Action potential duration (APD) restitution describes the relationship between APD and the preceding diastolic interval. Steep negative APD restitution is pro-arrhythmic and steep negative contractile restitution is a manifestation of an inability to cope with increased demand and is a defining characteristic of heart failure. In this study we wished to investigate the interdependence of APD restitution and contraction restitution in myocytes from rats with right ventricular failure (RVF) induced by pulmonary arterial hypertension (PAH). Male Wistar rats were injected with saline (controls, CON) or 60mg/kg of monocrotaline (FAIL) to induce PAH and RVF. Single RV myocytes were isolated from hearts on the day of heart failure signs (FAIL) or a time matched day (CON). Myocytes were whole cell patch clamped using discontinuous voltage clamp at stimulation frequencies of 1Hz and 5Hz using voltage waveforms based on previously measured APD restitution (Benoist et al., 2012). Cell shortening and time to 50% relaxation were simultaneously measured by video edge detection. All experiments were performed at 36°C. Statistical analysis was performed by repeated measures analysis of variance. When voltage clamp protocols mimicked the respective APD restitution (in CON myocytes depolarisation duration was 50ms at both 1Hz and 5Hz, in FAIL cells depolarisation duration was 125ms at 1Hz but 50ms at 5Hz) an increase in stimulation frequency did not significantly affect the amplitude or time course of contraction in CON myocytes (6.57 ± 1.05 µm and 33.16 ± 3.08 ms at 1 Hz vs 5.91 ± 1.12 µm and 38.42 ± 6.87 ms at 5 Hz, P>0.05, n=11 myocytes). In contrast both contractile parameters were significantly reduced in FAIL myocytes (5.72 ± 1.36 µm and 35.03 ± 2.82 ms at 1 Hz vs 4.29 ± 1.16 µm and 28.50 ± 1.48 ms at 5 Hz, P<0.05, n=11 myocytes). However, when stimulation frequency was increased but depolarisation duration was held constant, at either 50ms or 125ms, contractile parameters were not changed in either group of cells (e.g. for FAIL cells with 125ms depolarisation at 5Hz (5.43 ± 2.14 µm and 31.99 ± 4.88 ms, P<0.05 vs above data for 1Hz at 125ms depolarization, n=11 myocytes, P<0.05). Voltage clamp protocols mimicking steep negative APD restitution provoked negative contractile restitution in FAIL cells, however the effect of increasing stimulation frequency on contraction was attenuated with fixed depolarisation duration. We therefore conclude that negative APD restitution is at least in part responsible for negative contractile restitution in FAIL myocytes.