Figure 9. Schematic diagram of the model .

Human myocyte model (C) including ion pumps and exchangers responsible for action potential, Ca²⁺ management, force development, pH_i and Ca²⁺–calmodulin‐dependent protein kinase II (CaMKII) regulation. Our previous model (Lascano et al. 2013) was modified by the addition of a second dyadic cleft: DC₁ and DC₂. The model is coupled to the myofilament force development model consisting of 5‐state troponin systems (TS) with Ca²⁺ binding at the myofilament level (Negroni et al. 2015). CYTO, cytosol; LTCC, L‐type Ca²⁺ channels; NCX, Na⁺/Ca²⁺ exchanger; NKA, Na⁺/K⁺‐ATPase; Cap, membrane Ca²⁺‐ATPase; NHE, Na⁺/H⁺ exchanger; NBC, Na⁺–HCO₃ ⁻ cotransporter; CHE, Cl⁻/OH⁻ exchanger; AE, anion exchanger; I represents different ionic currents (see text for further details). A, detail of the DC structure where DC₁ is surrounded by 6 DC₂. DC₁ represents the dyadic clefts where RyR2 are facing the L‐type Ca²⁺ channel (LCC) and DC₂ the dyadic clefts where RyR2 are not facing LCC. In the original TP model (ten Tusscher & Panfilov, 2006), the single dyadic cleft involves 14.3% of the present total cleft space (DC₁+DC₂). B, dyadic cleft structure assumed as two concentric cylinders. Surface 1: lateral surface of the cylinder with radius R, representing DC₁. Surface 2: lateral surface of the cylinder with radius R2, representing DC₂. The planar surfaces limiting the height of the cylinders are the sarcolemmal membrane on one side and the SR membrane on the other (see text for further details).