Abstract

High frequency breathing (HF; >0.2 Hz) may limit the influence of respiration at the low frequency (LF; 0.07–0.2 Hz) where cerebrovascular control is assessed. We tested the hypotheses that: 1) LF breathing will increase, and HF breathing will decrease LF coherence (COH) between mean arterial pressure (MAP) and mean middle cerebral artery velocity (MCAvmean ); and 2) reductions of COH expected when subjects breathe at 0.25 Hz are due, in part, to reduced CO2 associated with faster breathing. We recorded ECG, finger arterial pressure (Finometer), MCAvmean (transcranial Doppler), respiratory rate, and end‐tidal CO2 in 20 volunteers (28 ± 2 yrs). Four 7‐min breathing protocols were followed: 1) spontaneous breathing (SB); 2) paced breathing at 0.1 Hz; 3) paced breathing at 0.25 Hz; and 4) paced breathing at 0.25 Hz with CO2 control (5% CO2 bled in continuously; 0.25 Hz C). LF COH was assessed between MCAvmean and MAP. End‐tidal CO2 was lower during 0.25 Hz breathing than all other conditions (P<0.05). COH was lower during 0.25 Hz breathing than both 0.1 Hz breathing and SB (P≤0.008). COH was indistinguishable during 0.25 Hz breathing with controlled and uncontrolled CO2 (P =0.299). Controlled breathing in the HF limits contributing influences of respiration on cerebrovascular control despite moderate reductions in end‐tidal CO2.

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