Effect of dietary nitrate on skeletal muscle energetics in normoxia and hypoxia

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Hypoxia is associated with a reduction in the maximal oxidative metabolic rate of skeletal muscle which is reflected in a slowing of muscle phosphocreatine (PCr) recovery kinetics following exercise. For the same metabolic rate, there is a greater muscle metabolic perturbation (e.g., greater fall in [PCr]) during exercise performed in hypoxia compared to normoxia. Nitric oxide (NO) is a key signalling molecule for hypoxic vasodilatation and it also modulates mitochondrial O2 consumption. Dietary nitrate intake, which increases NO bioavailability, might therefore improve O2 delivery to active muscle and reduce O2 demand during hypoxic exercise. It has been shown that nitrate supplementation lessens muscle metabolic perturbation during high-intensity exercise and considerably enhances exercise tolerance in moderate hypoxia. Nitrate supplementation has also been shown to abolish the reduction in the rate of PCr recovery which is typically observed in hypoxia, indicating enhanced muscle oxygenation and a restoration of muscle oxidative function. Further research is warranted to identify to what extent these effects can be attributed to changes in muscle energy metabolism and/or improved O2 delivery. These findings indicate that dietary nitrate supplementation may have important therapeutic applications for improving skeletal muscle energetics and functional capacity in conditions where muscle O2 delivery is compromised.