Article

Beetroot juice supplementation speeds O2 uptake kinetics and improves exercise tolerance during severe-intensity exercise initiated from an elevated baseline.

University of Exeter.
AJP Regulatory Integrative and Comparative Physiology (Impact Factor: 3.11). 10/2013; 305(12). DOI: 10.1152/ajpregu.00295.2013
Source: PubMed

ABSTRACT

Severe-intensity exercise initiated from an elevated metabolic rate would be expected to enhance the proportional activation of higher-order (type II) muscle fibers. The purpose of this study was therefore to test the hypothesis that, compared to placebo (PL), NO3--rich beetroot juice (BR) supplementation would speed the phase II vo2 kinetics (τp) and enhance exercise tolerance during severe-intensity exercise initiated from a baseline of moderate-intensity exercise. Nine healthy, physically-active subjects were assigned in a randomized, double-blind, crossover design to receive BR (140 mL/day, containing ~8 mmol of NO3(-)) and PL (140 mL/day, containing ~0.003 mmol of NO3(-)) for 6 days. On days 4, 5 and 6 of the supplementation periods, subjects completed a double-step exercise protocol that included transitions from unloaded-to-moderate intensity exercise (U→M) followed immediately by moderate-to-severe-intensity exercise (M→S). Compared to PL, BR elevated resting plasma nitrite concentration (PL: 65 ± 32 vs. BR: 348 ± 170 nM, P<0.01) and reduced the vo2 τp in M→S (PL: 46 ± 13 vs. BR: 36 ± 10 s, P<0.05) but not U→M (PL: 25 ± 4 vs. BR: 27 ± 6 s, P>0.05). During M→S exercise, the faster vo2 kinetics coincided with faster NIRS-derived muscle [deoxyhemoglobin] kinetics (τ; PL: 20 ± 9 vs. BR: 10 ± 3 s, P<0.05) and a 22% greater time-to-task failure (PL: 521 ± 158 vs. BR: 635 ± 258 s, P<0.05). Dietary supplementation with NO3(-)-rich BR juice speeds vo2 kinetics and enhances exercise tolerance during severe-intensity exercise when initiated from an elevated metabolic rate.

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    • "Also, dietary nitrate resulted in enhanced cardiorespiratory function [13] and improved glucose tolerance in diabetic rats [14]. Nitrate-rich beetroot juice intake prior to exercise achieved similar results, in particular improving exercise tolerance to high-intensity exercise [15], but also in patients with chronic obstructive pulmonary disease [16]. Further, an antiinflammatory effect has been linked to dietary nitrate and nitrite consumption [17], overall hinting towards an atherosclerosisprotective role of dietary nitrate supplementation. "
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    ABSTRACT: Background: Short term dietary nitrate or nitrite supplementation has nitric oxide (NO)-mediated beneficial effects on blood pressure and inflammation and reduces mitochondrial oxygen consumption, possibly preventing hypoxia. As these processes are implicated in atherogenesis, dietary nitrate was hypothesized to prevent plaque initiation, hypoxia and inflammation. Aims: Study prolonged nitrate supplementation on atherogenesis, hypoxia and inflammation in low density lipoprotein receptor knockout mice (LDLr(-/-)). Methods: LDLr(-/-) mice were administered sodium-nitrate or equimolar sodium-chloride in drinking water alongside a western-type diet for 14 weeks to induce atherosclerosis. Plasma nitrate, nitrite and hemoglobin-bound nitric oxide were measured by chemiluminescence and electron parametric resonance, respectively. Results: Plasma nitrate levels were elevated after 14 weeks of nitrate supplementation (NaCl: 40.29 ± 2.985, NaNO3: 78.19 ± 6.837, p < 0.0001). However, prolonged dietary nitrate did not affect systemic inflammation, hematopoiesis, erythropoiesis and plasma cholesterol levels, suggesting no severe side effects. Surprisingly, neither blood pressure, nor atherogenesis were altered. Mechanistically, plasma nitrate and nitrite were elevated after two weeks (NaCl: 1.0 ± 0.2114, NaNO3: 3.977 ± 0.7371, p < 0.0001), but decreased over time (6, 10 and 14 weeks). Plasma nitrite levels even reached baseline levels at 14 weeks (NaCl: 0.7188 ± 0.1072, NaNO3: 0.9723 ± 0.1279 p = 0.12). Also hemoglobin-bound NO levels were unaltered after 14 weeks. This compensation was not due to altered eNOS activity or conversion into peroxynitrite and other RNI, suggesting reduced nitrite formation or enhanced nitrate/nitrite clearance. Conclusion: Prolonged dietary nitrate supplementation resulted in compensation of nitrite and NO levels and did not affect atherogenesis or exert systemic side effects.
    Full-text · Article · Jan 2016 · Atherosclerosis
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    • "Although the C2C12 experiments lack an appropriate NO − 3 - depleted beetroot juice control ( see above ) , increased coupling efficiency of oxidative phosphorylation agrees with data reported by Larsen et al . ( 2011 ) , who show that skeletal muscle mitochondria isolated from NO − 3 - supplemented subjects exhibit higher respiratory control and P / O ratios ( defined in Brand and Nicholls , 2011 ) than mitochondria from non - supplemented controls , and that increases in P / O ratio correlate with NO − 3 - induced decreases in whole - body O 2 uptake during exercise . This increased efficiency of ATP synthesis in isolated mitochondria , however , emerges from decreased respiration linked to mitochondrial proton leak , not from stimulated O 2 uptake coupled to phosphorylation ( Larsen et al . "
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    ABSTRACT: Inorganic nitrate is present at high levels in beetroot and celery, and in green leafy vegetables such as spinach and lettuce. Though long believed inert, nitrate can be reduced to nitrite in the human mouth and, further, under hypoxia and/or low pH, to nitric oxide. Dietary nitrate has thus been associated favorably with nitric-oxide-regulated processes including blood flow and energy metabolism. Indeed, the therapeutic potential of dietary nitrate in cardiovascular disease and metabolic syndrome-both aging-related medical disorders-has attracted considerable recent research interest. We and others have shown that dietary nitrate supplementation lowers the oxygen cost of human exercise, as less respiratory activity appears to be required for a set rate of skeletal muscle work. This striking observation predicts that nitrate benefits the energy metabolism of human muscle, increasing the efficiency of either mitochondrial ATP synthesis and/or of cellular ATP-consuming processes. In this mini-review, we evaluate experimental support for the dietary nitrate effects on muscle bioenergetics and we critically discuss the likelihood of nitric oxide as the molecular mediator of such effects.
    Full-text · Article · Aug 2015 · Frontiers in Physiology
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    • "Surprisingly, a more recent study by Shepherd et al. [90], involving thirteen patients with chronic obstructive pulmonary disease (COPD), showed that a 4-fold rise in plasma nitrate concentration induced by two days of nitrate supplementation did not reduce the oxygen cost of moderate intensity cycling, increase distance covered in the six-minute walk test, or lower blood pressure. The recent study suggests that the ergogenic effect of nitrate supplementation is mostly present in type II muscle fibers, which is why its effect should be more pronounced during exercise of high intensity [91]. It should not be forgotten that NO can also have a potentially harmful effect on exercise capacity by inhibiting cytochrome c oxidase, as reported previously [84]. "
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    ABSTRACT: In this review, we present the relation between power generation capabilities and pulmonary oxygen uptake during incremental cycling exercise in humans and the effect of exercise intensity on the oxygen cost of work. We also discuss the importance of oxygen delivery to the working muscles as a factor determining maximal oxygen uptake in humans. Subsequently, we outline the importance of coronary blood flow, myocardial oxygen uptake and myocardial metabolic stability for exercise tolerance. Finally, we describe mechanisms of endothelium-dependent regulation of coronary and skeletal muscle blood flow, dysregulation of which may impair exercise capacity and increase the cardiovascular risk of exercise. Copyright © 2015 Institute of Pharmacology, Polish Academy of Sciences. All rights reserved.
    Preview · Article · Jun 2015 · Pharmacological reports: PR
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