Energetic dysfunction is important in the pathogenesis of multiple cardiac pathologies. Increasing evidence implicates causal links between energetic dysfunction and potentially arrhythmogenic, primary cardiac electrophysiological abnormalities (Adabag et al. 2015). The precise physiological mechanisms linking metabolic disturbance to arrhythmic tendency remain uncertain. These relationships were investigated in PGC-1β-/- mice known to display abnormal mitochondrial bioenergetics. Wild type (WT) and PGC-1β-/-, C57/B6, mice aged ≥ 12 weeks (Bar Harbour Laboratories, Maine), matched for baseline characteristics, were weighed and anaesthetised with tribromoethanol (240mg/kg i.p.) for lead I and lead II electrocardiogram (ECG) recordings. Three hundred seconds of intrinsic ECG recordings were followed by dobutamine (0.3mg/kg i.p.) challenge, and a further 300s of ECG recorded. ECG signals were analysed using a bespoke program in the open-source R programming language. Multivariate ANOVA examined for significant differences in ECG features between groups. Demonstration of significant differences between groups then prompted further, post hoc MANOVA decomposition and post hoc Tukey HSD tests for significance (P<0.05). WT (n=13) and PGC-1β-/- (n=15) mice showed indistinguishable pre-treatment baseline heart rates (WT 6.78 ± 0.16 Hz vs. PGC-1β-/- 6.52 ± 0.32 Hz, p > 0.05). However, PGC-1β-/- mice displayed chronotropic incompetence with dobutamine challenge (8.30 ± 0.10 Hz vs. 9.11 ± 0.28 Hz, p = 0.025) (Fig. 1). Dobutamine-treated PGC-1β-/- mice also showed shorter corrected QT (QTc) intervals than the corresponding WT mice (126.06 ± 1.15ms vs. 119.94 ± 2.23ms, p < 0.05). The late component of the murine R’ wave has previously been correlated with ventricular repolarisation (Boukens et al. 2014). QT waveforms were accordingly analysed in greater detail to clarify aspects of electrical activity affected. Mean QR’ durations were indistinguishable between groups whether before or after dobutamine challenge. However, R’Tc intervals were shorter in PGC-1β-/- mice following such challenge (25.91 ± 0.37ms vs. 24.24 ± 0.44, p < 0.05). The present study is the first report of a short QT phenotype associated with energetic dysfunction, secondary to PGC-1β-/- ablation in mice. In humans short QT has been correlated with increased arrhythmic risk (Gollob et al. 2011). Short QT syndromes are poorly characterised disorders for which there is limited understanding of arrhythmic mechanisms. The PGC-1β-/- mouse model will enable exploration to its underlying mechanistic pathways.