Post-Exercise Hypotension (PEH) is a common physiological response leading to lower blood pressure during the recovery period after an acute bout of exercise. However, the mechanism triggering PEH is still not fully understood. Here, we investigated whether oral nitrite synthesis during the recovery period is a key mechanism inducing PEH in healthy individuals. Twenty-three individuals participated in this randomized, double-blind and crossover study. They performed two treadmill trials, separated by a week running four sets of 7 min at 65% of VO2peak interspersed with 3 minutes of passive recovery. At 1, 30, 60 and 90 minutes after exercise, participants rinsed their mouth for 1 minute with antibacterial mouthwash to inhibit activity of oral bacteria, or a placebo mouthwash. Blood pressure was measured before, 1 and 2 hours after exercise. The microvascular response was assessed measuring the tissue oxygen index (TOI) in the forearm (extensor digitorum) before and 2 hours post-exercise as determined by near-infrared spectroscopy (NIRS). TOI levels from the rectus femoris were also measured at the same time using a second NIRS channel. Saliva and blood samples were also taken before and 2 hours after exercise. Exercise induced a significant reduction of systolic blood pressure (SBP) (1h: -5.2 ± 5.0 mmHg, P < 0.001; 2h: -3.8 ± 5.3 mmHg, P = 0.005) compared to baseline in the placebo condition. Similarly, diastolic blood pressure (DBP) fall in the first hour of recovery (1h: -2.4 ± 3.4 mmHg; P = 0.004), but not at 2 hours in the placebo treatment (2h: -0.9 ± 3.3 mmHg; P = 0.167) compared to baseline levels. These changes were associated with higher plasma nitrite availability (pre-exercise: 59 ± 34.3 nM; 2h post-exercise: 100 ± 50 nM, P = 0.013) and a greater peak of TOI following the occlusion period of reactive hyperamia (+1.2 ± 2.0 %, P = 0.010) after exercise in the placebo condition. Average TOI values from the rectus femoris were also higher after exercise (77.7 ± 5.8%) compared to baseline (74.2 ± 5.6%, P < 0.001). Antibacterial mouthwash reduced significantly nitrite availability in saliva (P < 0.001) and plasma (P < 0.001) compared to placebo. Consequently, reduction of SBP was attenuated by 61% at 1h (+ 2.4 ± 4.6 mmHg, P = 0.021) and fully inhibited at 2h (+ 4.1 ± 4.6 mmHg, P = 0.026) after exercise. A similar response was observed in DBP as its reduction was attenuated by 29% at 1h and fully inhibited at 2h after exercise in the antibacterial mouthwash treatment compared to placebo, but differences between treatments were not stastistically different (P > 0.05). TOI levels in the forearm (reactive hyperamia test) and leg did not differ (P > 0.05) after exercise compared to baseline when oral bacteria was inhibited with actibacterial mouthwash. Nitrate-reducing activity of oral bacteria is a key regulator of PEH and skeletal muscle oxygenation, and this response is disabled by using antibacterial mouthwash in healthy individuals.