Effects of Slow-paced Breathing on Heart Rate Variability in Patients With Heart Failure

Overview

Background: Heart failure (HF) is a major global public health concern characterized by impaired cardiac function, high mortality, frequent hospital readmissions, and substantial healthcare burden. Autonomic nervous system (ANS) dysfunction plays a critical role in the pathophysiology of HF, typically presenting as increased sympathetic activity and reduced parasympathetic activity. Heart rate variability (HRV), a non-invasive marker of cardiac autonomic regulation, has been widely used to evaluate autonomic function and predict clinical outcomes in patients with HF. Reduced HRV is associated with increased risks of sudden cardiac death, cardiovascular events, and hospital readmission. Although cardiac rehabilitation (CR) has been demonstrated to improve exercise capacity, quality of life, and clinical outcomes in HF patients, its effects on autonomic modulation, particularly during Phase I cardiac rehabilitation, remain insufficiently investigated. Slow-paced breathing (SPB) has emerged as a potential non-pharmacological intervention for enhancing autonomic regulation. By synchronizing respiratory rhythm with cardiovascular oscillations, SPB may enhance baroreflex sensitivity, increase vagal activity, and improve HRV. Previous studies have suggested beneficial effects of SPB on autonomic function; however, the findings remain inconsistent, and evidence regarding its short-term effects on HRV among hospitalized HF patients undergoing early cardiac rehabilitation is limited. Therefore, further investigation is warranted to determine whether SPB can provide additional autonomic benefits when incorporated into Phase I cardiac rehabilitation. Objective: This study aims to investigate the effects of slow-paced breathing combined with Phase I cardiac rehabilitation on autonomic nervous system function in patients with heart failure, using HRV as the primary outcome measure. Methods: This study will employ a parallel randomized controlled trial design. Hospitalized patients diagnosed with heart failure will be randomly allocated into either the SPB intervention group or the control group. Both groups will receive standard Phase I cardiac rehabilitation, while the intervention group will additionally receive slow-paced breathing training. The primary outcomes will include changes in HRV parameters, including time-domain indices (standard deviation of NN intervals \[SDNN\] and root mean square of successive differences \[RMSSD\]) and frequency-domain indices (low-frequency power \[LF\], high-frequency power \[HF\], and LF/HF ratio), to evaluate changes in cardiac autonomic regulation before and after intervention.

Physiological Link Between Slow-Paced Breathing and Autonomic Nervous System Regulation Although conventional breathing exercises (e.g., diaphragmatic breathing and deep breathing) facilitate lung expansion, prevent premature alveolar and airway collapse, and maintain normal respiratory function and adequate gas exchange, these techniques primarily focus on the quantity of breathing and respiratory muscle activity. In contrast, slow-paced breathing (SPB) is a controlled breathing technique that primarily regulates the breathing frequency and maintains a fixed inspiratory-to-expiratory ratio, allowing synchronization with intrinsic cardiovascular oscillations to enhance cardiopulmonary function and autonomic regulation. Slow-paced breathing, also referred to as slow breathing, resonance frequency breathing, or paced breathing, is considered a method that influences autonomic nervous system (ANS) function through modulation of respiratory frequency. The interaction between respiration and cardiovascular regulation is mediated through the autonomic nervous system, which regulates heart rate, blood pressure, and respiratory patterns. This physiological coupling is known as respiratory sinus arrhythmia (RSA), which is considered one of the primary contributors to HRV. Under normal RSA conditions, heart rate slightly increases during inspiration and decreases during expiration. This phenomenon reflects parasympathetic modulation of cardiac activity and serves as an important physiological indicator of vagal function. The interaction between respiratory and cardiovascular systems involves three major components: the respiratory network, the cardiovascular network, and their central synaptic interactions. The respiratory network within the central nervous system generates respiratory commands that activate respiratory motor neurons, leading to respiratory muscle activity. During this process, two major types of afferent feedback signals are generated from the lungs: chemical feedback and mechanical feedback. Chemical feedback is mediated through the aortic arch and carotid bodies, which detect changes in oxygen, carbon dioxide, and hydrogen ion concentrations and transmit these signals back to the brain. Mechanical feedback occurs through lung expansion during inspiration, which activates lung stretch receptors; meanwhile, respiratory-induced changes in intrathoracic pressure also generate afferent signals transmitted to the central nervous system. Meanwhile, the cardiovascular network regulates cardiac activity and vascular smooth muscle function through the autonomic nervous system, resulting in changes in heart rate and vascular resistance. The vascular system determines systolic arterial pressure (SAP) and diastolic arterial pressure (DAP), leading to alterations in blood pressure and arterial blood conditions. Changes in blood pressure stimulate baroreceptors located in the aortic arch and carotid sinus, which subsequently transmit sensory information back to the brain. Ultimately, these signals are integrated within the nucleus tractus solitarius (NTS) in the brainstem, resulting in respiratory-mediated modulation of cardiovascular autonomic control