Relationship of middle cerebral artery blood flow velocity to intensity during dynamic exercise in normal subjects

Moraine, Jean-Jacques; Lamotte, Michel; Berré, Jacques; Niset, Georges; Leduc, Albert; Naeije, Robert

doi:10.1007/bf00377701

Cited by 105 publications

(100 citation statements)

References 14 publications

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“…However, MCAv at 70 % HRR was similar or slightly reduced compared with that observed at 30 % HRR. This is in accordance with previous reports that the increase in MCAv is intensity dependent up until 60 % of V Á O2 max, after which it declines back towards resting levels due to hyperventilation-induced hypocapnia (Hellstrom et al 1996;Moraine et al 1993). Below ventilatory threshold, the increase in CBF with exercise is likely driven by increases in cerebral metabolism and PaCO 2 , as a result of increased functional activation with motor activity (Hellstrom et al 1996;Moraine et al 1993); however, above this, the large disproportional increase in ventilation reduces PaCO 2 and thus CBF despite progressive elevations in cerebral metabolism (Hellstrom et al 1996;Moraine et al 1993).…”

Section: Discussionsupporting

confidence: 93%

“…This magnitude of increase is similar to that observed by other authors using transcranial Doppler to assess blood flow velocity in the MCA during exercise (Hellstrom et al 1996;Jorgensen et al 1992;Linkis et al 1995;Moraine et al 1993;Ogoh et al 2005). However, MCAv at 70 % HRR was similar or slightly reduced compared with that observed at 30 % HRR.…”

Section: Discussionsupporting

confidence: 90%

See 1 more Smart Citation

Cerebral blood flow and cerebrovascular reactivity at rest and during sub-maximal exercise: Effect of age and 12-week exercise training

Murrell

Cotter

Thomas

et al. 2012

AGE

160

180

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Chronic reductions in cerebral blood flow (CBF) and cerebrovascular reactivity to CO 2 are risk factors for cerebrovascular disease. Higher aerobic fitness is associated with higher CBF at any age; however, whether CBF or reactivity can be elevated following an exercise training intervention in healthy individuals is unknown. The aim of this study was to assess the effect of exercise training on CBF and cerebrovascular reactivity at rest and during exercise in young and older individuals. Ten young (23±5 years; body mass index ) previously sedentary individuals breathed 5 % CO 2 for 3 min at rest and during steady-state cycling exercise (30 and 70 % heart rate range (HRR)) prior to and following a 12-week aerobic exercise intervention. Effects of training on middle cerebral artery blood velocity (MCAv) at rest were unclear in both age groups. The absolute MCAv response to exercise was greater in the young (9 and 9 cm s −1 (30 and 70 % HRR, respectively) vs. 5 and 4 cm s −1 (older), P<0.05) and was similar following training. Cerebrovascular reactivity was elevated following the 12-week training at rest (2.87±0.76 vs. 2.54± 1.12 cm s −1 mm Hg −1 , P00.01) and during exercise, irrespective of age. The finding of a training-induced elevation in cerebrovascular reactivity provides further support for exercise as a preventative tool in cerebrovascular and neurological disease with ageing.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 90%

Cerebral blood flow and cerebrovascular reactivity at rest and during sub-maximal exercise: Effect of age and 12-week exercise training

Murrell

Cotter

Thomas

et al. 2012

AGE

160

180

View full text Add to dashboard Cite

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“…This increase is reflected with a parallel increase in regional CBF, neuronal activity and metabolism (reviewed in Ogoh and Ainslie 2009). In contrast, at least in young healthy subjects, CBF declines towards baseline values (Moraine et al 1993) when exercise intensity is >60% VO 2peak , regardless of the progressive increase in neuronal activity and metabolism. This reduction in CBF is attributed to increased cerebral vasoconstriction (Moraine et al 1993;Hellstrom et al 1996;Nybo and Rasmussen 2007) secondary to hyperventilatory-induced hypocapnia.…”

mentioning

confidence: 86%

“…In contrast, at least in young healthy subjects, CBF declines towards baseline values (Moraine et al 1993) when exercise intensity is >60% VO 2peak , regardless of the progressive increase in neuronal activity and metabolism. This reduction in CBF is attributed to increased cerebral vasoconstriction (Moraine et al 1993;Hellstrom et al 1996;Nybo and Rasmussen 2007) secondary to hyperventilatory-induced hypocapnia. This observation indicates that, during heavy exercise, CBF decreases despite progressive increases in cerebral metabolic demand (reviewed in Ogoh and Ainslie 2009).…”

mentioning

confidence: 86%

Aging blunts hyperventilation-induced hypocapnia and reduction in cerebral blood flow velocity during maximal exercise

Marsden

Haykowsky

Smirl

et al. 2011

AGE

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Cerebral blood flow (CBF) increases from rest to ∼60% of peak oxygen uptake (VO 2peak ) and thereafter decreases towards baseline due to hyperventilation-induced hypocapnia and subsequent cerebral vasoconstriction. It is unknown what happens to CBF in older adults (OA), who experience a decline in CBF at rest coupled with a blunted ventilatory response during VO 2peak . In 14 OA (71±10 year) and 21 young controls (YA; 23±4 years), we hypothesized that OA would experience less hyperventilationinduced cerebral vasoconstriction and therefore an attenuated reduction in CBF at VO 2peak . Incremental exercise was performed on a cycle ergometer, whilst bilateral middle cerebral artery blood flow velocity (MCA V mean ; transcranial Doppler ultrasound), heart rate (HR; ECG) and end-tidal PCO 2 (P ET CO 2 ) were monitored continuously. Blood pressure (BP) was monitored intermittently. From rest to 50% of VO 2peak , despite greater elevations in BP in OA, the change in MCA V mean was greater in YA compared to OA (28% vs. 15%, respectively; P<0.0005). In the YA, at intensities >70% of VO 2peak , the hyperventilationinduced declines in both P ET CO 2 (14 mmHg (YA) vs. 4 mmHg (OA); P<0.05) and MCA V mean (−21% (YA) vs. −7% (OA); P<0.0005) were greater in YA compared to OA. Our findings show (1), from rest-tomild intensity exercise (50% VO 2peak ), elevations in CBF are reduced in OA and (2) age-related declines in hyperventilation during maximal exercise result in less hypocapnic-induced cerebral vasoconstriction.

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“…77 vascular function (as detailed above), exercising above~70% _ VO 2 max induces a hyperventilation-induced hypocapnia and subsequent cerebral vasoconstriction, reducing CBF toward resting values. [32][33][34] This constrictive effect may serve as a neuroprotective response to prevent BBB disruption and hyperperfusion injury, and has been associated with improved CBF regulation during changes in blood pressure (i.e., autoregulation). [92][93][94] However, whether this vasoconstriction is sufficient to counteract the increased cerebral perfusion pressure induced from HIT is not known.…”

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

J Cereb Blood Flow Metab

157

179

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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.

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Relationship of middle cerebral artery blood flow velocity to intensity during dynamic exercise in normal subjects

Cited by 105 publications

References 14 publications

Cerebral blood flow and cerebrovascular reactivity at rest and during sub-maximal exercise: Effect of age and 12-week exercise training

Cerebral blood flow and cerebrovascular reactivity at rest and during sub-maximal exercise: Effect of age and 12-week exercise training

Aging blunts hyperventilation-induced hypocapnia and reduction in cerebral blood flow velocity during maximal exercise

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

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