Heart Rate Variability Biofeedback Increases Baroreflex Gain and Peak Expiratory Flow PAUL M. LEHRER,PHD, EVGENY VASCHILLO,PHD, BRONYA VASCHILLO, MD, SHOU-EN LU,PHD, DWAIN L. ECKBERG, MD, ROBERT EDELBERG,PHD, WEICHUNG JOE SHIH,PHD, YONG LIN,PHD, TOM A. KUUSELA,PHD, KARI U. O. TAHVANAINEN, MD, AND ROBERT M. HAMER,PHD Objective: We evaluated heart rate variability biofeedback as a method for increasing vagal baroreflex gain and improving pulmonary function among 54 healthy adults. Methods: We compared 10 sessions of biofeedback training with an uninstructed control. Cognitive and physiological effects were measured in four of the sessions. Results: We found acute increases in low-frequency and total spectrum heart rate variability, and in vagal baroreflex gain, correlated with slow breathing during biofeedback periods. Increased baseline baroreflex gain also occurred across sessions in the biofeedback group, independent of respiratory changes, and peak expiratory flow increased in this group, independently of cardiovascular changes. Biofeedback was accompanied by fewer adverse relaxation side effects than the control condition. Conclusions: Heart rate variability biofeedback had strong long-term influences on resting baroreflex gain and pulmonary function. It should be examined as a method for treating cardiovascular and pulmonary diseases. Also, this study demonstrates neuroplasticity of the baroreflex. Key words: biofeedback, heart rate variability, baroreflex, pulmonary function, neuroplasticity. BP = blood pressure; HF = high frequency; HR = heart rate; HRV = heart rate variability; LF = low frequency; RSA = respiratory sinus arrhythmia. INTRODUCTION B iofeedback can enable people to obtain voluntary control over various physiological processes (1), and some biofeedback methods have been used widely as adjuncts to, or substitutes for, medical treatment. Typically, a biofeedback trainee views an instantaneous electronic display of a physi- ological function and attempts to change it. Most biofeedback methods involve teaching patients to control a level of a physiological function, such as muscle tension, HR, or finger temperature. Recently we have reported using biofeedback to produce increases in heart rate variability (HRV). This method has been used by Russian clinicians to treat autonomic dys- function with a variety of clinical manifestations, including anxiety and high BP (2), and we recently used it to improve airway function in asthmatic patients (3). These results tenta- tively suggest that the method can produce long-term changes in multiple organ systems that are affected by autonomic control. This study focuses on arterial baroreflexes and pul- monary function in a healthy population. Arterial baroreflex responses, triggered by stretch receptors in the walls of the aortic arch and carotid artery, modulate vagus nerve traffic to the sinoatrial node, and mediate beat- by-beat HR responses to changing arterial pressures (4). Risk for cardiac events (including sudden death) in patients with heart disease is inversely related to the robustness of their baroreflex responses. La Rovere et al. (5) showed that in patients recovering from myocardial infarction, those with subnormal vagal baroreflex gains have a high risk of fatal cardiac events, especially if the patient also has low HRV. The linkage between vagal baroreflex impairment and mor- tality may partially reflect patients’ autonomic responses to cardiac rhythm changes. Ventricular tachycardia, a rapid rhythm that commonly precedes sudden death (6), precip- itously lowers arterial pressure, and increases muscle-sym- pathetic (7) and reduces vagal-cardiac (8) nerve activity. During ventricular tachycardia, arterial perfusion pressures recover more rapidly in patients with stronger than weaker vagal and sympathetic baroreflexes (9). In an exercise/ ischemia dog model of sudden cardiac death, ventricular fibrillation occurs when baroreflexes are weak, but does not occur when they are strong (10). Vagal mechanisms also figure importantly in asthma, because the parasympathetic nervous system plays a major role in modulating airway smooth muscle tone (11). Just as increased baroreflex responsiveness may promote success- ful responses to abrupt rhythm disturbances in cardiac patients, increased vagal activity can cause bronchocon- striction in asthma, and asthma exacerbations can be asso- ciated with cholinergic hyperreactivity (12). The therapeu- tic effects of HRV biofeedback may be through influencing the body’s modulatory processes (eg, the well-known mod- ulation of BP changes by baroreflex activity), through which vagal as well as sympathetic reflexes may be controlled. The levels of baroreflex gain and vagal bronchoconstriction both vary over time, influenced by various neurobehavioral factors. The earliest quantitative analysis of human baroreflex function (13) documented elevated baroreflex gain during sleep. Fritsch et al. (14) reported that changes of arterial pressure lasting only seconds reset the relation between arte- rial pressure and vagal and sympathetic neural outflows. Sys- tematic changes in pulmonary function also occur during behavioral laboratory tasks (12) and relaxation (15). From the Department of Psychiatry Robert Wood Johnson Medical School (P.M.L., R.E., Y.L.), Piscataway, New Jersey; UMDNJ–New Jersey Medical School, Department of Neurosciences, Newark, New Jersey (E.V., B.V.); UMDNJ–School of Public Health, Division of Bio- metrics (S-E.L., W.J.S.); Medical College of Virginia at Virginia Common- wealth University (D.L.E.), Richmond, Virginia; Department of Physics, University of Turku (T.A.K.), Turku, Finland; Department of Clinical Physiology, Kuopio University Hospital (K.U.O.T.), Kuopio, Finland; and Department of Psychiatry University of North Carolina, School of Medicine, Chapel Hill, North Carolina (R.M.H.). Address reprint requests to: Paul Lehrer, Ph.D., Department of Psychiatry, Robert Wood Johnson Medical School, 671 Hoes Lane, Piscataway, NJ 08854, USA. Email: lehrer@umdnj.edu Received for publication June 12, 2002; revision received January 6, 2003. This research was supported by Grant R01HL58805 from the National Heart, Lung, and Blood Institute of the National Institutes of Health. DOI: 10.1097/01.PSY.0000089200.81962.19 796 Psychosomatic Medicine 65:796 – 805 (2003) 0033-3174/03/6505-0796 Copyright © 2003 by the American Psychosomatic Society