<scp>¹⁵N</scp>‐labeled dietary nitrate supplementation increases human skeletal muscle nitrate concentration and improves muscle torque production

Abstract

Abstract Aim Dietary nitrate (NO 3 − ) supplementation increases nitric oxide bioavailability and can enhance exercise performance. We investigated the distribution and metabolic fate of ingested NO 3 − at rest and during exercise with a focus on skeletal muscle. Methods In a randomized, crossover study, 10 healthy volunteers consumed 12.8 mmol 15 N‐labeled potassium nitrate (K 15 NO 3 ; 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 [NO 3 − ] and [NO 2 − ], and by mass spectrometry to determine the proportion of NO 3 − and NO 2 − that was 15 N‐labeled. Results Neither muscle [NO 3 − ] nor [NO 2 − ] were altered by PLA. Following NIT, muscle [NO 3 − ] (but not [NO 2 − ]) was elevated at 1‐h (from ~35 to 147 nmol/g, p &lt; 0.001) and 3‐h, with almost all of the increase being 15 N‐labeled. There was a significant reduction in 15 N‐labeled muscle [NO 3 − ] 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 15 N‐labeled muscle [NO 3 − ] and the magnitude of decline in 15 N‐labeled muscle [NO 3 − ] during exercise ( r = 0.66 and r = 0.62, respectively; p &lt; 0.01). Conclusion This study shows, for the first time, that skeletal muscle rapidly takes up dietary NO 3 − , the elevated muscle [NO 3 − ] following NO 3 − ingestion declines during exercise, and muscle NO 3 − dynamics are associated with enhanced torque production during maximal intermittent muscle contractions.

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