Slow Breathing Improves Arterial Baroreflex Sensitivity and Decreases Blood Pressure in Essential Hypertension

Nevner hvordan 6 pust i minuttet øker HRV og vagus nervens effekt på hjertet. Nevner også hvordan CO2 synker ved 15 pust i minuttet og holdes normalt ved 6 pust i minuttet. De med hjerteproblemer har mye større reaksjon på CO2 enn andre, og generelt lavere nivå.

Sympathetic hyperactivity and parasympathetic withdrawal may cause and sustain hypertension. This autonomic imbalance is in turn related to a reduced or reset arterial baroreflex sensitivity and chemoreflex-induced hyperventilation. Slow breathing at 6 breaths/min increases baroreflex sensitivity and reduces sympathetic activity and chemoreflex activation, suggesting a potentially beneficial effect in hypertension. We tested whether slow breathing was capable of modifying blood pressure in hypertensive and control subjects and improving baroreflex sensitivity. Continuous noninvasive blood pressure, RR interval, respiration, and end-tidal CO2 (CO2-et) were monitored in 20 subjects with essential hypertension (56.4±1.9 years) and in 26 controls (52.3±1.4 years) in sitting position during spontaneous breathing and controlled breathing at slower (6/min) and faster (15/min) breathing rate. Baroreflex sensitivity was measured by autoregressive spectral analysis and “alpha angle” method. Slow breathing decreased systolic and diastolic pressures in hypertensive subjects (from 149.7±3.7 to 141.1±4 mm Hg, P<0.05; and from 82.7±3 to 77.8±3.7 mm Hg, P<0.01, respectively). Controlled breathing (15/min) decreased systolic (to 142.8±3.9 mm Hg; P<0.05) but not diastolic blood pressure and decreased RR interval (P<0.05) without altering the baroreflex. Similar findings were seen in controls for RR interval. Slow breathing increased baroreflex sensitivity in hypertensives (from 5.8±0.7 to 10.3±2.0 ms/mm Hg; P<0.01) and controls (from 10.9±1.0 to 16.0±1.5 ms/mm Hg; P<0.001) without inducing hyperventilation. During spontaneous breathing, hypertensive subjects showed lower CO2 and faster breathing rate, suggesting hyperventilation and reduced baroreflex sensitivity (P<0.001 versus controls). Slow breathing reduces blood pressure and enhances baroreflex sensitivity in hypertensive patients. These effects appear potentially beneficial in the management of hypertension.

However, breathing at 6 breaths/min significantly increased the baroreflex sensitivity in hypertensive (from 5.8±0.7 to 10.3±2.0 ms/mm Hg; P<0.01) and control subjects (from 10.9±1.0 to 16.0±1.5 ms/mm Hg; P<0.001;Figure 2).

Hypertensive subjects showed a significantly higher resting respiratory rate (14.55±0.82 versus 11.76±1.00; P<0.05) and a significantly lower CO2-et values compared with control subjects (Figure 3). During controlled breathing at 6/min, there were no significant changes in CO2-et and in Vm. The lack of change in Vm, despite lower breathing rate, was attributable to a significant increase in Vt in hypertensives and controls. Controlled breathing at 15/min induced a marked decrease in CO2-et, particularly in hypertensive subjects, and a marked relative increase in Vm and Vt (Figure 3).

We found that paced breathing, and particularly slow breathing at 6 cycle/min, reduces blood pressure in hypertensive patients. The reduction in blood pressure during slow breathing is associated with an increase in the vagal arm of baroreflex sensitivity, indicating a change in autonomic balance, related to an absolute or relative reduction in sympathetic activity.

This demonstrated that slow breathing is indeed capable of inducing a modification in respiratory and cardiovascular control, and that appropriate training could induce a long-term effect. In subjects with chronic congestive heart failure, a condition known to induce sympathetic and chemoreflex activation, slow breathing induced a reduction in chemoreflexes and an increase in baroreflex.10,25 We have also shown that in these patients, 1-month training in slow breathing could induce prolonged benefits, even in terms of exercise capacity.25

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