title: The Effects of Involuntary Respiratory Contractions on Cerebral Blood Flow during Maximal Apnoea in Trained Divers.
abstract: The effects of involuntary respiratory contractions on the cerebral blood flow response to maximal apnoea is presently unclear. We hypothesised that while respiratory contractions may augment left ventricular stroke volume, cardiac output and ultimately cerebral blood flow during the struggle phase, these contractions would simultaneously cause marked 'respiratory' variability in blood flow to the brain. Respiratory, cardiovascular and cerebrovascular parameters were measured in ten trained, male apnoea divers during maximal 'dry' breath holding. Intrathoracic pressure was estimated via oesophageal pressure. Left ventricular stroke volume, cardiac output and mean arterial pressure were monitored using finger photoplethysmography, and cerebral blood flow velocity was obtained using transcranial ultrasound. The increasingly negative inspiratory intrathoracic pressure swings of the struggle phase significantly influenced the rise in left ventricular stroke volume (R (2) = 0.63, P<0.05), thereby contributing to the increase in cerebral blood flow velocity throughout this phase of apnoea. However, these contractions also caused marked respiratory variability in left ventricular stroke volume, cardiac output, mean arterial pressure and cerebral blood flow velocity during the struggle phase (R (2) = 0.99, P<0.05). Interestingly, the magnitude of respiratory variability in cerebral blood flow velocity was inversely correlated with struggle phase duration (R (2) = 0.71, P<0.05). This study confirms the hypothesis that, on the one hand, involuntary respiratory contractions facilitate cerebral haemodynamics during the struggle phase while, on the other, these contractions produce marked respiratory variability in blood flow to the brain. In addition, our findings indicate that such variability in cerebral blood flow negatively impacts on struggle phase duration, and thus impairs breath holding performance.
authors.affiliation: Griffith Health Institute and Heart Foundation Research Centre, Griffith University, Gold Coast Campus, Queensland, Australia ; Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota, United States of America.
authors.forename: Troy J
authors.initials: TJ
authors.lastname: Cross
authors.forename: Justin J
authors.initials: JJ
authors.lastname: Kavanagh
authors.forename: Toni
authors.initials: T
authors.lastname: Breskovic
authors.forename: Petra
authors.initials: P
authors.lastname: Zubin Maslov
authors.forename: Mihajlo
authors.initials: M
authors.lastname: Lojpur
authors.forename: Bruce D
authors.initials: BD
authors.lastname: Johnson
authors.forename: Zeljko
authors.initials: Z
authors.lastname: Dujic
mesh_terms: D000328:Adult; D001049:Apnea / Q000378:metabolism / Q000503:physiopathology*; D062186:Arterial Pressure; D062485:Breath Holding; D002560:Cerebrovascular Circulation; D004242:Diving / Q000502:physiology*; D005260:Female; D006439:Hemodynamics; D006801:Humans; D008297:Male; D010100:Oxygen / Q000378:metabolism; D013318:Stroke Volume
chemical_list: D010100:Oxygen