title: Dietary nitrate accelerates postexercise muscle metabolic recovery and O2 delivery in hypoxia.
abstract: We tested the hypothesis that the time constants (τ) of postexercise T2* MRI signal intensity (an index of O2 delivery) and muscle [PCr] (an index of metabolic perturbation, measured by (31)P-MRS) in hypoxia would be accelerated after dietary nitrate (NO3 (-)) supplementation. In a double-blind crossover design, eight moderately trained subjects underwent 5 days of NO3 (-) (beetroot juice, BR; 8.2 mmol/day NO3 (-)) and placebo (PL; 0.003 mmol/day NO3 (-)) supplementation in four conditions: normoxic PL (N-PL), hypoxic PL (H-PL; 13% O2), normoxic NO3 (-) (N-BR), and hypoxic NO3 (-) (H-BR). The single-leg knee-extension protocol consisted of 10 min of steady-state exercise and 24 s of high-intensity exercise. The [PCr] recovery τ was greater in H-PL (30 ± 4 s) than H-BR (22 ± 4 s), N-PL (24 ± 4 s) and N-BR (22 ± 4 s) (P < 0.05) and the maximal rate of mitochondrial ATP resynthesis (Qmax) was lower in the H-PL (1.12 ± 0.16 mM/s) compared with H-BR (1.35 ± 0.26 mM/s), N-PL (1.47 ± 0.28 mM/s), and N-BR (1.40 ± 0.21 mM/s) (P < 0.05). The τ of postexercise T2* signal intensity was greater in H-PL (47 ± 14 s) than H-BR (32 ± 10 s), N-PL (38 ± 9 s), and N-BR (27 ± 6 s) (P < 0.05). The postexercise [PCr] and T2* recovery τ were correlated in hypoxia (r = 0.60; P < 0.05), but not in normoxia (r = 0.28; P > 0.05). These findings suggest that the NO3 (-)-NO2 (-)-NO pathway is a significant modulator of muscle energetics and O2 delivery during hypoxic exercise and subsequent recovery.
authors.affiliation: College of Life and Environmental Sciences, St. Luke's Campus, University of Exeter, Exeter, United Kingdom; a.vanhatalo@exeter.ac.uk.
authors.forename: Anni
authors.initials: A
authors.lastname: Vanhatalo
authors.affiliation: College of Life and Environmental Sciences, St. Luke's Campus, University of Exeter, Exeter, United Kingdom;
authors.forename: Andrew M
authors.initials: AM
authors.lastname: Jones
authors.affiliation: College of Life and Environmental Sciences, St. Luke's Campus, University of Exeter, Exeter, United Kingdom;
authors.forename: James R
authors.initials: JR
authors.lastname: Blackwell
authors.affiliation: University of Exeter Medical School, Exeter, United Kingdom, University of Exeter, Exeter, United Kingdom; and.
authors.forename: Paul G
authors.initials: PG
authors.lastname: Winyard
authors.affiliation: NIHR Exeter Clinical Research Facility, University of Exeter Medical School, St. Luke's Campus, University of Exeter, Exeter, United Kingdom.
authors.forename: Jonathan
authors.initials: J
authors.lastname: Fulford
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000284:Administration, Oral; D000293:Adolescent; D000328:Adult; D027461:Beta vulgaris; D001628:Beverages; D015415:Biomarkers / Q000378:metabolism; D018592:Cross-Over Studies; D004032:Diet; D004311:Double-Blind Method; D004734:Energy Metabolism / Q000187:drug effects*; D004739:England; D005260:Female; D006801:Humans; D000860:Hypoxia / Q000097:blood / Q000378:metabolism* / Q000503:physiopathology; D007700:Kinetics; D008279:Magnetic Resonance Imaging; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D008931:Mitochondria, Muscle / Q000187:drug effects / Q000378:metabolism; D009119:Muscle Contraction / Q000187:drug effects*; D018482:Muscle, Skeletal / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D009566:Nitrates / Q000008:administration & dosage*; D009569:Nitric Oxide / Q000378:metabolism; D009573:Nitrites / Q000378:metabolism; D010100:Oxygen / Q000097:blood*; D010101:Oxygen Consumption; D010725:Phosphocreatine / Q000378:metabolism; D028321:Plant Preparations; D018517:Plant Roots; D020127:Recovery of Function; D055815:Young Adult
chemical_list: D015415:Biomarkers; D009566:Nitrates; D009573:Nitrites; D028321:Plant Preparations; D010725:Phosphocreatine; D009569:Nitric Oxide; D000255:Adenosine Triphosphate; D010100:Oxygen
keywords: hypoxia; nitric oxide; nitrite; phosphocreatine; skeletal muscle