The influence of controlled breathing on cerebrovascular control

Arterial pressures oscillate with the frequency of respiration, and these oscillations are translated directly to the cerebrovasculature. For this reason, intrinsic cerebrovascular control is assessed at the low frequency (LF; 0.07- 0.2 Hz). When humans breathe at a high frequency (HF; >0.2 Hz) it is possible that respiratory influence on these non-respiratory rhythms could be eliminated, thereby allowing the interpretation of intrinsic cerebrovascular control. Additionally, the impact of variations in carbon dioxide (CO©ü) occurring during HF breathing has not been explained, and could be a primary factor of improved interpretation of control; that is, if such is exhibited during HF breathing. The purpose of this study is two-fold: 1) to test the hypothesis that LF breathing will increase, and HF breathing will decrease LF coherence (COH) between mean arterial pressure (MAP) and middle cerebral artery velocity (MCAvmean); and 2) to test the hypothesis that reductions of COH expected when subjects breathe at 0.25 Hz are due, in part, to hyperventilation associated with faster breathing. We recorded ECG, finger arterial pressure (Finometer), transcranial Doppler ultrasound of the MCA, pneumobelt tracings and end-tidal CO©ü in 20 healthy volunteers (28 ¡¾ 2 yrs). All subjects breathed in time to a digital tracing displayed on a laptop monitor while in a seated position. Three breathing protocols were followed: 1) spontaneous breathing (SB); 2) fixed-frequency breathing at 6 breaths/minutes (0.1 Hz); 3) fixed-frequency breathing at 15 breaths/minutes (0.25 Hz); and 4) fixed-frequency breathing at 15 breaths/minute with CO2 control (5% CO2 bled in continuously; 0.25 Hz C). Each breathing frequency was maintained for seven minutes with two minute intermissions. Reliance of MCAvmean on MAP was assessed over the LF with cross-spectral COH analysis. End-tidal CO©ü was not different between SB and CB 0.25 Hz C (P =0.491). COH was lower during 0.25 Hz breathing compared to both LF breathing and SB (P ¡Â0.035). COH was indistinguishable during HF breathing with controlled and uncontrolled CO©ü (P =0.299). Slow, deep breaths occurring at the LF could cause underestimated cerebrovascular control. Therefore, in the clinical and research setting where cerebrovascular control is most commonly assessed, controlled breathing outside the LF range could eliminate confounding results despite associated hyperventilation.