In addition to the Ca 2+ switch, heart muscle possesses a unique adrenergic regulatory mechanism that allows it to meet increased oxygen demand from the rest of the body. Stimulation of β1-adrenergic receptors leads to activation of protein kinase A (PKA) which phosphorylates a number of membrane and contractile proteins including two serines (22 and 23) located in a 32 amino-acid N-terminal cardiac specific extension to cardiac troponin I (cTnI) . Phosphorylation of serines 22 and 23 causes no more than a 2-3 fold decrease in myofilament Ca 2+ -sensitivity and a corresponding increase in the Ca 2+ dissociation rate that determines relaxation rate . Nevertheless, this small change is sufficient to allow the lusitropic response to adrenergic stimulation since the faster relaxation rate of the cardiac muscle due to cTnI phosphorylation (lusitropy) results in shortening the cardiac muscle contractionrelaxation cycle, allowing for efficient contraction at a faster heart rate.