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Free Radic Biol Med. 2019 Jul 29;143:252-259. doi: 10.1016/j.freeradbiomed.2019.07.035. [Epub ahead of print]

Post-exercise hypotension and skeletal muscle oxygenation is regulated by nitrate-reducing activity of oral bacteria.

Author information

1
Institute of Health & Community, University of Plymouth, Plymouth, UK.
2
Peninsula Medical School, University of Plymouth, Plymouth, UK.
3
Centre for Genomic Regulation (CRG), The Barcelona Institute of Science & Technology, Barcelona, Spain.
4
Research Group on Community Nutrition and Oxidative Stress, University of Balearic Islands & CIBEROBN (CB12/03/30038), Palma de Mallorca, Spain.
5
Centre for Genomic Regulation (CRG), The Barcelona Institute of Science & Technology, Barcelona, Spain; Universitat Pompeu Fabra (UPF), Barcelona, Spain; Institució Catalana de Recerca I Estudis Avançats (ICREA), Barcelona, Spain.
6
Institute of Health & Community, University of Plymouth, Plymouth, UK. Electronic address: Raul.Bescos@plymouth.ac.uk.

Abstract

Post-exercise hypotension (PEH) is a common physiological phenomenon leading to lower blood pressure after acute exercise, but it is not fully understood how this intriguing response occurs. This study investigated whether the nitrate-reducing activity of oral bacteria is a key mechanism to trigger PEH. Following a randomized, double blind and crossover design, twenty-three healthy individuals (15 males/8 females) completed two treadmill trials at moderate intensity. After exercise, participants rinsed their mouth with antibacterial mouthwash to inhibit the activity of oral bacteria or a placebo mouthwash. Blood pressure was measured before, 1h and 2 h after exercise. The microvascular response to a reactive hyperaemia test, as well as blood and salivary samples were taken before and 2 h after exercise to analyse nitrate and nitrite concentrations and the oral microbiome. As expected, systolic blood pressure (SBP) was lower (1 h: -5.2 ± 1.0 mmHg; P < 0.001); 2 h: -3.8 ± 1.1 mmHg, P = 0.005) after exercise compared to baseline in the placebo condition. This was accompanied by an increase of circulatory nitrite 2 h after exercise (2h: 100 ± 13 nM) compared to baseline (59 ± 9 nM; P = 0.013). Additionally, an increase in the peak of the tissue oxygenation index (TOI) during the reactive hyperaemia response was observed after exercise (86.1 ± 0.6%) compared to baseline levels (84.8 ± 0.5%; P = 0.010) in the placebo condition. On the other hand, the SBP-lowering effect of exercise was attenuated by 61% at 1 h in the recovery period, and it was fully attenuated 2 h after exercise with antibacterial mouthwash. This was associated with a lack of changes in circulatory nitrite (P > 0.05), and impaired microvascular response (peak TOI baseline: 85.1 ± 3.1%; peak TOI post-exercise: 84.6 ± 3.2%; P > 0.05). Diversity of oral bacteria did not change after exercise in any treatment. These findings show that nitrite synthesis by oral commensal bacteria is a key mechanism to induce the vascular response to exercise over the first period of recovery thereby promoting lower blood pressure and greater muscle oxygenation.

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