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The effects of two paradigms of intermittent hypoxia on human cardio-ventilatory responses and cerebral tissue oxygenation Foster, Glen Edward
The purpose of this study was to determine the ventilatory, cardiovascular, and cerebral tissue oxygen responses to two paradigms of normobaric, isocapnic, intermittent hypoxia (IH). Eighteen male subjects were randomly assigned to one of two IH groups; short duration IH (SDIH) was exposed to 5 minutes of 12% O₂ separated by 5 minutes of normoxia for one hour, and long duration IH (LDIH) was exposed to 30 minutes of 12% O₂. Both groups had 10 daily exposures over a twelve day period. The isocapnic hypoxic ventilatory response was measured before (preHVR) and after (postHVR) each daily exposure on day 1, 3, 5, 8, 10, 12 and again 3 and 5 days following the end o f IH. The hyperoxic hypercapnic ventilatory response (HCVR) was determined following rest on days 1, 12, 15, and 17. During all procedures, ventilation, beat-by-beat blood pressure, heart rate (HR) arterial oxyhemoglobin saturation (SaO₂), and cerebral tissue oxygenation (SCO₂) were measured. The preHVR increased throughout IH exposure regardless o f paradigm and returned to resting levels by day 17 (Day 1: 0.84 ± 0.50; Day 12: 1.20 ± 1.01; Day 17: 0.95 ± 0.58 1 min⁻¹ %SaO₂⁻¹; p= 0.002). The H C V R did not change throughout IH. The postHVR was blunted compared with the preHVR (p= 0.02). There were no differences in the change in systolic blood pressure sensitivity (ΔSBP/ΔSaO₂), diastolic blood pressure sensitivity (ΔDBP/ΔSaO₂), heart rate sensitivity (ΔHR/ΔSaO₂), cardiac output sensitivity (ΔCO/ΔSaO₂), stroke volume sensitivity (ΔSV/ΔSaO₂), and total peripheral resistance sensitivity (ΔTPR/ΔSaO₂) to hypoxia following IH. The change in cerebral tissue oxygen saturation sensitivity to hypoxia (ΔScO₂/ΔSaO₂) was less on day 12 (Day 1: -0.51 ± 0.13; Day 12: -0.64 ± 0.181 p= 0.0002) and the change in cerebral tissue deoxyhemoglobin concentration (ΔHHb/ΔSaO₂) was more on day 12 (Day 1: 0.34 ± 0.21; Day 12: 0.44 ± 0.14 uM %SaO₂⁻¹; p= 0.007). These differences had returned to baseline by day 17. Acute exposure to SDIH increased mean arterial pressure (MAP; p= 0.005) but LDIH did not (p>0.05). Intermittent hypoxia did not improve exercise ventilatory efficiency during exercise. In conclusion, exposures to SDIH and LDIH have similar effects on the ventilatory, cardiovascular, and cerebral oxygen responses to acute progressive hypoxia. However, acute exposure to SDIH increases MAP while LDIH does not.
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