Dietary nitrate supplementation and exercise performance

Andrew M Jones, Andrew M Jones

Abstract

Dietary nitrate is growing in popularity as a sports nutrition supplement. This article reviews the evidence base for the potential of inorganic nitrate to enhance sports and exercise performance. Inorganic nitrate is present in numerous foodstuffs and is abundant in green leafy vegetables and beetroot. Following ingestion, nitrate is converted in the body to nitrite and stored and circulated in the blood. In conditions of low oxygen availability, nitrite can be converted into nitric oxide, which is known to play a number of important roles in vascular and metabolic control. Dietary nitrate supplementation increases plasma nitrite concentration and reduces resting blood pressure. Intriguingly, nitrate supplementation also reduces the oxygen cost of submaximal exercise and can, in some circumstances, enhance exercise tolerance and performance. The mechanisms that may be responsible for these effects are reviewed and practical guidelines for safe and efficacious dietary nitrate supplementation are provided.

Figures

Fig. 1
Fig. 1
Pathways of NO production. NO is produced from the substrates l-arginine and oxygen in a reaction catalyzed by the NO synthases and is subsequently oxidized to nitrite and nitrate. Nitrate can be reduced to nitrite by xanthine oxidase and by anaerobic bacteria in the oral cavity, and nitrite can be further reduced to NO and other reactive nitrogen species, an effect that is accentuated when tissue oxygen availability is low. In this way, the products of NO production can be recycled. In addition to endogenous production, body stores of nitrate and nitrite can be increased through the consumption of foods that are rich in inorganic nitrate such as green leafy vegetables and some fruits. NO is important in several physiological processes that may support or enhance exercise performance. It is possible that the reliance on the nitrate–nitrite–NO pathway for NO production is increased during exercise. Dashed arrows show that NO can be oxidized to NO2 − and NO3 −. Ca2+ calcium, NO nitric oxide, NO3− nitrate, NO2− nitrite, NOS nitric oxide synthase, SR sarcoplasmic reticulum
Fig. 2
Fig. 2
Influence of acute and chronic dietary nitrate supplementation with 0.5 l/day of beetroot juice on a pulmonary oxygen uptake during submaximal exercise and b peak power output achieved during ramp incremental exercise. The nitrate condition is shown in filled symbols, the placebo condition is shown in open symbols, and the non-supplemented control condition is shown in grey symbols. The steady-state V˙O2 during moderate-intensity exercise was reduced 2.5 h after nitrate ingestion and this was maintained after 5 and 15 days of continued supplementation. The peak power output was higher than the other conditions after 15 days of supplementation. Values are mean ± SD. *Significantly different from the non-supplemented control condition (p < 0.05); #significantly different from the placebo condition (p < 0.05). BL baseline, V˙O2 oxygen uptake
Fig. 3
Fig. 3
Influence of dietary nitrate (black symbols) and placebo (white symbols) supplementation on 50-mile cycling time trial performance. The lines in the upper part of the figure show the ratio of power output to V˙O2 and the bars in the lower part of the figure show the split times taken to complete consecutive 10-mile splits. The power output to V˙O2 ratio was higher for the 20- to 30-mile (*p = 0.05) and 40- 50-mile (*p < 0.05) splits, and the 40- to 50-mile split was completed in a faster time (#p < 0.05) following nitrate supplementation compared with placebo. However, there was no significant difference in overall performance between treatments (beetroot juice 136.7 ± 5.6 vs. placebo 137.9 ± 6.4 min). Values are shown as mean ± SD. V˙O2 oxygen uptake

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