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 levels have a great impact on heart rate and contractility: increased calcium levels cause an increase in both. High levels of calcium ions result in hypercalcemia and excessive levels can induce cardiac arrest. Drugs known as calcium channel blockers slow HR by binding to these channels and blocking or slowing the inward movement of calcium ions. Caffeine and nicotine are both stimulants of the nervous system and of the cardiac centres causing an increased heart rate. Caffeine works by increasing the rates of depolarization at the SA node, whereas nicotine stimulates the activity of the sympathetic neurons that deliver impulses