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

We tested the hypothesis that the time constants (tau) of postexercise T2* MRI signal intensity (an index of O-2 delivery) and muscle [PCr] (an index of metabolic perturbation, measured by P-31-MRS) in hypoxia would be accelerated after dietary nitrate (NO3-) supplementation. In a doubleblind 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% O-2), 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 tau 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 (Q(max)) 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 tau 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 tau 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 O-2 delivery during hypoxic exercise and subsequent recovery.