Hypoxia Disrupts Blood Pressure Control in Men

Episodes of hypoxia, such as those occurring during sleep apnea or high-altitude exposure, can disrupt BP regulation and other physiologic processes. To determine how BP affects that disruption, a recent small study published in Clinical Autonomic Research investigated its effects in men with untreated hypertension and control participants with BP in the normal range.

The researchers hypothesized that hypoxia would cause greater BP variability (BPV) in individuals with hypertension compared with control participants without hypertension. They recruited nine men with untreated stage 1-2 hypertension (hypertensive group)  and nine men with BP in the normal range (normotensive group). Both groups were exposed to two breathing conditions: normal oxygen levels (21% O₂) and isocapnic hypoxia (IH; 10% O₂). During both sessions, oxygen saturation, beat-to-beat BP, muscle sympathetic nerve activity (MSNA), and end-tidal carbon dioxide (PetCO₂) were continuously monitored, with PetCO₂ maintained at baseline levels.

To assess BPV, the researchers calculated standard deviation; coefficient of variation; and average real variability for systolic, diastolic, and mean BP. Sympathetic transduction was determined using a time-domain signal averaging technique. Cardiac baroreflex sensitivity (cBRS) was assessed using the sequence method, and sympathetic baroreflex sensitivity (sBRS) was calculated through MSNA-diastolic pressure regression.

The results showed that IH induced comparable oxygen desaturation in both normotensive (−25.7 ± 3.3%) and hypertensive (−21.2 ± 4.0%; P>0.05) groups.  Although overall BP and PetCO₂ levels remained stable, the MSNA response to hypoxia was significantly greater in the hypertensive group (normotensive group: +8 ± 2 vs hypertensive group: +12 ± 2 bursts/min; P=0.03).

Under hypoxic conditions, both groups showed increased BPV across all indices and similar impairment in cBRS and sBRS. Both groups also showed increased sympathetic transduction and reduced cardiac and sympathetic baroreflex function.

These findings indicate that IH disrupts multiple components of neurovascular regulation regardless of baseline BP status.