ABSTRACT
NEW FINDINGS: 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. ABSTRACT: 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 15 min experimental conditions: (1) normoxia (partial pressure of end-tidal oxygen, PETO2 = 100 mmHg), (2) hypoxia ( PETO2 = 50 mmHg), (3) normoxia with breathing volitionally matched to levels observed during hypoxia (hyperpnoea; PETO2 = 100 mmHg) and (4) hypoxia ( PETO2 = 50 mmHg) 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 ± 12 cm/s, P = 0.04) and hypoxia + RB (61 ± 14 cm/s, P < 0.001) compared to normoxia (55 ± 11 cm/s), while it was unchanged during hyperpnoea (52 ± 13 cm/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.
Subject(s)
Cerebrovascular Circulation , Middle Cerebral Artery , Blood Flow Velocity , Cerebrovascular Circulation/physiology , Humans , Hypoxia , Oxygen , RespirationABSTRACT
NEW FINDINGS: What is the central question of this study? Does facial cooling-mediated stimulation of cutaneous trigeminal afferents associated with the diving response increase cerebral blood flow or are factors associated with breath-holding (e.g. arterial carbon dioxide accumulation, pressor response) more important in humans? What is the main finding and its importance? Physiological factors associated with breath-holding such as arterial carbon dioxide accumulation and the pressor response, but not facial cooling (trigeminal nerve stimulation), make the predominant contribution to diving response-mediated increases in cerebral blood flow in humans. ABSTRACT: Diving evokes a pattern of physiological responses purported to preserve oxygenated blood delivery to vital organs such as the brain. We sought to uncouple the effects of trigeminal nerve stimulation on cerebral blood flow (CBF) from other modifiers associated with the diving response, such as apnoea and changes in arterial carbon dioxide tension. Thirty-seven young healthy individuals participated in separate trials of facial cooling (FC, 3 min) and cold pressor test (CPT, 3 min) under poikilocapnic (Protocol 1) and isocapnic conditions (Protocol 2), facial cooling while either performing a breath-hold (FC +BH) or breathing spontaneously for a matched duration (FC -BH) (Protocol 3), and BH during facial cooling (BH +FC) or without facial cooling (BH -FC) (Protocol 4). Under poikilocapnic conditions neither facial cooling nor CPT evoked a change in middle cerebral artery blood flow velocity (MCA vmean ; transcranial Doppler) (P > 0.05 vs. baseline). Under isocapnic conditions, facial cooling did not change MCA vmean (P > 0.05), whereas CPT increased MCA vmean by 13% (P < 0.05). Facial cooling with a concurrent BH markedly increased MCA vmean (Δ23%) and internal carotid artery blood flow (ICAQ ; duplex Doppler ultrasound) (Δ26%) (P < 0.001), but no change in MCA vmean and ICAQ was observed when facial cooling was accompanied by spontaneous breathing (P > 0.05). Finally, MCA vmean and ICAQ were similarly increased by BH either with or without facial cooling. These findings suggest that physiological factors associated with BH, and not facial cooling (i.e. trigeminal nerve stimulation) per se, make the predominant contribution to increases in CBF during diving in humans.
