Sodium nitrate ingestion increases skeletal muscle nitrate content in humans

Nitrate (NO₃^-) ingestion has been shown to have vasoactive and ergogenic effects that have been attributed to increased nitric oxide (NO) production. Recent observations in rodents suggest skeletal muscle tissue to serve as an endogenous NO₃^- "reservoir". The current study determined NO₃^- contents in human skeletal muscle tissue in a post-absorptive state, and following ingestion of a sodium nitrate bolus (NaNO3). Seventeen male, type 2 diabetes patients (age 72±1 y; BMI 26.5±0.5 m·kg^-2) were randomized to ingest a dose of NaNO3 (NIT; 9.3 mg NO₃^- per kg bodyweight) or placebo (PLA; 8.8 mg NaCl per kg bodyweight). Blood and muscle biopsy samples were taken before and up to 7 h following NO₃^- or placebo ingestion to assess NO₃^- (and plasma nitrite (NO₂^-)) concentrations. Additionally, basal plasma and muscle NO₃^- concentrations were assessed in 10 healthy young (CON-Y: age 21±1 y) and 10 healthy older (CON-O: age 75±1 y) control subjects. In all groups, baseline NO₃^- concentrations were higher in muscle (NIT: 57±7, PLA: 61±7, CON-Y: 80±10, CON-O: 54±6 µmol·L^-1) than in plasma (NIT: 35±3, PLA: 32±3, CON-Y: 38±3, CON-O: 33±3 µmol·L^-1;P≤0.011). Ingestion of NaNO3 resulted in a sustained increase in plasma NO₃^-, plasma NO₂^-, and muscle NO₃^- concentrations (up to 185±25 µmol·L^-1) in the NIT group (time effect P<0.001), when compared with PLA (treatment effect P<0.05). In conclusion, basal NO₃^- concentrations are substantially higher in human skeletal muscle tissue when compared with plasma. Ingestion of a bolus of dietary NO₃^- increases both plasma and muscle NO₃^- contents in humans.

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