Dietary nitrate supplementation reduces the O2cost of low-intensity exercise and enhances tolerance to high-intensity exercise in humans

Author:

Bailey Stephen J.1,Winyard Paul2,Vanhatalo Anni1,Blackwell Jamie R.1,DiMenna Fred J.1,Wilkerson Daryl P.1,Tarr Joanna2,Benjamin Nigel2,Jones Andrew M.1

Affiliation:

1. School of Sport and Health Sciences and

2. Peninsula College of Medicine and Dentistry, University of Exeter, Exeter, United Kingdom

Abstract

Pharmacological sodium nitrate supplementation has been reported to reduce the O2cost of submaximal exercise in humans. In this study, we hypothesized that dietary supplementation with inorganic nitrate in the form of beetroot juice (BR) would reduce the O2cost of submaximal exercise and enhance the tolerance to high-intensity exercise. In a double-blind, placebo (PL)-controlled, crossover study, eight men (aged 19–38 yr) consumed 500 ml/day of either BR (containing 11.2 ± 0.6 mM of nitrate) or blackcurrant cordial (as a PL, with negligible nitrate content) for 6 consecutive days and completed a series of “step” moderate-intensity and severe-intensity exercise tests on the last 3 days. On days 4–6, plasma nitrite concentration was significantly greater following dietary nitrate supplementation compared with PL (BR: 273 ± 44 vs. PL: 140 ± 50 nM; P < 0.05), and systolic blood pressure was significantly reduced (BR: 124 ± 2 vs. PL: 132 ± 5 mmHg; P < 0.01). During moderate exercise, nitrate supplementation reduced muscle fractional O2extraction (as estimated using near-infrared spectroscopy). The gain of the increase in pulmonary O2uptake following the onset of moderate exercise was reduced by 19% in the BR condition (BR: 8.6 ± 0.7 vs. PL: 10.8 ± 1.6 ml·min−1·W−1; P < 0.05). During severe exercise, the O2uptake slow component was reduced (BR: 0.57 ± 0.20 vs. PL: 0.74 ± 0.24 l/min; P < 0.05), and the time-to-exhaustion was extended (BR: 675 ± 203 vs. PL: 583 ± 145 s; P < 0.05). The reduced O2cost of exercise following increased dietary nitrate intake has important implications for our understanding of the factors that regulate mitochondrial respiration and muscle contractile energetics in humans.

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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