Abstract
Inorganic nitrate is present at high levels in beetroot and celery, and in green leafy vegetables such as spinach and lettuce. Though long believed inert, nitrate can be reduced to nitrite in the human mouth and, further, under hypoxia and/or low pH, to nitric oxide. Dietary nitrate has thus been associated favorably with nitric-oxide-regulated processes including blood flow and energy metabolism. Indeed, the therapeutic potential of dietary nitrate in cardiovascular disease and metabolic syndrome—both aging-related medical disorders—has attracted considerable recent research interest. We and others have shown that dietary nitrate supplementation lowers the oxygen cost of human exercise, as less respiratory activity appears to be required for a set rate of skeletal muscle work. This striking observation predicts that nitrate benefits the energy metabolism of human muscle, increasing the efficiency of either mitochondrial ATP synthesis and/or of cellular ATP-consuming processes. In this mini-review, we evaluate experimental support for the dietary nitrate effects on muscle bioenergetics and we critically discuss the likelihood of nitric oxide as the molecular mediator of such effects.
Highlights
Inorganic nitrate (NO−3 ) has long been considered an undesirable food component and pollutant of drinking water as nitrosation of secondary amines may produce carcinogenic N-nitrosamines (Magee and Barnes, 1956)
Consistent with this, nitric oxide (NO)−3 benefit on V pulmonary oxygen uptake (O2) adjustment following the onset of exercise and on tolerance to high-intensity exercise is relatively large when the contribution of type II muscle fibers to force production is increased in human skeletal muscle (Breese et al, 2013; Bailey et al, 2015)
Dietary NO−3 benefits on the O2 cost of exercise likely arise from increased efficiency of ATP synthesis and/or of skeletal muscle work (Figure 1)
Summary
Inorganic nitrate (NO−3 ) has long been considered an undesirable food component and pollutant of drinking water as nitrosation of secondary amines may produce carcinogenic N-nitrosamines (Magee and Barnes, 1956). It has recently been found that dietary NO−3 lowers the O2 cost of human exercise as less respiratory activity is required for a set rate of skeletal muscle work (Larsen et al, 2007, 2010; Bailey et al, 2009, 2010) This finding is interesting as it challenges exercise physiology dogma that the steady-state O2 consumption for any individual is immutable at a given sub-maximal workload irrespective of age, fitness, diet, or pharmacological intervention (Poole and Richardson, 1997). This mini-review aims to evaluate the mechanistic understanding of NO−3 effects on skeletal muscle function. Acute (2.5 h post-ingestion) lowering of TABLE 1 | Dietary nitrate improves the economy and/or performance of human locomotion
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