The greater reduction in systolic blood pressure using loaded breathing training in the

present Panobinostat supplier study indicates that this method could be a valuable adjunct treatment for older hypertensive people and in cases of isolated systolic hypertension. Our findings differ from previous work involving breathing training in that there was a consistent reduction of 5 to 8 beats/min in resting heart rate as a result of both loaded and unloaded breathing whereas previous studies of breathing training report no change in heart rate (Schein et al 2001, Grossman et al 2001, Rosenthal et al 2001, Viskoper et al 2003). These previous studies used devices which guided the breathing rate but did not necessarily control the depth of inspiration, as is evident from the high variation in the ratio of inspiratory to expiratory times during breathing training with RESPeRate ( Schein et al 2007). With the pressure threshold device we have used, it is necessary to maintain a certain inspiratory pressure to obtain any air flow. With the 20-cmH2O threshold the minimal airflow maintained for the 4-s inspiratory time ensured a relatively large chest expansion. This lung

inflation and the negative intrathoracic pressures generated may have activated pulmonary stretch receptors and the Hering-Breuer inflation reflex, which would reduce heart rate and systemic vascular resistance. The mechanisms by which breathing training results in reductions of blood pressure are not clear. It has been suggested below that in essential hypertension there is enhanced sympathetic activity (Guzzetti et al 1988, Goldstein, 1993) pressor http://www.selleckchem.com/products/epacadostat-incb024360.html hyper-responsiveness (Goldstein 1993), and reduced vagal activity at rest (Guzzetti et al 1988). Since the breathing training reduced resting systolic and diastolic blood pressure together with heart rate, one mechanism of its action may be that the training increased cardiac vagal tone and reduced sympathetic activity to the cardiac

and peripheral arterioles. It is known that resistive slow deep breathing at elevated tidal volumes – as in this study – leads to decreased sympathetic excitation (Seals et al 1993). Hyperventilation and low end-tidal carbon dioxide pressures at rest have been described in essential hypertension (Joseph et al 2005), which could enhance peripheral chemoreflex sensitivity (Trzebski et al 1982) and sympathetic activity. Slow breathing training may reduce hyperventilation at rest, as seen in yoga practice, thereby altering the chemoreflex sensitivity (Spicuzza et al 2000). A change in baroreflex sensitivity is another possibility as the baroreflex-cardiac sensitivity is shown to be decreased in hypertension (Goldstein 1993), and the effects of slow deep breathing reducing blood pressure have been suggested to be mediated via an increase in baroreflex sensitivity (Joseph et al 2005).