Dietary nitrate (NO3–) supplementation increases systemic nitric oxide (NO) bioavailability, and can reduce the oxygen cost of submaximal exercise and enhance exercise tolerance. However, the influence of dietary NO3– supplementation on the efficiency of mitochondrial respiration is unclear. Purpose: To investigate the effects of acute and chronic dietary NO3– ingestion on mitochondrial respiration in young healthy adults. Methods: Using a randomized, double-blind crossover design, 8 participants (6 males: 27 ± 7 years, 2 females: 23 ± 1 years) consumed NO3– rich beetroot juice (BR) (~12.8 mmol NO3–) and NO3– depleted placebo beetroot juice (PL) (~0.08 mmol NO3–) acutely and then chronically every day for 2 weeks, separated by at least 1-week washout period. Skeletal muscle samples were collected from vastus lateralis at 3 h following supplement ingestion on day 1 and day 14. 2-3 mg permeabilized muscle fibres, 2 ml mitochondrial respiration medium, and 25 ml oxygen were added to a two-channel, high-resolution Oroboros Oxygraph-2K (Oroboros, Oxygraphy, Innsbruk, Austria) prior to analysis. Glutamate and malate, Adenosine 5’-diphosphate (ADP), cytochrome c, succinate, carbonyl cyanide 4 phenylhydrazone (FCCP), rotenone and antimycin A were injected to measure leak respiration, maximal oxidative phosphorylation (OXPHOS) and uncoupled electron transfer capacity. The OXPHOS-leak control efficiency (P-L control efficiency) was calculated as the 1-leak respiration/OXPHOS (1-L/P). Two-way repeated ANOVA was used to assess the differences in mitochondrial respiration between groups (PL vs BR) and across time (acute vs chronic). Results: There were no significant differences in leak respiration (acute PL: 7.17 ± 1.21 pmol O2 mg-1 sec-1, acute BR: 6.99 ± 1.48 pmol O2 mg-1 sec-1, P=0.75; chronic PL: 8.72 ± 3.70 pmol O2 mg-1 sec-1, chronic BR: 8.02 ± 2.28 pmol O2 mg-1 sec-1, P=0.65) and P-L control efficiency (acute PL: 0.83 ± 0.05, acute BR: 0.84 ± 0.05, P=0.76; chronic PL: 0.83 ± 0.05, chronic BR: 0.86 ± 0.04, P=0.26) between BR and PL ingestion. Similarly, no differences in maximal OXPHOS (acute PL: 46.89 ± 16.63 pmol O2 mg-1 sec-1, acute BR: 46.19 ± 11.51 pmol O2 mg-1 sec-1, P=0.86; chronic PL: 54.02 ± 20.40 pmol O2 mg-1 sec-1, chronic BR: 59.63 ± 22.40 pmol O2 mg-1 sec-1, P=0.52) and uncoupled electron transfer capacity (acute PL: 56.04 ± 15.85 pmol O2 mg-1 sec-1, acute BR: 59.34 ± 10.85 pmol O2 mg-1 sec-1, P=0.44; chronic PL: 64.51 ± 19.63 pmol O2 mg-1 sec-1, chronic BR: 70.08 ± 24.23 pmol O2 mg-1 sec-1, P=0.61) were found between BR and PL supplementation. Conclusion: Neither acute nor chronic dietary NO3– ingestion improved mitochondrial respiration in young healthy adults. These results indicate that the lower oxygen cost of submaximal exercise that has been reported previously following dietary NO3– ingestion is not related to enhanced mitochondrial respiration efficiency.
Dietary Manipulations for Health and in the Prevention and Management of Disease (Manchester Metropolitan University, UK) (2024) Proc Physiol Soc 56, C07
Oral Communications: No effect of dietary nitrate supplementation on mitochondrial respiration in young healthy adults
Chenguang Wei1, Anni Vanhatalo1, Jamie R Blackwell1, Matthew I Black1, Nicolas Place1, Andrew M Jones1,
1University of Exeter Exeter United Kingdom, 2University of Lausanne Lausanne Switzerland,
View other abstracts by:
Where applicable, experiments conform with Society ethical requirements.