blocher, Marmarou, & Sugerman, 1997;Stembridge et al, 2017) during static breath holding in elite apneists suggest notable increases in ICP [IJVP is strongly correlated with direct measures of ICP in humans(Myerson & Loman, 1932)]. It is speculated that intrathoracic vessel (e.g.…”