In response to exercise training the human heart can undergo hypertrophy and electrophysiological changes in the ECG can mimic those seen in response pathological stimuli such as hypertension (Maron, 2005). In single rat ventricular myocytes too, both hypertension (McCrossan et al., 2004) and exercise (Natali et al., 2002) can cause hypertrophy and action potential prolongation. These changes are typically thought to pre-dispose to arrhythmia but conversely, regular exercise is known to be beneficial to the heart. We therefore wished to test whether electrical remodelling (and hypertrophy) could be detected in whole rat hearts in response to voluntary exercise and whether these changes pre-disposed the exercised hearts to arrhythmia. Female Sprague-Dawley rats were given free access to a running wheel for a 5 week voluntary exercise training period (TRN) and compared to sedentary control animals (SED). After 5 weeks animals were humanely killed and hearts removed and weighed, then perfused with a bicarbonate-based physiological solution at 37°C on a Langendorff apparatus at constant perfusion pressure and paced at a stimulation frequency of 5 Hz. Left ventricular, epicardial monophasic action potentials (MAPs) were recorded and the response to the following arrhythmic stimuli were tested; a) 2 s of rapid pacing at 50 Hz b) 10 min of perfusion with high (8.6 mM) K⁺ plus (1 µM) noradrenaline c) a combination of (a) + (b). Heart rate variability (the standard deviation of the inter-beat interval) was used to assess arrhythmic susceptibility. We observed that TRN hearts had significantly larger heart weight:body weight (TRN 5.9 ± 0.13 mg/g n=22 vs. SED 5.16 ± 0.15 mg/g n=20, mean ± SEM, P<0.001 unpaired t-test) and significantly longer MAP durations at 50% (TRN 26.6 ± 1.5 ms vs. SED 23.5 ± 1.1 ms), 75% (TRN 50.3 ± 0.8 ms vs. SED 42.8 ± 1.0 ms) and 90% repolarisation (TRN 66.3 ± 1.0 ms vs. SED 60.5 ± 1.2 ms) than SED hearts (P<0.05 unpaired t-test n = 10-12). However, heart rate variability in response to the arrhythmic stimuli was not significantly different between TRN and SED hearts (P > 0.05 unpaired t-test n = 9-10). We suggest that despite the occurrence of both cardiac hypertrophy and electrical remodelling in response to voluntary exercise, these changes do not pre-dispose the exercise trained heart to arrhythmias. Our findings are consistent with the overall beneficial effect of mild exercise on the heart.