INTRODUCTION:
Hypoxic conditions are known to alter cerebrovascular and cardiovascular physiology. While the factors that facilitate cerebral autoregulation are not completely understood, it is thought to involve cardiac, myogenic, neural, endothelial, and metabolic factors. Some research suggests that acute hypoxia does influence cerebral autoregulatory mechanisms shown by increases in the very-low-frequency cerebral blood flow oscillations at 15% O2, and other research has shown that cerebrovascular neurogenic activity and sympathoexcitatory pathways maintain cerebral blood flow velocity (CBFV) in hypoxia. However, limited research is available to show cerebral haemodynamic (oxygenation) changes. This study was conducted to observe cerebrovascular and cardiovascular responses during repeated squat-stands in normoxia and normobaric hypoxia to assess cerebral autoregulation.
METHODS:
Healthy participants had a near-infrared spectroscopy (NIRS) device fitted over the right prefrontal cortex to measure oxyhemoglobin (HbO2), total hemoglobin (tHb), and hemoglobin difference (HbD) concentrations. A near‐infrared transillumination‐backscattering sounding (NIRT) device was placed over the left prefrontal cortex to measure subarachnoid space width (SASLeft). Blood pressure was collected using finger photoplethysmography. Thirty-one participants (3 females, age = 31 ± 13 years, Body Mass Index = 24 ± 2 kg/m2) completed 30 minutes of supine rest followed by 5 minutes of repeated squat-stands (0.05 Hz) under normoxic (577 m, 711 mmHg) conditions prior to moving inside a normobaric hypoxic (2750 m, 14.8% O2) environmental chamber and repeating the protocol. Wavelet transformations were used to analyze the amplitudes and phase coherence of the simultaneously collected signals.
RESULTS:
Significant decreases were found for the HbO2 (0.0139±0.0087 vs 0.0209±0.0096 1/s), tHb (0.0159±0.0093 vs 0.0229±0.0133 1/s), and HbD (0.0119±0.0084 vs 0.0164±0.0091 1/s) (p<0.01) wavelet amplitudes, and for the blood pressure (0.1035 ±0.0562 vs 0.1232 ± 0.0285 1/s) (p<0.05) wavelet amplitude at the cardiac interval (I, 0.6-2 Hz) in the normobaric hypoxic condition compared to the normoxic condition, respectively. However, no significant differences were observed in the wavelet coherence analyses between any of the collected signals.
CONCLUSION:
We showed that there was a suppression in the amplitude of the cardiac interval to cerebral oxygenation and blood pressure during repeated squat-stands in normobaric hypoxia. Therefore, there is altered cardiac activity contribution to the right prefrontal cortex oxygen and blood pressure oscillations in hypoxia during a task that facilitates cerebral autoregulation. The inclusion of cerebral blood flow in future research along with wavelet analysis would help to increase our understanding of factors contributing to hypoxia on the brain.