Human cerebrovascular responses to diving are not related to facial cooling.

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.