Beetroot juice supplementation reduces whole body oxygen consumption but does not improve indices of mitochondrial efficiency in human skeletal muscle
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Key pointsOral consumption of nitrate (NO3−) in beetroot juice has been shown to decrease the oxygen cost of submaximal exercise; however, the mechanism of action remains unresolved.We supplemented recreationally active males with beetroot juice to determine if this altered mitochondrial bioenergetics.Despite reduced submaximal exercise oxygen consumption, measures of mitochondrial coupling and respiratory efficiency were not altered in muscle.In contrast, rates of mitochondrial hydrogen peroxide (H2O2) emission were increased in the absence of markers of lipid or protein oxidative damage.These results suggest that improvements in mitochondrial oxidative metabolism are not the cause of beetroot juice‐mediated improvements in whole body oxygen consumption.AbstractIngestion of sodium nitrate (NO3−) simultaneously reduces whole body oxygen consumption () during submaximal exercise while improving mitochondrial efficiency, suggesting a causal link. Consumption of beetroot juice (BRJ) elicits similar decreases in but potential effects on the mitochondria remain unknown. Therefore we examined the effects of 7‐day supplementation with BRJ (280 ml day−1, ∼26 mmol NO3−) in young active males (n = 10) who had muscle biopsies taken before and after supplementation for assessments of mitochondrial bioenergetics. Subjects performed 20 min of cycling (10 min at 50% and 70% ) 48 h before ‘Pre’ (baseline) and ‘Post’ (day 5 of supplementation) biopsies. Whole body decreased (P < 0.05) by ∼3% at 70% following supplementation. Mitochondrial respiration in permeabilized muscle fibres showed no change in leak respiration, the content of proteins associated with uncoupling (UCP3, ANT1, ANT2), maximal substrate‐supported respiration, or ADP sensitivity (apparent Km). In addition, isolated subsarcolemmal and intermyofibrillar mitochondria showed unaltered assessments of mitochondrial efficiency, including ADP consumed/oxygen consumed (P/O ratio), respiratory control ratios and membrane potential determined fluorometrically using Safranine‐O. In contrast, rates of mitochondrial hydrogen peroxide (H2O2) emission were increased following BRJ. Therefore, in contrast to sodium nitrate, BRJ supplementation does not alter key parameters of mitochondrial efficiency. This occurred despite a decrease in exercise , suggesting that the ergogenic effects of BRJ ingestion are not due to a change in mitochondrial coupling or efficiency. It remains to be determined if increased mitochondrial H2O2 contributes to this response.
