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al o f P hy si ol og y Genetically modified mice provide unique models for investigating the roles of specific proteins in cardiac excitation–contraction coupling and helping to understand molecular alterations that contribute to cardiac diseases (James et al. 1998). The mouse is, however, a relatively recent model in cardiac physiology and data published in the literature are sparse and often contradictory. For instance, in most mammalian animal models, ventricular myocardium exhibits a positive relationship between force development and stimulation rate (Braveny & Sumbera