The fundamental characteristics of calcium cycling are poorly characterized in heart failure with preserved ejection fraction (HFpEF). Abnormal diastolic function is the hallmark of HFpEF, but several lines of evidence hint that systolic function is also defective. To characterize excitation-contraction (EC) coupling in HFpEF, we measured L-type Ca current (ICa) and intracellular calcium (Ca) in left ventricular myocytes isolated from Dahl salt-sensitive (DS) rats with phenotypically-verified HFpEF produced by feeding them a high salt diet (8% NaCl). DS rats fed normal salt served as controls (Con). Whole-cell patch clamp revealed a 24% increase in ICa density in HFpEF myocytes depolarized to 0 mV (n=17 Con; n=29 HFpEF; p<0.01) with a leftward shift in the peak voltage, despite a 37% reduction in Cav1.2 protein expression by mass spectroscopy. ICa inactivation kinetics were slowed in HFpEF (τfast: 7.2 ± 0.4 vs. 9.0 ± 0.7, p<0.03; τslow: 59.8 ± 2.8 vs. 86.8 ± 5.8, p<0.001; n=20 Con, n=17 HFpEF). Steady-state activation of ICawas left-shifted 4 mV in HFpEF (n=13 Con vs. n=17 HFpEF), and steady-state inactivation was right-shifted 4 mV (n=21 Con vs. n=15 HFpEF). Consequently, window current doubled. These findings are consistent with an increase in phosphorylation of Cav1.2 and/or its modulating proteins. Simultaneous recordings of Ca release using high-speed laser scanning confocal imaging in fluo-4 loaded myocytes showed that Ca spark recruitment was similar in the two groups, but spark latency was shortened in HFpEF (8.0 ± 0.1 ms Con vs.7.3 ± 0.1 ms HFpEF; p<0.01, n=12 each), indicating earlier ryanodine receptor (RyR) triggering. However, Ca transient amplitude in response to ICa and SR Ca measured by caffeine release were unchanged. Thus Ca-induced Ca release appears to operate near its maximum in HFpEF myocytes: ICa is increased, its gating kinetics are shifted so as to increase steady-state Ca influx, and the latency of couplon activation is abbreviated, but nevertheless Ca transient amplitude is unchanged. These findings hint that EC coupling reserve may be limited in HFpEF, which would help rationalize the limited systolic functional reserve seen in HFpEF patients. Larger window currents may also increase susceptibility to triggered arrhythmia.