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.

Détails

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Etat: Public
Version: Final published version
ID Serval
serval:BIB_4B467D558313
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
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.
Périodique
Frontiers in physiology
Auteur(s)
Fan J.L., Bourdillon N., Meyer P., Kayser B.
ISSN
1664-042X (Print)
ISSN-L
1664-042X
Statut éditorial
Publié
Date de publication
2018
Peer-reviewed
Oui
Volume
9
Langue
anglais
Notes
Article 869
Résumé
<b>Background:</b> 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 O <sub>2</sub> saturation < 70%) have not been explored. <b>Methods:</b> 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 (O <sub>2</sub> Hb and HHb, respectively) during 15 km cycling time trials (TT) in normoxia and severe hypoxia (11% inspired O <sub>2</sub> , peripheral O <sub>2</sub> 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 O <sub>2</sub> Hb during TT in severe hypoxia. <b>Results:</b> During TT in normoxia, nitrate supplementation lowered MCAv by ∼2.3 cm/s and increased cerebral O <sub>2</sub> Hb by ∼6.8 μM and HHb by ∼2.1 μM compared to normoxia placebo ( <i>p</i> ≤ 0.01 for all), while BP tended to be lowered ( <i>p</i> = 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 ( <i>p</i> < 0.01 for both), while it had no effect on cerebral O <sub>2</sub> Hb ( <i>p</i> = 0.98), HHb ( <i>p</i> = 0.07) or PETCO <sub>2</sub> ( <i>p</i> = 0.12). Dietary nitrate had no effect of CVR during TT in normoxia or hypoxia ( <i>p</i> = 0.19). <b>Conclusion:</b> 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.
Mots-clé
Physiology (medical), Physiology, NO bioavailability, cerebral tissue oxygenation, exercise, hypoxia, nitrate
Pubmed
Web of science
Open Access
Oui
Création de la notice
21/08/2018 10:56
Dernière modification de la notice
20/08/2019 14:59
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