Regional brain blood flow in man during acute changes in arterial blood gases

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.

Section: Measurementsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Willie

Ainslie

Drviš

et al. 2014

“…Although the internal carotid/MCA provides 475% of total CBF, arteries responsible for perfusing the brainstem (i.e., vertebral/posterior cerebral arteries (PCA)) have been shown to be more responsive to various cognitive stimuli. [20][21][22] Considering the different responsiveness of the posterior cerebral vasculature, a global evaluation of NVC incorporating an assessment of both the MCA and PCA is likely to increase sensitivity for detecting changes in cerebrovascular reserve.…”

Section: Introductionmentioning

confidence: 99%

Regional Neurovascular Coupling and Cognitive Performance in Those with Low Blood Pressure Secondary to High-Level Spinal Cord Injury: Improved by Alpha-1 Agonist Midodrine Hydrochloride

Phillips

Warburton

Ainslie

et al. 2014

Individuals with high-level spinal cord injury (SCI) experience low blood pressure (BP) and cognitive impairments. Such dysfunction may be mediated in part by impaired neurovascular coupling (NVC) (i.e., cerebral blood flow responses to neurologic demand). Ten individuals with SCI 4T6 spinal segment, and 10 age-and sex-matched controls were assessed for beat-by-beat BP, as well as middle and posterior cerebral artery blood flow velocity (MCAv, PCAv) in response to a NVC test. Tests were repeated in SCI after 10 mg midodrine (alpha 1 -agonist). Verbal fluency was measured before and after midodrine in SCI, and in the control group as an index of cognitive function. At rest, mean BP was lower in SCI (70 ± 10 versus 92 ± 14 mm Hg; Po0.05); however, PCAv conductance was higher (0.56 ± 0.13 versus 0.39 ± 0.15 cm/second/mm Hg; Po0.05). Controls exhibited a 20% increase in PCAv during cognition; however, the response in SCI was completely absent (Po0.01). When BP was increased with midodrine, NVC was improved 70% in SCI, which was reflected by a 13% improved cognitive function (Po0.05). Improvements in BP were related to improved cognitive function in those with SCI (r 2 ¼ 0.52; Po0.05). Impaired NVC, secondary to low BP, may partially mediate reduced cognitive function in individuals with high-level SCI. INTRODUCTIONSpinal cord injury (SCI) is a devastating condition often resulting in disturbed motor, sensory, and autonomic function. As a result of disrupted descending autonomic spinal pathways after SCI, sympathetic vasomotor tone is impaired, often resulting in arterial hypotension. 1 Those with injury at or above T 6 spinal segment, because of a myriad of potential mechanisms (including decentralization of sympathetically mediated vasomotor tone in the splanchnic region and legs) have more profound autonomic disturbances including resting hypotension and orthostatic hypotension as compared with those with lower level SCI. 2 An abundance of evidence, from both animal and human studies, demonstrated that there is an association between low blood pressure (BP) and a variety of cognitive impairments. 3,4 There is well-established evidence that individuals with SCI have a high rate of traumatic brain injury that can result in a significant number of cognitive dysfunctions. 5 However, the high prevalence of cognitive dysfunction (i.e., between 10% and 60%) in SCI 6,7 is likely to be at least partially due to widespread hypotension. 8 This notion is further highlighted by a significant positive relationship between systolic BP (SBP) and cognitive function in the SCI population. 9

“…32 Regional differences in cerebrovascular reactivity to CO 2 between the anterior and posterior cerebral circulations could partly explain this differential response, with CBF-CO 2 reactivity during hypercapnia reportedly blunted in the posterior circulation (i.e., VA and posterior cerebral artery velocity) compared with the anterior circulation (ICA and/or MCAv); 98,99 although this is not a universal finding. 100 Thus, the acute and chronic effect of exercise-induced changes in PaCO 2 on regional CBF during and after HIT requires future research.…”

Section: Optimizing Cerebrovascular Adaptation and Safety For High-inmentioning

confidence: 99%

High-Intensity Interval Exercise and Cerebrovascular Health: Curiosity, Cause, and Consequence

Lucas

Cotter

Brassard

et al. 2015

157

171

Exercise is a uniquely effective and pluripotent medicine against several noncommunicable diseases of westernised lifestyles, including protection against neurodegenerative disorders. High-intensity interval exercise training (HIT) is emerging as an effective alternative to current health-related exercise guidelines. Compared with traditional moderate-intensity continuous exercise training, HIT confers equivalent if not indeed superior metabolic, cardiac, and systemic vascular adaptation. Consequently, HIT is being promoted as a more time-efficient and practical approach to optimize health thereby reducing the burden of disease associated with physical inactivity. However, no studies to date have examined the impact of HIT on the cerebrovasculature and corresponding implications for cognitive function. This review critiques the implications of HIT for cerebrovascular function, with a focus on the mechanisms and translational impact for patient health and well-being. It also introduces similarly novel interventions currently under investigation as alternative means of accelerating exercise-induced cerebrovascular adaptation. We highlight a need for studies of the mechanisms and thereby also the optimal dose-response strategies to guide exercise prescription, and for studies to explore alternative approaches to optimize exercise outcomes in brain-related health and disease prevention. From a clinical perspective, interventions that selectively target the aging brain have the potential to prevent stroke and associated neurovascular diseases.