Abstract
What is the central question of this study? Does the ventilatory response to moderate acute hypoxia increase cerebral perfusion independently of changes in arterial oxygen tension in humans? What is the main finding and its importance? The ventilatory response does not increase middle cerebral artery mean blood velocity during moderate isocapnic acute hypoxia beyond that elicited by reduced oxygen saturation. Hypoxia induces ventilatory, cardiovascular and cerebrovascular adjustments to defend against reductions in systemic oxygen delivery. We aimed to determine whether the ventilatory response to moderate acute hypoxia increases cerebral perfusion independently of changes in arterial oxygenation. Eleven young healthy individuals were exposed to four 15min experimental conditions: (1) normoxia (partial pressure of end-tidal oxygen, =100mmHg), (2) hypoxia ( =50mmHg), (3) normoxia with breathing volitionally matched to levels observed during hypoxia (hyperpnoea; =100mmHg) and (4) hypoxia ( =50mmHg) with respiratory frequency and tidal volume volitionally matched to levels observed during normoxia (i.e., restricted breathing (RB)). Isocapnia was maintained in all conditions. Middle cerebral artery mean blood velocity (MCA Vmean ), assessed by transcranial Doppler ultrasound, was increased during hypoxia (58±12cm/s, P=0.04) and hypoxia + RB (61±14cm/s, P<0.001) compared to normoxia (55±11cm/s), while it was unchanged during hyperpnoea (52±13cm/s, P=0.08). MCA Vmean was not different between hypoxia and hypoxia + RB (P>0.05). These findings suggest that the hypoxic ventilatory response does not increase cerebral perfusion, indexed using MCA Vmean , during moderate isocapnic acute hypoxia beyond that elicited by reduced oxygen saturation.
Highlights
Hypoxia induces ventilatory, cardiovascular and cerebrovascular adjustments to defend against reductions in convective oxygen delivery to organs such as the heart, brain and kidneys (Guyenet, 2000, 2014; Marshall, 1994)
Eleven young healthy individuals were exposed to four 15 min experimental conditions: (1) normoxia, (2) hypoxia (PETO2 = 50 mmHg), (3) normoxia with breathing volitionally matched to levels observed during hypoxia and (4) hypoxia (PETO2 = 50 mmHg) with respiratory frequency and tidal volume volitionally matched to levels observed during normoxia (i.e., restricted breathing (RB))
SpO2 was lower during hypoxic conditions (Hypoxia 87 ± 2%; Hypoxia + RB 85 ± 1%) than normoxic conditions (Normoxia 98 ± 1%; Hyperpnoea 98 ± 1%; P < 0.001), but no main effect of breathing or interaction was observed
Summary
Cardiovascular and cerebrovascular adjustments to defend against reductions in convective oxygen delivery to organs such as the heart, brain and kidneys (Guyenet, 2000, 2014; Marshall, 1994). Isocapnic hypoxia increases internal carotid and vertebral artery blood flows (Ogoh et al, 2013), along with middle cerebral artery mean blood velocity (MCA Vmean) (Willie et al, 2012). The breathing changes that occur in hypoxia lead to changes in ventilation efficiency, blood oxygenation, systemic and pulmonary pressure (Bilo et al, 2012) – all with the potential to increase cerebral blood flow (Willie et al, 2014). The partial pressure of end-tidal CO2 (PETCO2 ) was higher during the restricted breathing condition, potentially confounding the results It remains unclear whether ventilation independently modulates the cerebrovascular response to acute hypoxia
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