Impaired dynamic cerebral autoregulation in trained breath-hold divers

Abstract

Breath-hold divers (BHD) experience repeated bouts of severe hypoxia and hypercapnia with large increases in blood pressure. However, the impact of long-term breath-hold diving on cerebrovascular control remains poorly understood. The ability of cerebral blood vessels to respond rapidly to changes in blood pressure represents the property of dynamic autoregulation. The current investigation tested the hypothesis that breath-hold diving impairs dynamic autoregulation to a transient hypotensive stimulus. Seventeen BHD (3 women, 11 ± 9 yr of diving) and 15 healthy controls (2 women) completed two or three repeated sit-to-stand trials during spontaneous breathing and poikilocapnic conditions. Heart rate (HR), finger arterial blood pressure (BP), and cerebral blood flow velocity (BFV) from the right middle cerebral artery were measured continuously with three-lead electrocardiography, finger photoplethysmography, and transcranial Doppler ultrasonography, respectively. End-tidal carbon dioxide partial pressure was measured with a gas analyzer. Offline, an index of cerebrovascular resistance (CVRi) was calculated as the quotient of mean BP and BFV. The rate of the drop in CVRi relative to the change in BP provided the rate of regulation [RoR; (∆CVRi/∆T)/∆BP]. The BHD demonstrated slower RoR than controls ( P ≤ 0.001, d = 1.4). Underlying the reduced RoR in BHD was a longer time to reach nadir CVRi compared with controls ( P = 0.004, d = 1.1). In concert with the longer CVRi response, the time to reach peak BFV following standing was longer in BHD than controls ( P = 0.01, d = 0.9). The data suggest impaired dynamic autoregulatory mechanisms to hypotension in BHD. NEW & NOTEWORTHY Impairments in dynamic cerebral autoregulation to hypotension are associated with breath-hold diving. Although weakened autoregulation was observed acutely in this group during apneic stress, we are the first to report on chronic adaptations in cerebral autoregulation. Impaired vasomotor responses underlie the reduced rate of regulation, wherein breath-hold divers demonstrate a prolonged dilatory response to transient hypotension. The slower cerebral vasodilation produces a longer perturbation in cerebral blood flow velocity, increasing the risk of cerebral ischemia.

Physiology, pathophysiology and (mal)adaptations to chronic apnoeic training: a state-of-the-art review

“…Similarly, during static apnoeas, EBHDs are known to exhibit greater increases in cerebral blood flow, higher cerebrovascular reactivity (Joulia et al 2009 ; Vestergaard and Larsson 2019 ) and are able to withstand greater hypoxaemic and hypercapnic levels than NDs (Bain et al 2016 , 2018 ; Willie et al 2015 ). Additionally, there is also evidence to suggest that trained BHDs exhibit a blunted ventilatory chemosensitivity to hypercapnia at rest and post-exercise (Delapille et al 2001 ; Grassi et al 1994 ; Roecker et al 2014 ) that is distinct from scuba divers and controls (Roecker et al 2014 ), in addition to displaying a reduced cerebral autoregulation compared with ND controls (Moir et al 2019 ). Yet the nature of the latter adaptation remains to be determined whether it serves a protective purpose (i.e., preserving cerebral oxygen perfusion/delivery) or rather represents a more menacing phenomenon (i.e., exposing BHDs to a greater risk of cerebral hypoperfusion).…”

Rapid changes in vascular compliance contribute to cerebrovascular adjustments during transient reductions in blood pressure in young, healthy adults

“…To date, characterization of autoregulation has focused primarily on alterations in cerebrovascular resistance achieved by adjustments in vessel diameter through myogenic, metabolic, and/or neural mechanisms. Indeed, impairments in cerebral autoregulation accompany abnormal cerebrovascular resistance responses to deviations in BP (1,4,21). However, solely focusing on cerebrovascular resistance conceals the contribution of broader mechanical features of the cerebral circulation to dynamic cerebral blood flow regulation.…”

Cognitive impairment caused by hypoxia: from clinical evidences to molecular mechanisms

“…The dysregulated neurovascular coupling may be induced by injured neurovascular unit via the interplay between oxidative stress and inflammation (Moretti and Caruso 2020) in acute stage. In addition, dynamic cerebrovascular autoregulation is reported to be impaired both in acute and chronic stage (Moir et al 2019). However, neurons in the frontal cortex and hippocampus are abnormally activated in chronic stage, which requires increased effective blood flow (Iadecola et al 1997).…”