Device-guided slow-breathing effects on end-tidal CO(2) and heart-rate variability

Previous studies have reported that regular practice of a device-guided slow-breathing (DGB) exercise decreases resting blood pressure (BP) in hypertensive patients. The performance of DGB is associated with acute decreases in sympathetic vascular tone, and it has been suggested that the decreases in resting BP produced by regular practice of DGB over periods of weeks are due to chronic decreases in sympathetic nervous system activity. However, the kidneys respond to sympathetically mediated changes in BP by readjusting blood volume levels within a few days. Thus, the mechanism by which DGB could produce long-term BP changes remains to be clarified. Previous research with laboratory animals and human subjects has shown that slow, shallow breathing that increases pCO(2) potentiates BP sensitivity to high sodium intake. These findings raise the possibility that deeper breathing during DGB that decreases BP might involve opposite changes in pCO(2). The present study tested the hypothesis that performance of DGB acutely decreases a marker of pCO(2), end-tidal CO(2) (PetCO(2)). Breathing rate, tidal volume, and PetCO(2) were monitored before, during, and after a 15-min session of DGB by patients with elevated BP. BP, heart rate, and heart-rate variability (HRV) were also measured under these conditions. A control group was also studied before, during, and after a 15-min session of spontaneous breathing (SB). The DGB group, but not the SB group, showed progressive and substantial increases in tidal volume and low-frequency HRV and decreases in PetCO(2) and systolic BP. The PetCO(2) effects persisted into the posttask, rest period. The findings are consistent with the hypothesis that habitual changes in breathing patterns of the kind observed during DGB could potentiate an antihypertensive adaptation via effects on pCO(2) and its role in cardiovascular homeostasis.