Dietary nitrate supplementation and exercise performance

Abstract

Abstract

Dietary nitrate supplementation, primarily delivered through beetroot juice, has emerged as a well-characterized ergogenic strategy with consistent evidence of improving exercise efficiency and performance. This review by Jones, Vanhatalo, and Bailey (2018) comprehensively examined the mechanisms, evidence base, and practical applications of nitrate supplementation for exercise performance across a range of athletic populations and exercise modalities.

The nitrate-nitrite-nitric oxide pathway represents the primary mechanism: ingested nitrate is reduced by oral bacteria to nitrite, which is subsequently reduced to nitric oxide in hypoxic tissues during exercise, enhancing mitochondrial efficiency, reducing the oxygen cost of exercise, and improving blood flow to contracting muscles [1]. Meta-analytic evidence supports a meaningful improvement in exercise economy of approximately 2-3%, translating to significant performance gains in time-trial and endurance-dominated activities [2].

The review identified important population moderators: the ergogenic effect is most consistent in recreational to moderately trained athletes, while elite athletes may show attenuated responses, possibly due to habitually higher plasma nitrate levels [3]. A loading protocol of 2-3 days and an acute dose equivalent to 6-8 mmol of nitrate (approximately 500mL of beetroot juice) were identified as optimal for maximizing plasma nitrite availability at the time of exercise.

Keywords: dietary nitrate, beetroot juice, nitric oxide, exercise economy, mitochondrial efficiency, ergogenic, endurance performance

Introduction

Introduction

Nitric oxide (NO) occupies a central position in exercise physiology as a signaling molecule that regulates vascular tone, mitochondrial respiration, muscle contractile function, and glucose uptake. For decades, researchers recognized NO's importance to exercise capacity, but the primary focus was on endogenous NO synthesis via the L-arginine-eNOS pathway [1]. The discovery that inorganic nitrate in dietary sources could serve as an alternative, oxygen-independent source of NO production fundamentally expanded the nutritional strategies available to athletes seeking to enhance NO bioavailability.

The nitrate-nitrite-NO pathway operates through a series of reduction reactions that become increasingly favored in conditions of low oxygen availability — precisely the tissue environment during intense exercise. Dietary nitrate (NO₃⁻) consumed through food or supplements is absorbed in the small intestine and enters the circulation, where approximately 25% is taken up by salivary glands and secreted into saliva [2]. Commensal bacteria on the tongue reduce salivary nitrate to nitrite (NO₂⁻), which is then swallowed and absorbed. In hypoxic tissues with low pH — conditions that characterize intensely exercising skeletal muscle — nitrite is further reduced to nitric oxide by a variety of reductases including deoxyhemoglobin and xanthine oxidoreductase.

This pathway has several appealing pharmacological characteristics relative to L-arginine supplementation. First, because it produces NO through an oxygen-independent mechanism, it is most active precisely when conventional eNOS activity is most limited (during heavy exercise with tissue hypoxia). Second, dietary nitrate from food sources such as beetroot, spinach, arugula, and celery provides a naturally occurring, unprocessed source that avoids the pharmacokinetic problems associated with amino acid supplements [3].

Jones and colleagues at the University of Exeter were among the first to systematically characterize the exercise performance effects of beetroot juice supplementation, demonstrating in a landmark 2009 study that 500mL of beetroot juice for 6 days reduced the oxygen cost of submaximal exercise by approximately 5% and increased time to exhaustion [4]. Subsequent work from their group and others expanded the understanding of optimal dosing, timing, population responsiveness, and the specific exercise modalities that benefit most from nitrate supplementation.

Evidence Review

Discussion

Discussion

Contextualizing the 2-3% Performance Improvement

A 2-3% improvement in time-trial performance may appear modest in absolute terms, but within the context of competitive athletics, this magnitude of improvement can represent the difference between medal and non-medal outcomes. In Olympic-distance triathlon events lasting 1-2 hours, a 2% improvement in run-bike-swim performance represents minutes of time advantage [1]. Even for recreational athletes, improved exercise economy translates to either faster performance at the same subjective effort, or equivalent performance at lower physiological cost — a meaningful quality-of-life improvement for regular exercisers.

The mechanism of economy improvement — reduced oxygen cost at given exercise intensities — represents a qualitatively different performance enhancement than most ergogenic compounds. Rather than stimulating greater energy production, nitrate makes the same amount of energy production more metabolically efficient. This fundamental mechanism has parallels with altitude acclimatization and heat adaptation, both of which improve exercise economy through related NO-dependent vascular and mitochondrial adaptations [2].

Antifungal Mouthwash: An Unexpected Confounder

An important and somewhat unexpected practical finding in the nitrate literature is that antibacterial mouthwash can completely abolish the ergogenic effects of nitrate supplementation. By eliminating the oral bacteria responsible for nitrate-to-nitrite reduction, chlorhexidine-containing mouthwash prevents the conversion of dietary nitrate to the active nitrite precursor [3].

This finding has two practical implications. First, athletes supplementing with beetroot juice should avoid using antibacterial mouthwash in the hours preceding and following supplementation. Second, the mouthwash interference provides compelling mechanistic evidence that the oral bacteria-dependent reduction step is essential for nitrate's ergogenic effect, ruling out alternative mechanisms that don't require this conversion.

Nitrate Source: Beetroot Juice vs. Sodium Nitrate vs. Vegetables

Most research has used beetroot juice as the nitrate vehicle due to its high nitrate concentration (3-5 mmol per 100mL of concentrated juice), commercial availability, and the ability to create nitrate-depleted beetroot juice as a visually identical placebo. However, equivalent nitrate from sodium nitrate supplements or high-nitrate vegetables (spinach, arugula, lettuce) provides similar performance benefits, confirming that nitrate is the active component rather than beetroot-specific phytochemicals [4].

Practical considerations favor commercially concentrated beetroot shots (typically 70mL providing 5-8 mmol nitrate) for athletic use due to portion control precision and convenience, though athletes who can reliably consume adequate quantities of high-nitrate vegetables achieve similar benefits through dietary means.

Interaction with Training Status and Oxygen Availability

The gradient of nitrate responsiveness across training levels reflects a fundamental characteristic of the nitrate-nitrite-NO pathway: its benefits are greatest when conventional oxygen-dependent NO synthesis is most limited. In conditions of tissue hypoxia and acidosis — the state of intensely working muscles — nitrite reduction to NO is strongly favored, while less trained individuals who experience more pronounced exercise-induced hypoxia show greater pathway activation [5].

This interaction also explains why the benefits are most pronounced at moderate rather than near-maximal exercise intensities: at near-maximal intensities, oxygen delivery (cardiovascular capacity) rather than mitochondrial efficiency becomes the primary limiting factor, shifting performance determinants away from the specific mechanisms nitrate addresses.

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