Excitation-Contraction Coupling: This is the mechanism by which electrical depolarization (excitation), results in contracton in a cardiac myocyte. Calcium acts as the secondary messenger making that coupling.
Adult Cardiac Myocyte - Calcium Regulation during contraction and relaxation:

Neonatal cardiac myocyte - Calcium regulation during contraction and relaxation:
In neonatal cardiac myocyte, SR is sparsely developed and poorly organized. So, CICR can not fully function/support cardiac contraction in the newborn. Therefore, neonatal cardiac myocytes depend on trans-sarcolemmal influx of calcium (via L-type Calcium channels & NCX). NCX operates in "reverse" direction during systole in this situation and "forwards" during diastole. NCX plays a major role in calcium homeostasis in neonate.

1) T-tubules: Invaginations of sarcolemma that help to increase the cell surface area for a given cell volume. T-tubules bring more of the sarcolemmal L-type Calcium Channels in proximity to ryanodine receptors of the SR. Thus, T-tubules enhance the efficiency of CICR. However, in neonatal cardiac myocyte, the T-tubules are absent, which impose a substantial impediment to sarcolemma to SR coupling.
2) Sodium-Pottasium Pump (Na,K-ATPase): This pump, present in sarcolemma maintains an appropriate Na gradient across the membrane. This pump exists in different isoforms. Different isoforms have different senstivity and response to cardiac glycosides - which may explain the relatively high tolerability of neonates and infants to Digoxin.
3) Calsequestrin: Major calcium storing protein inside SR. Activity of calsequestrin increases progressively with development.
4) Actin and Myosin have different isoforms for heavy and light chains - which increase in sensitivity to calcium with increasing maturity, thus influencing inotropy and lusitropy of the cardiac myocyte.
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