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Aim: Dietary nitrate (NO3−) supplementation increases nitric oxide bioavailability and can enhance exercise performance. We investigated the distribution and metabolic fate of ingested NO3− at rest and during exercise with a focus on skeletal muscle. Methods: In a randomized, crossover study, 10 healthy volunteers consumed 12.8 mmol 15N‐labeled potassium nitrate (K15NO3; NIT) or potassium chloride placebo (PLA). Muscle biopsies were taken at baseline, at 1‐ and 3‐h post‐supplement ingestion, and immediately following the completion of 60 maximal intermittent contractions of the knee extensors. Muscle, plasma, saliva, and urine samples were analyzed using chemiluminescence to determine absolute [NO3−] and [NO2−], and by mass spectrometry to determine the proportion of NO3− and NO2− that was 15N‐labeled. Results: Neither muscle [NO3−] nor [NO2−] were altered by PLA. Following NIT, muscle [NO3−] (but not [NO2−]) was elevated at 1‐h (from ~35 to 147 nmol/g, p < 0.001) and 3‐h, with almost all of the increase being 15N‐labeled. There was a significant reduction in 15N‐labeled muscle [NO3−] from pre‐ to post‐exercise. Relative to PLA, mean muscle torque production was ~7% greater during the first 18 contractions following NIT. This improvement in torque was correlated with the pre‐exercise 15N‐labeled muscle [NO3−] and the magnitude of decline in 15N‐labeled muscle [NO3−] during exercise (r = 0.66 and r = 0.62, respectively; p < 0.01). Conclusion: This study shows, for the first time, that skeletal muscle rapidly takes up dietary NO3−, the elevated muscle [NO3−] following NO3− ingestion declines during exercise, and muscle NO3− dynamics are associated with enhanced torque production during maximal intermittent muscle contractions. [ABSTRACT FROM AUTHOR]

Key points: Nitric oxide (NO), a potent vasodilator and a regulator of many physiological processes, is produced in mammals both enzymatically and by reduction of nitrite and nitrate ions.We have previously reported that, in rodents, skeletal muscle serves as a nitrate reservoir, with nitrate levels greatly exceeding those in blood or other internal organs, and with nitrate being reduced to NO during exercise.In the current study, we show that nitrate concentration is substantially greater in skeletal muscle than in blood and is elevated further by dietary nitrate ingestion in human volunteers. We also show that high‐intensity exercise results in a reduction in the skeletal muscle nitrate store following supplementation, likely as a consequence of its reduction to nitrite and NO.We also report the presence of sialin, a nitrate transporter, and xanthine oxidoreductase in human skeletal muscle, indicating that muscle has the necessary apparatus for nitrate transport, storage and metabolism. Rodent skeletal muscle contains a large store of nitrate that can be augmented by the consumption of dietary nitrate. This muscle nitrate reservoir has been found to be an important source of nitrite and nitric oxide (NO) via its reduction by tissue xanthine oxidoreductase. To explore if this pathway is also active in human skeletal muscle during exercise, and if it is sensitive to local nitrate availability, we assessed exercise‐induced changes in muscle nitrate and nitrite concentrations in young healthy humans, under baseline conditions and following dietary nitrate consumption. We found that baseline nitrate and nitrite concentrations were far higher in muscle than in plasma (∼4‐fold and ∼29‐fold, respectively), and that the consumption of a single bolus of dietary nitrate (12.8 mmol) significantly elevated nitrate concentration in both plasma (∼19‐fold) and muscle (∼5‐fold). Consistent with these observations, and with previous suggestions of active muscle nitrate transport, we present western blot data to show significant expression of the active nitrate/nitrite transporter sialin in human skeletal muscle. Furthermore, we report an exercise‐induced reduction in human muscle nitrate concentration (by ∼39%), but only in the presence of an increased muscle nitrate store. Our results indicate that human skeletal muscle nitrate stores are sensitive to dietary nitrate intake and may contribute to NO generation during exercise. Together, these findings suggest that skeletal muscle plays an important role in the transport, storage and metabolism of nitrate in humans. Key points: Nitric oxide (NO), a potent vasodilator and a regulator of many physiological processes, is produced in mammals both enzymatically and by reduction of nitrite and nitrate ions.We have previously reported that, in rodents, skeletal muscle serves as a nitrate reservoir, with nitrate levels greatly exceeding those in blood or other internal organs, and with nitrate being reduced to NO during exercise.In the current study, we show that nitrate concentration is substantially greater in skeletal muscle than in blood and is elevated further by dietary nitrate ingestion in human volunteers. We also show that high‐intensity exercise results in a reduction in the skeletal muscle nitrate store following supplementation, likely as a consequence of its reduction to nitrite and NO.We also report the presence of sialin, a nitrate transporter, and xanthine oxidoreductase in human skeletal muscle, indicating that muscle has the necessary apparatus for nitrate transport, storage and metabolism. [ABSTRACT FROM AUTHOR]

It is possible that dietary nitrate (NO) supplementation may improve both physical and cognitive performance via its influence on blood flow and cellular energetics. Purpose: To investigate the effects of dietary NO supplementation on exercise performance and cognitive function during a prolonged intermittent sprint test (IST) protocol, which was designed to reflect typical work patterns during team sports. Methods: In a double-blind randomised crossover study, 16 male team-sport players received NO-rich (BR; 140 mL day; 12.8 mmol of NO), and NO-depleted (PL; 140 mL day; 0.08 mmol NO) beetroot juice for 7 days. On day 7 of supplementation, subjects completed the IST (two 40-min 'halves' of repeated 2-min blocks consisting of a 6-s 'all-out' sprint, 100-s active recovery and 20 s of rest), on a cycle ergometer during which cognitive tasks were simultaneously performed. Results: Total work done during the sprints of the IST was greater in BR (123 ± 19 kJ) compared to PL (119 ± 17 kJ; P < 0.05). Reaction time of response to the cognitive tasks in the second half of the IST was improved in BR compared to PL (BR first half: 820 ± 96 vs. second half: 817 ± 86 ms; PL first half: 824 ± 114 vs. second half: 847 ± 118 ms; P < 0.05). There was no difference in response accuracy. Conclusions: These findings suggest that dietary NO enhances repeated sprint performance and may attenuate the decline in cognitive function (and specifically reaction time) that may occur during prolonged intermittent exercise. [ABSTRACT FROM AUTHOR]