Dynamic Cerebral Autoregulation Is Acutely Impaired During Maximal Apnoea In Trained Divers

Cross, Troy J.; Kavanagh, Justing J.; Brešković, Toni; Johnson, Bruce D.; Dujić, Željko

doi:10.1249/01.mss.0000494467.53181.62

Cited by 5 publications

(6 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Compared to other studies our measured MAP increase was higher (31 mmHg at Cross et al [12], 32 mmHg at Heusser et al [22], and 17 mmHg at Perini et al [36]). The mean apnea time lasted 247 ± 76 s, which is longer than those reported by the mentioned studies (199 ± 11 s [12] and 210 ± 70 s [36]) for trained divers and in the same range as the 234 ± 66 s published by Heusser et al [22] for elite divers. Thus, the divers in this study may be classified as well-trained in the field of static apnea and the detected apnea dependent compensatory mechanisms can be classified as relatively distinct.…”

Section: Blood Pressure Apnea Duration and Cocontrasting

confidence: 87%

Influence of Apnea-induced Hypoxia on Catecholamine Release and Cardiovascular Dynamics

et al. 2016

View full text Add to dashboard Cite

Prolonged breath-hold causes complex compensatory mechanisms such as increase in blood pressure, redistribution of blood flow, and bradycardia. We tested whether apnea induces an elevation of catecholamine-concentrations in well-trained apneic divers.11 apneic divers performed maximal dry apnea in a horizontal position. Parameters measured during apnea included blood pressure, ECG, and central, in addition to peripheral hemoglobin oxygenation. Peripheral arterial hemoglobin oxygenation was detected by pulse oximetry, whereas peripheral (abdominal) and central (cerebral) tissue oxygenation was measured by Near Infrared Spectroscopy (NIRS). Exhaled O and CO, plasma norepinephrine and epinephrine concentrations were measured before and after apnea.Averaged apnea time was 247±76 s. Systolic blood pressure increased from 135±13 to 185±25 mmHg. End-expiratory CO increased from 29±4 mmHg to 49±6 mmHg. Norepinephrine increased from 623±307 to 1 826±984 pg ml and epinephrine from 78±22 to 143±65 pg ml during apnea. Heart rate reduction was inversely correlated with increased norepinephrine (correlation coefficient -0.844, p=0.001). Central (cerebral) O desaturation was time-delayed compared to peripheral O desaturation as measured by NIRS and SpO.Increased norepinephrine caused by apnea may contribute to blood shift from peripheral tissues to the CNS and thus help to preserve cerebral tissue O saturation longer than that of peripheral tissue.

show abstract

Section: Blood Pressure Apnea Duration and Cocontrasting

confidence: 87%

Influence of Apnea-induced Hypoxia on Catecholamine Release and Cardiovascular Dynamics

et al. 2016

View full text Add to dashboard Cite

show abstract

“…Here, despite further increases in MAP with apnoea, the elevations in CBF are attenuated (probably via increases in ICP). In contrast, when reported using a transfer function analysis (Cross, Kavanagh, Breskovic, Johnson, & Dujic, ), cerebral autoregulation appears impaired. Nonetheless, a caveat to both studies is the negation of ICP in determining the CPP.…”

Section: Cerebrovascular Regulationmentioning

confidence: 89%

Physiology of static breath holding in elite apneists

Bain

Drviš

Dujić

et al. 2018

Experimental Physiology

Self Cite

View full text Add to dashboard Cite

Breath-hold-related activities have been performed for centuries, but only recently, within the last ∼30 years, has it emerged as an increasingly popular competitive sport. In apnoea sport, competition relates to underwater distances or simply maximal breath-hold duration, with the current (oxygen-unsupplemented) static breath-hold record at 11 min 35 s. Remarkably, many ultra-elite apneists are able to suppress respiratory urges to the point where consciousness fundamentally limits a breath-hold duration. Here, arterial oxygen saturations as low as ∼50% have been reported. In such cases, oxygen conservation to maintain cerebral functioning is critical, where responses ascribed to the mammalian dive reflex, e.g. sympathetically mediated peripheral vasoconstriction and vagally mediated bradycardia, are central. In defence of maintaining global cerebral oxygen delivery during prolonged breath holds, the cerebral blood flow may increase by ∼100% from resting values. Interestingly, near the termination of prolonged dry static breath holds, recent studies also indicate that reductions in the cerebral oxidative metabolism can occur, probably attributable to the extreme hypercapnia and irrespective of the hypoxaemia. In this review, we highlight and discuss the recent data on the cardiovascular, metabolic and, particularly, cerebrovascular function in competitive apneists performing maximal static breath holds. The physiological adaptation and maladaptation with regular breath-hold training are also summarized, and future research areas in this unique physiological field are highlighted; particularly, the need to determine the potential long-term health impacts of extreme breath holding.

show abstract

“…Indeed, it has been recently shown that the diameter of the MCA is not static. 5,7,11,39 Cross et al 40 interpreted increased phase synchronization during apnea to indicate impaired cerebral autoregulation, but various metrics that ostensibly quantify the efficacy of cerebral autoregulation have been shown to yield disparate results. 32 However, that CBF did not increase further than during clamp despite a much greater increase in MAP is evidence of cerebral autoregulatory efficacy without the confounding influence of more quantitatively complex metrics of autoregulation and the potentially invalid assumptions of transcranial Doppler ultrasound.…”

Section: Cerebral Autoregulation During Apneamentioning

confidence: 99%

Regulation of Brain Blood Flow and Oxygen Delivery in Elite Breath-Hold Divers

Willie

Ainslie

Drviš

et al. 2014

J Cereb Blood Flow Metab

Self Cite

View full text Add to dashboard Cite

The roles of involuntary breathing movements (IBMs) and cerebral oxygen delivery in the tolerance to extreme hypoxemia displayed by elite breath-hold divers are unknown. Cerebral blood flow (CBF), arterial blood gases (ABGs), and cardiorespiratory metrics were measured during maximum dry apneas in elite breath-hold divers (n = 17). To isolate the effects of apnea and IBM from the concurrent changes on ABG, end-tidal forcing ('clamp') was then used to replicate an identical temporal pattern of decreasing arterial PO 2 (PaO 2 ) and increasing arterial PCO 2 (PaCO 2 ) while breathing. End-apnea PaO 2 ranged from 23 to 37 mm Hg (30 ± 7 mm Hg). Elevation in mean arterial pressure was greater during apnea than during clamp reaching +54 ± 24% versus 34 ± 26%, respectively; however, CBF increased similarly between apnea and clamp (93.6 ± 28% and 83.4 ± 38%, respectively). This latter observation indicates that during the overall apnea period IBM per se do not augment CBF and that the brain remains sufficiently protected against hypertension. Termination of apnea was not determined by reduced cerebral oxygen delivery; despite 40% to 50% reductions in arterial oxygen content, oxygen delivery was maintained by commensurately increased CBF.

show abstract

Dynamic Cerebral Autoregulation Is Acutely Impaired During Maximal Apnoea In Trained Divers

Cited by 5 publications

References 43 publications

Influence of Apnea-induced Hypoxia on Catecholamine Release and Cardiovascular Dynamics

Influence of Apnea-induced Hypoxia on Catecholamine Release and Cardiovascular Dynamics

Physiology of static breath holding in elite apneists

Regulation of Brain Blood Flow and Oxygen Delivery in Elite Breath-Hold Divers

Contact Info

Product

Resources

About