Myocardial Ca
2+ handling during excitation-contraction coupling has been modelled mathematically to gain a better insight into the expectation that Ca
2+ sensitization of contractile machinery may save myocardial energy utiliza-tion for Ca
2+ handling. The basic model of myocardial Ca
2+ kinetics and mechanoenergetics involved the sarcoplasmic reticulum (SR), sarcoplasm, tro-ponin C (Tn) and crossbridges (CB). The relations among the released Ca
2+ ions from the SR, peak concentrations of sarcoplasmic free Ca
2+ ([Ca
2+]i) and Ca
2+-bound troponin ([TnCa]) and peak contractile force were computed, based upon the assumptions that the released Ca2
+ ions diffuse as free Ca
2+ in sarcoplasm, bind kinetically with Tn with an association rate constant of k
1, dissociate from TnCa with a dissociation rate constant of k
2, and are seques-tered into the SR with consumption of ATP. TnCa was associated with GB cycling to develop force with a set of given on and off rate constants. The association constant Ka (=k
1/k
2) of TnCa as an index of Ca
2+ sensitivity of Tn was varied 32-fold from 0.25 to 8/μM. Results showed that Ca
2+ sensitization from a lower Ka level could most sharply decrease the total Ca2+ release re-quired to develop the same contractile force. Thus, it would reduce the total Ca
2+ handling energy that the SR uses to maintain the same contractility.
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