Whitfield, J., Ludzki, A., Heigenhauser, G. J, Senden, J. M, Verdijk, L. B, van Loon, L. J, Spriet, L. L & Holloway, GP. (2016). Beetroot juice supplementation reduces whole body oxygen consumption but does not improve indices of mitochondrial efficiency in human skeletal muscle. Journal of Physiology,594(2), 421-435. United Kingdom: Wiley-Blackwell Publishing Ltd.. Retrieved from https://doi.org/10.1113/JP270844
Ingestion 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.
Mary MacKillop Institute for Health Research
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