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Introduction: In failing (F) hearts, rate and adrenergic dependent contractile reserve are impaired and the ability to increase contractility (CY) in response to physiologic stress is diminished. The inability to increase CY in response to increases in heart rate has been linked to a reduced ability of the SR to sequester Ca2þ. The goal of this research was to determine whether alterations in the competition between SERCA and the NCX contribute to impaired rate-dependent reserve and whether CY could be restored in F muscle by increasing extracellular bath Ca2þ. Methods: Steady state isometric force was measured (1.75 mM Ca2þ, 37 C, 80% Lmax-Lo) in control (C) (n 5 9) and F (via pulmonary artery banding) right ventricular trabeculae (n 5 11) at varying stimulation frequencies (0.5e2.5Hz). Altered bath Ca2þ experiments (1.0e7.0mM) were also performed in these trabeculae (0.5Hz). Single and paired rapid cooling contractures (RCCs) were employed to define SR Ca2þ load and the competition between SERCA and the NCX, respectively. Results: C trabeculae exhibited a positive forcefrequency response which was paralleled by a rate-dependent increase in RCC amplitude and the RCC2/RCC1 ratio. F trabeculae exhibited a blunted response to increases in stimulation frequency which was paralleled by a reduced RCC amplitude and RCC2/ RCC1 ratio. Increases in extracellular bath Ca2þ evoked similar increases in both RCC amplitude and developed tension (DT) in F trabeculae compared to C, although DTwas not normalized. Conclusion: This data suggests that under basal conditions (0.5Hz), supraphysiologic application of Ca2þ can evoke similar increases in both SR Ca2þ load and DT in F compared to C trabeculae. This implies that the blunted forcefrequency response representative of F hearts is largely due to an alteration in the functional competition between SERCA and the NCX during relaxation. During increased rates of stimulation, SERCA is not able to adequately compete with the NCX for Ca2þ due to an increase in the NCX/SERCA activity ratio. Thus, Ca2þ extrusion exceeds SR re-sequestration in failing myocardium.