Response of Cerebral Blood Flow and Blood Pressure to Dynamic Exercise: A Study Using PET

Hiura, Mikio; Nariai, Tadashi; Sakata, Muneyuki; Muta, Akitaka; Ishibashi, Kenji; Wagatsuma, Kei; Tago, Tetsuro; Toyohara, Jun; Maehara, Taketoshi

doi:10.1055/s-0043-123647

Cited by 9 publications

(34 citation statements)

References 33 publications

(45 reference statements)

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“…These findings support an enhanced neurovascular coupling with dietary nitrate, mediated by higher cortical tissue oxygenation and lower CBF response during cortical activation. Using positron emission tomography, Hiura et al (2014 , 2018 ) found moderate steady-state cycling (∼50% estimated max HR) selectively increased regional blood flow to cerebellar vermis and primary sensorimotor cortex, insular cortex and brain stem. Since prefrontal cortical tissue oxygenation changes during exercise reflect those of the sensorimotor cortex ( Subudhi et al, 2009 ), an enhanced neurovascular coupling with dietary nitrate could account for the elevated prefrontal tissue oxygenation and reduced MCAv during TT in normoxia.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, we observed a progressive rise in MCAv and Borg score during TT in hypoxia, in absence of significant changes in BP or exercise workload ( Fan et al, 2013 ). Since exercise selectively increases regional CBF to the sensorimotor cortex ( Hiura et al, 2014 , 2018 ) – presumably due to greater afferent feedback, we speculated that the progressive increase in RPE (and associated greater sensorimotor cortex activation) could account for the progressive rise in MCAv during TT in hypoxia. In the present study, we found RPE to be elevated during TT in hypoxia but unaffected with dietary nitrate.…”

Section: Discussionmentioning

confidence: 99%

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Oral Nitrate Supplementation Differentially Modulates Cerebral Artery Blood Velocity and Prefrontal Tissue Oxygenation During 15 km Time-Trial Cycling in Normoxia but Not in Hypoxia

et al. 2018

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Background: Nitrate is a precursor of nitric oxide (NO), an important regulator of cerebral perfusion in normoxic and hypoxic conditions. Nitrate supplementation could be used to improve cerebral perfusion and oxygenation during exercise in hypoxia. The effects of dietary nitrate supplementation on cerebral haemodynamics during exercise in severe hypoxia (arterial O2 saturation < 70%) have not been explored.Methods: In twelve trained male cyclists, we measured blood pressure (BP), middle cerebral artery blood velocity (MCAv), cerebrovascular resistance (CVR) and prefrontal oxyhaemoglobin and deoxyhaemoglobin concentration (O2Hb and HHb, respectively) during 15 km cycling time trials (TT) in normoxia and severe hypoxia (11% inspired O2, peripheral O2 saturation ∼66%) following 3-day oral supplementation with placebo or sodium nitrate (0.1 mmol/kg/day) in a randomised, double-blinded manner. We tested the hypothesis that dietary nitrate supplementation increases MCAv and cerebral O2Hb during TT in severe hypoxia.Results: During TT in normoxia, nitrate supplementation lowered MCAv by ∼2.3 cm/s and increased cerebral O2Hb by ∼6.8 μM and HHb by ∼2.1 μM compared to normoxia placebo (p ≤ 0.01 for all), while BP tended to be lowered (p = 0.06). During TT in severe hypoxia, nitrate supplementation elevated MCAv (by ∼2.5 cm/s) and BP (by ∼5 mmHg) compared to hypoxia placebo (p < 0.01 for both), while it had no effect on cerebral O2Hb (p = 0.98), HHb (p = 0.07) or PETCO2 (p = 0.12). Dietary nitrate had no effect of CVR during TT in normoxia or hypoxia (p = 0.19).Conclusion: Our findings indicate that during normoxic TT, the modulatory effect of dietary nitrate on regional and global cerebral perfusion is heterogeneous. Meanwhile, the lack of major changes in cerebral perfusion with dietary nitrate during hypoxic TT alludes to an exhausted cerebrovascular reserve.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Oral Nitrate Supplementation Differentially Modulates Cerebral Artery Blood Velocity and Prefrontal Tissue Oxygenation During 15 km Time-Trial Cycling in Normoxia but Not in Hypoxia

et al. 2018

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“…In one study, 11 healthy individuals were assessed using PET oxygen-15-labeled water following 20 min of mostly very low intensity exercise (30% of estimated HRR). Results revealed that regional CBF decreased 8–13% during PEH compared to rest (234).…”

Section: Protecting the Brain After And During Aerobic Exercisementioning

confidence: 99%

Aerobic Training and Mobilization Early Post-stroke: Cautions and Considerations

Marzolini

Robertson

et al. 2019

Front. Neurol.

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Knowledge gaps exist in how we implement aerobic exercise programs during the early phases post-stroke. Therefore, the objective of this review was to provide evidence-based guidelines for pre-participation screening, mobilization, and aerobic exercise training in the hyper-acute and acute phases post-stroke. In reviewing the literature to determine safe timelines of when to initiate exercise and mobilization we considered the following factors: arterial blood pressure dysregulation, cardiac complications, blood-brain barrier disruption, hemorrhagic stroke transformation, and ischemic penumbra viability. These stroke-related impairments could intensify with inappropriate mobilization/aerobic exercise, hence we deemed the integrity of cerebral autoregulation to be an essential physiological consideration to protect the brain when progressing exercise intensity. Pre-participation screening criteria are proposed and countermeasures to protect the brain from potentially adverse circulatory effects before, during, and following mobilization/exercise sessions are introduced. For example, prolonged periods of standing and static postures before and after mobilization/aerobic exercise may elicit blood pooling and/or trigger coagulation cascades and/or cerebral hypoperfusion. Countermeasures such as avoiding prolonged standing or incorporating periodic lower limb movement to activate the venous muscle pump could counteract blood pooling after an exercise session, minimize activation of the coagulation cascade, and mitigate potential cerebral hypoperfusion. We discuss patient safety in light of the complex nature of stroke presentations (i.e., type, severity, and etiology), medical history, comorbidities such as diabetes, cardiac manifestations, medications, and complications such as anemia and dehydration. The guidelines are easily incorporated into the care model, are low-risk, and use minimal resources. These and other strategies represent opportunities for improving the safety of the activity regimen offered to those in the early phases post-stroke. The timeline for initiating and progressing exercise/mobilization parameters are contingent on recovery stages both from neurobiological and cardiovascular perspectives, which to this point have not been specifically considered in practice. This review includes tailored exercise and mobilization prescription strategies and precautions that are not resource intensive and prioritize safety in stroke recovery.

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“…30% HR reserve) supine cycling exercise, indicating reflex cardiovascular control of CBF distribution during exercise (Hiura et al . ). Additionally, Sato et al .…”

Section: Discussionmentioning

confidence: 97%

“…Such increases in regional CBF supplying the brainstem, cerebellum and hypothalamus were reportedly consistent with the exercise‐induced elevations in MAP (Hiura et al . ); as such, regional CBF distribution may support improved reflex cardiovascular control (e.g. autonomic regulation of MAP and HR responses) during exercise.…”

Section: Discussionmentioning

confidence: 99%

Evidence for temperature‐mediated regional increases in cerebral blood flow during exercise

Caldwell

Coombs

Howe

et al. 2020

The Journal of Physiology

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Key points Aerobic exercise elicits increases in cerebral blood flow (CBF), as well as core body temperature; however, the isolated influence of temperature on CBF regulation during exercise has not been investigated The present study assessed CBF regulation and neurovascular coupling during submaximal cycling exercise and temperature‐matched passive heat stress during isocapnia (i.e. end‐tidal PnormalCO2 was held constant) Submaximal cycling exercise and temperature‐matched passive heat stress provoked ∼16% increases in vertebral artery blood flow, independent of changes in end‐tidal PnormalCO2 and blood pressure External carotid artery blood flow increased by ∼43% during both exercise and passive heat stress, with no change in internal carotid artery blood flow Neurovascular coupling (i.e. the relationship between local increases in cerebral metabolism and appropriately matched increases in regional cerebral blood flow) is preserved during both exercise and temperature‐matched passive heat stress Abstract Acute moderate‐intensity exercise increases core temperature (Tc; +0.7‐0.8°C); however, such exercise increases cerebral blood flow (CBF; +10‐20%) mediated via small elevations in arterial PnormalCO2 and metabolism. The present study aimed to isolate the role of Tc from PnormalCO2 on CBF regulation during submaximal exercise. Healthy adults (n = 11; 10 males/one female; 26 ± 4 years) participated in two interventions each separated by ≥48 h: (i) 60 min of semi‐recumbent cycling (EX; 50% workload max) and (ii) 75 min of passive heat stress (HS; 49°C water‐perfused suit) to match the exercise‐induced increases in Tc (EX: Δ0.75 ± 0.33°C vs. HS: Δ0.77 ± 0.33°C, P = 0.855). Blood flow (Q) in the internal and external carotid arteries (ICA and ECA, respectively) and vertebral artery (VA) (Duplex ultrasound) was measured. End‐tidal PnormalCO2 and PnormalO2 were effectively clamped to resting values within each condition. The QICA was unchanged with EX and HS interventions (P = 0.665), consistent with the unchanged end‐tidal PnormalCO2 (P = 0.327); whereas, QVA was higher throughout both EX and HS (EX: Δ16 ± 21% vs. HS: Δ16 ± 23%, time effect: P = 0.006) with no between condition differences (P = 0.785). These increases in QVA contributed to higher global CBF throughout both EX and HS (EX: Δ12 ± 20% vs. HS: Δ14 ± 14%, time effect: P = 0.029; condition effect: P = 0.869). The QECA increased throughout both EX and HS (EX: Δ42 ± 58% vs. HS: Δ53 ± 28%, time effect: P < 0.001; condition effect: P = 0.628). Including blood pressure as a covariate did not alter these CBF findings (all P > 0.05). Overall, these data provide new evidence for temperature‐mediated elevations in posterior CBF during exercise that are independent of changes in PnormalCO2 and blood pressure.

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Response of Cerebral Blood Flow and Blood Pressure to Dynamic Exercise: A Study Using PET

Cited by 9 publications

References 33 publications

Oral Nitrate Supplementation Differentially Modulates Cerebral Artery Blood Velocity and Prefrontal Tissue Oxygenation During 15 km Time-Trial Cycling in Normoxia but Not in Hypoxia

Oral Nitrate Supplementation Differentially Modulates Cerebral Artery Blood Velocity and Prefrontal Tissue Oxygenation During 15 km Time-Trial Cycling in Normoxia but Not in Hypoxia

Aerobic Training and Mobilization Early Post-stroke: Cautions and Considerations

Evidence for temperature‐mediated regional increases in cerebral blood flow during exercise

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