Dietary nitrate accelerates postexercise muscle metabolic recovery and O2 delivery in hypoxia.

We tested the hypothesis that the time constants (τ) of postexercise T2* MRI signal intensity (an index of O2 delivery) and muscle [PCr] (an index of metabolic perturbation, measured by (31)P-MRS) in hypoxia would be accelerated after dietary nitrate (NO3 (-)) supplementation. In a double-blind crossover design, eight moderately trained subjects underwent 5 days of NO3 (-) (beetroot juice, BR; 8.2 mmol/day NO3 (-)) and placebo (PL; 0.003 mmol/day NO3 (-)) supplementation in four conditions: normoxic PL (N-PL), hypoxic PL (H-PL; 13% O2), normoxic NO3 (-) (N-BR), and hypoxic NO3 (-) (H-BR). The single-leg knee-extension protocol consisted of 10 min of steady-state exercise and 24 s of high-intensity exercise. The [PCr] recovery τ was greater in H-PL (30 ± 4 s) than H-BR (22 ± 4 s), N-PL (24 ± 4 s) and N-BR (22 ± 4 s) (P < 0.05) and the maximal rate of mitochondrial ATP resynthesis (Qmax) was lower in the H-PL (1.12 ± 0.16 mM/s) compared with H-BR (1.35 ± 0.26 mM/s), N-PL (1.47 ± 0.28 mM/s), and N-BR (1.40 ± 0.21 mM/s) (P < 0.05). The τ of postexercise T2* signal intensity was greater in H-PL (47 ± 14 s) than H-BR (32 ± 10 s), N-PL (38 ± 9 s), and N-BR (27 ± 6 s) (P < 0.05). The postexercise [PCr] and T2* recovery τ were correlated in hypoxia (r = 0.60; P < 0.05), but not in normoxia (r = 0.28; P > 0.05). These findings suggest that the NO3 (-)-NO2 (-)-NO pathway is a significant modulator of muscle energetics and O2 delivery during hypoxic exercise and subsequent recovery.