Muscle contraction RyRs are activated by a calcium trigger, which is brought about by the flow of through the L-type calcium channels. Furthermore, cardiac muscle tend to exhibit diad (or dyad) structures, rather than triads. Excitation-contraction coupling in cardiac muscle cells occurs when an action potential is initiated by pacemaker cells in the sinoatrial node or Atrioventricular node and conducted to all cells in the heart via gap junctions. The action potential travels along the surface membrane into T-tubules (the latter are not seen in all cardiac cell types) and the depolarisation causes extracellular to enter the cell via L-type calcium channels
Heart rate turbulence normal cardiac cycle, so the ventricles of the heart haven't had time to fill up to their normal level, before contracting and pumping their contents out. This results in a pulse (blood pressure) weaker than expected and triggers normal homeostatic mechanisms that try to compensate by constricting arteries and increasing heart rate (the turbulence onset part of HRT). This is accomplished by the brain reflexively withdrawing the parasympathetic nerve signals and increasing the sympathetic nerve signals it sends to the heart. The compensatory constriction of the arteries and increased heart rate frequently cause blood pressure to oveshoot normal values (overcompensates),