Donald C. McKenzie

Effects of two protocols of intermittent hypoxia on human ventilatory, cardiovascular and cerebral responses to hypoxia

We determined the ventilatory, cardiovascular and cerebral tissue oxygen response to two protocols of normobaric, isocapnic, intermittent hypoxia. Subjects (n= 18, male) were randomly assigned to short‐duration intermittent hypoxia (SDIH, 12% O2 separated by 5 min of normoxia for 1 h) or long‐duration intermittent hypoxia (LDIH, 30 min of 12% O2). Both groups had 10 exposures over a 12 day period. The hypoxic ventilatory response (HVR) was measured before each daily intermittent hypoxia exposure on days 1, 3, 5, 8, 10 and 12. The HVR was measured again 3 and 5 days after the end of intermittent hypoxia. During all procedures, ventilation, blood pressure, heart rate, arterial oxyhaemoglobin saturation and cerebral tissue oxygen saturation were measured. The HVR increased throughout intermittent hypoxia exposure regardless of protocol, and returned to baseline by day 17 (day 1, 0.84 ± 0.50; day 12, 1.20 ± 1.01; day 17, 0.95 ± 0.58 l min−1%SaO2−1; P < 0.01). The change in systolic blood pressure sensitivity (r=+0.68; P < 0.05) and the change in diastolic blood pressure sensitivity (r=+0.73; P < 0.05) were related to the change in HVR, while the change in heart rate sensitivity was not (r=+0.32; NS). The change in cerebral tissue oxygen saturation sensitivity to hypoxia was less on day 12, and returned to baseline by day 17 (day 1, −0.51 ± 0.13; day 12, −0.64 ± 0.18; day 17, −0.51 ± 0.13; P < 0.001). Acute exposure to SDIH increased mean arterial pressure (+5 mmHg; P < 0.01), but LDIH did not (P > 0.05). SDIH and LDIH had similar effects on the ventilatory and cardiovascular response to acute progressive hypoxia and hindered cerebral oxygenation. Our findings indicate that the vascular processes required to control blood flow and oxygen supply to cerebral tissue in a healthy human are hindered following exposure to 12 days of isocapnic intermittent hypoxia.

Exercise‐induced arterial hypoxaemia and the mechanics of breathing in healthy young women

•u2002 By virtue of their smaller lung volumes and airway diameters, women develop more mechanical ventilatory constraints during exercise, which may result in increased vulnerability to hypoxaemia during exercise. •u2002 Hypoxaemia developed at all exercise intensities with varying patterns and was more common in aerobically trained subjects; however, some untrained women also developed hypoxaemia. •u2002 Mechanical respiratory constraints directly lead to hypoxaemia in some women and prevent adequate reversal of hypoxaemia in most women. •u2002 Experimentally reversing mechanical constraints with heliox gas partially reversed the hypoxaemia in subjects who developed expiratory flow limitation. •u2002 Due in part to increased mechanical ventilatory constraints, the respiratory systems response to exercise is less than ideal in most women.