Respiratory sinus arrhythmia (RSA) is the physiological phenomenon whereby heart rate (HR) is modulated by respiration. Whilst the physiological function of RSA is not well defined, mathematical modelling predicts that RSA improves cardiac function (Ben-Tal et al. 2012). Some cardiovascular diseases, including heart failure, are associated with a loss of RSA (La Rovere et al. 1998). We investigated the physiological importance of RSA in rats after myocardial infarction (MI) using a novel central pattern generator (CPG) that couples HR to respiration (Nogaret et al. 2013). Wistar rats (male, 250-300g) were anaesthetised with ketamine (60mg kg-1) and medetomidine (250μg kg-1, both i.m.) and either the left anterior coronary artery was ligated (n = 8) or sham operation (n = 9) was performed. After 3 days of recovery, rats were anaesthetised with isofluorane (1.2-1.8% in pure oxygen). The CPG respiratory input signal was generated from real-time diaphragm EMG and the stimulus output delivered to the right cervical vagus nerve via bipolar cuff electrodes. Arterial pressures, HR, respiratory rate, expired air CO2, body temperature and instantaneous flow from the ascending aorta were monitored simultaneously. The effect of artificial RSA versus tonic bradycardia on cardiac function was tested. Treatment effects were considered statistically significant when P<0.05 (Two-way ANOVA between post-MI and Sham data and paired T test within post-MI and Sham groups). Data are presented as mean ± SEM. Using the CPG, RSA of magnitude between 15 and 76 beats per minute (bpm) was generated for 5 min (average RSA amplitude 33±3bpm) in post-MI and Sham rats. Post-MI (infarct size 43±7%) rats had a prolonged duration of systole (55±2ms vs. Sham 48±3ms, P<0.05) and reduced peak aortic flow (189±31 vs. Sham 265±19 mL/min, P<0.05) confirming left ventricular dysfunction (Pfeffer et al. 1979). Enhancement of RSA in post-MI and Sham rats significantly increased stroke volume (11±2% and 11±4% respectively, P<0.05) to the same degree, although this improvement was not different to tonic vagal nerve stimulation at matched average HR (8±1% vs. 9±2% in Sham). The amplitude of RSA was not correlated to a greater increase in stroke volume in Sham or post-MI rats (R2 = 0.21 and 0.00 respectively). We have shown that a novel CPG is capable of inducing RSA in anaesthetised rats. Using this device we have demonstrated that, in an acute setting, stroke volume in post-MI rats increases with RSA but that this is to the same extent as tonic vagal nerve stimulation. We next hope to understand the physiological effects of RSA in conscious, healthy and heart failure rats to understand the purpose of this highly conserved physiological phenomenon.