Abstract

Recent evidence indicates that five minutes of breathing hypoxic gas elicits cutaneous vasodilation. However, it is unclear if skin blood flow is influenced by a brief hypoxic exposure. PURPOSE: We tested the hypothesis that cutaneous vasodilation is increased following a brief hypoxic exposure. METHODS: Seven healthy participants (2 women, 25 ± 2 years, BMI 26 ± 3 kg/m2) breathed 4–6 breaths of 100% nitrogen. We continuously measured skin blood flow on the ventral side of the forearm (laser Doppler), arterial oxygen saturation (finger pulse oximeter), mean arterial pressure (Finometer), and heart rate (ECG) at baseline and following the hypoxic exposure for one minute, during which data were analyzed in 15 s time bins. Skin blood flow was also normalized to mean arterial pressure (MAP) and expressed as a percentage of the local heating induced maximal cutaneous vascular conductance (%CVCmax). RESULTS: Arterial oxygen saturation was lower at 45 s (89 ± 7%; P < 0.05) and 60 s (90 ± 5%; P < 0.05) vs. baseline (97 ± 1%). Skin blood flow was lower 15 s after the hypoxic exposure when compared to baseline (4.2 ± 0.9 vs. 5.1 ± 0.9 PU, P = 0.001). MAP was greater at 15 s vs. baseline (94 ± 7 vs. 88 ± 7 mmHg; P < 0.05) and returned to baseline values at 30 s. %CVCmax was reduced within the first 15 s following the hypoxic exposure compared to baseline (4.3 ± 1.0 vs. 5.6 ± 1.2%; P < 0.05). Skin blood flow and %CVCmax returned to baseline values 30 s following the hypoxic exposure. Heart rate was significantly greater than baseline (64 ± 9 bpm) at 15 s (76 ± 13 bpm; P < 0.01), 30 s (76 ± 14 bpm; P < 0.01), 45 s (69 ± 11 bpm; P < 0.01), and 60 s (67 ± 11 bpm; P < 0.05). CONCLUSIONS: Contrary to our hypothesis, a brief hypoxic exposure induces cutaneous vasoconstriction and attenuates skin blood flow. This suggests that activation of the peripheral chemoreceptors acutely lowers skin blood flow.

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