Purpose: The aim of this study was to verify the acute effects of hypoxic high intensity interval exercise (HIIE) on blood pressure (BP) responses. Methods: Ten healthy male volunteers (23.70 ± 1.06 years old; 67.37 ± 5.91 kg, and 173.45 ± 5.26 cm) participated and undertook the four random exercise trials: rest in hypoxia (RH), rest in normoxia (RN), normoxic HIIE (NH), and hypoxic HIIE (HH). Subjects were required to undergo a resting period on a chair for approximately five minutes before each of the four trials started. For RH and RN trials, another five-minute of resting period was required during the test; while for NH and HH trials, participants performed a five-minute test of HIIE, which consisted of two 30-second bouts of sprint with a 7.5% of body mass load separated by four minutes of recovery. Hypoxia was set to 2500 m. Systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), heart rate (HR), stroke volume (SV), cardiac output (CO) and total peripheral resistance (TPR) were evaluated before, during and 30 min after each trial. Results: SBP during HIIE ranged from 148 ± 14 to 209 ± 26 mmHg in NH trial and from 151 ± 12 to 206 ± 15 in HH trial. Both HH and NH led to post-exercise hypotension (PEH) during the post-test 30 minutes in trials compared with RN trial, but the decrease magnitude of SBP, DBP and MAP did not reach significant trial iii differences (p > .05). Significant decrease in SBP was only found in HH trial, and the duration of PEH in HH was longer than that in NH during the 30-minute post-test observation. Moreover, the area under the curve (AUC) of DBP in HH trial (-230 ± 142 mmHg*min) was significantly (p < .05) higher than that in NH trial (-187 ± 153 mmHg*min). During the 30-minute post-test observation, CO and HR both increased significantly (p < .05), SV remained unchanged (p > .05), and TPR decreased significantly (p < .05) along with PEH in NH and HH trial. Weight, height, BMI, and fat of the subjects significantly influenced the AUC of SBP in HH trial (R 2 = 0.777, F = 8.852, p = 0.017). Conclusion: HIIE can lead to PEH in both normoxic and hypoxic environment, while hypoxia strengthens this effect. Additionally, PEH is produced by larger reduction in TPR, which offsets the increase in CO. The fat mass may predict the change of SBP in HIIE in moderate hypoxia.