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This Article Full Text Full Text (PDF) All Versions of this Article: 107/3/718    most recent 00548.2009v1 Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Tzeng, Y. C. Articles by Ainslie, P. N. PubMed PubMed Citation Articles by Tzeng, Y. C. Articles by Ainslie, P. N.

Respiratory modulation of cardiovagal baroreflex sensitivity

¹Department of Surgery and Anaesthesia, University of Otago, Wellington; ²Department of Physiology, University of Otago, Dunedin, New Zealand; and ³Department of Human Kinetics, Faculty of Health and Social Development, University of British Columbia, Kelowna, British Columbia, Canada

Submitted 20 May 2009 ; accepted in final form 15 July 2009

Emerging evidence has suggested that with minimal prerequisite training, slow deep breathing around 0.10 Hz can acutely enhance cardiovagal baroreflex sensitivity (BRS) in humans. Such reports have led to the speculation that behavioral interventions designed to reduce breathing frequency may serve a therapeutic role in ameliorating depressed baroreflex function in conditions such as chronic heart failure, essential hypertension, and obstructive airway disease. This study sought to test the hypothesis that slow controlled breathing acutely enhances cardiovagal baroreflex function in young healthy volunteers. Distinct from earlier studies, however, baroreflex function was examined (n = 30) using the classical pharmacological modified Oxford method, which enabled the assessment of cardiovagal BRS through experimentally driven baroreceptor stimulation across a wide range of blood pressures. For a comparison against existing evidence, spontaneous cardiovagal BRS was also assessed using the -index and sequence method. Compared with fast breathing (0.25 Hz), slow breathing (0.10 Hz) was associated with an increase in the -index (8.1 ± 14 ms/mmHg, P < 0.01) and spontaneous up-sequence BRS (10 ± 11 ms/mmHg, P < 0.01). In contrast, BRS derived from spontaneous down sequences and the modified Oxford method were unaltered by slow breathing. The lack of change in BRS derived from the modified Oxford method challenges the concept that slow breathing acutely augments arterial baroreflex function in otherwise healthy humans. Our results also provide further evidence that spontaneous BRS may not reflect the BRS determined by experimentally driven baroreceptor stimulation.

baroreceptors; blood pressure; heart rate; parasympathetic