Experimental Physiology Exp Physiol 98.1 (2013) pp 161–171 161 Research Paper Research Paper Effects of testosterone on cardiomyocyte calcium homeostasis and contractile function in female rats Ronald D. Beesley 1 , Bradley M. Palmer 2 , Peter R. Casson 1 and Michael J. Toth 1,2,3 Departments of 1 Obstetrics and Gynecology, 2 Molecular Physiology and 3 Medicine, University of Vermont College of Medicine, Burlington, VT, USA New Findings  What is the central question of this study? Androgen excess in women is associated with an elevated risk for heart disease. Whether some portion of this elevated risk is related to an effect of androgens on cariomyoctye function, however, has not been examined. To our knowledge, this is the first study to directly address the role of androgens in regulating cardiomyocyte contractile dynamics and calcium homeostasis.  What is the main finding and its importance? Our results suggest minimal acute or chronic effects of testosterone on cardiomyocyte shortening dynamics, calcium homeostasis or myosin heavy chain expression, suggesting that the detrimental effect of androgen excess on cardiovascular risk is not mediated through alterations in cardiomyocyte biology. The role of testosterone (T) in the regulation of cardiovascular function in females is not well understood. Our goal was to examine the effect of T on cardiomyocyte biology by measuring sarcomere shortening/relaxation and intracellular calcium cycling in adult female Sprague–Dawley rats. The rats were divided into the following four groups: (1) sham operated; (2) ovariectomized (OVX); (3) OVX plus T; and (4) OVX + T plus an aromatase inhibitor (AI). The final group was added to rule out effects from bioconversion of T to oestradiol. Sarcomere/calcium dynamics were measured after 4 weeks at 2 and 6 Hz, then at 6 Hz following exposure to 300 nm isoprenaline. Additionally, the acute (i.e. non-genomic) effects of T were evaluated in sham-operated and OVX + T + AI rats. There were no group differences, nor was there evidence for an effect of T on frequency or isoprenaline response. Additionally, there were no findings to indicate an acute, non-genomic T effect. Moreover, the relative α- and β-myosin heavy chain isoform complement was unchanged by OVX or T replacement. Our results argue against acute or chronic effects of T on cardiomyocyte shortening dynamics, calcium cycling or myosin heavy chain expression, arguing against any direct effect of T on cardiomyocyte function in adult females. (Received 28 April 2012; accepted after revision 13 July 2012; first published online 13 July 2012) Corresponding author M. J. Toth: University of Vermont, Health Science Research Facility 126B, 149 Beaumont Avenue, Burlington, VT 05405, USA. Email: michael.toth@uvm.edu The role of testosterone (T) in the regulation of cardiovascular function and subsequent development of cardiovascular disease in women is not well understood. Most studies that have explored the effect of T on the development of cardiovascular disease risk in women have focused on its role on regulating the vasculature, lipid lipoprotein levels and/or adiposity (Mendelsohn & Karas, 2005). Epidemiological studies show adverse effects of elevated androgen levels on cardiovascular disease risk (Kritz-Silverstein et al . 1997). However, the effects of T on cardiomyocyte function per se have received less attention, despite early studies demonstrating a role for C  2012 The Authors. Experimental Physiology C  2012 The Physiological Society DOI: 10.1113/expphysiol.2012.067009