 This video will cover the following objective from muscle physiology. Compare skeletal muscle and cardiac muscle based on their innervation, structure, and contraction mechanisms. Cardiac muscle is found in the heart, in the wall of the heart, in a layer of the heart wall known as the myocardium. There are three layers of the heart wall, the endocardium, and epicardium are layers of epithelial tissue surrounding the thick middle layer, the myocardium, where the cardiac muscle is found. Cardiac muscle differs from skeletal muscle in that cardiac muscle is stimulated or excited by auto-rhythmic cells located within the heart. These auto-rhythmic cells spontaneously depolarize, producing an action potential that then spreads through the rest of the cardiac muscle tissue, through the other cells known as the contractile cells. So there are two major types of heart muscle cells or cardiomyocytes. There are the auto-rhythmic cells found within the SA node or sinoatrial node, the AV node, the atrial ventricular node, and also throughout the fibers of the intrinsic conduction system, shown in yellow here, there are the atrial ventricular bundle, or bundle of his, the bundle branches, and purkinje fibers. This intrinsic conduction system allows the action potential to spread rapidly through the heart, and then that action potential spreads into the contractile cells, which are the majority of cardiomyocytes found in cardiac muscle, the cells that are responsible for producing the contraction. So this intrinsic excitation mechanism of the auto-rhythmic cells is distinct from skeletal muscle, where we see that the nervous system stimulates excitation, where a somatic, efferent neuron releases neurotransmitter to stimulate contraction of skeletal muscle. Instead, the cardiac muscle is regulated by the autonomic nervous system, and that the autonomic nervous system can increase or decrease the heart rate, or increase or decrease the force of contraction. However, the excitation mechanism is generated by pacemaker cells, the auto-rhythmic cells that are found within the SA node of the heart, and then the action potential spreads from the SA node through the cardiac muscle to stimulate the contractile cells that produce the contraction to pump blood. Here we see an illustration showing the structure of contractile cells, the cardiac muscle fibers or cardiomyocytes that are responsible for producing contraction in the heart. Like skeletal muscle fibers, these contractile cells are striated, so cardiac muscle is striated like skeletal muscle, and the striations are alternating light and dark bands resulting from the overlapping thick and thin filaments arranged into sarcomeres. Another feature of cardiac muscle is that there are intercalated discs. So intercalated discs are the junctions where two cells meet. When two contractile cells meet, they're attached to each other through intercalated discs, and within these intercalated discs are cell junctions known as desmosomes and gap junctions. So the desmosomes anchor the filaments of the adjacent cytoskeletons together in order to prevent the cells from being pulled apart during contraction, and the gap junctions connect the cytosol of the adjacent cells, allowing ions to flow from one cell into the next, and this allows the action potential to spread throughout cardiac muscle. Here we see a graph of the auto-rhythmic cell action potential. The orange line is the region known as the pre-potential phase, or I prefer to call it the pacemaker potential because this phase of the action potential in auto-rhythmic cells of the SA node determines the heart rate. Increasing the slope of the pacemaker potential leads to increased heart rate because the membrane potential reaches threshold faster. Spontaneous depolarization occurs during the pacemaker potential when HCN channels open allowing a slow influx of sodium. HCN stands for hyperpolarization activated cyclic nucleotide gated channels. Understanding this name will help us understand how these channels function. Hyperpolarization activated tells us that decreasing the value of the membrane potential triggers opening of this voltage gated sodium channel. The voltage gated sodium channels we studied previously were all activated by depolarization, so it is unusual or funny that this channel is activated by hyperpolarization. This led to the term funny current to describe the flow of ions through this channel. Cyclic nucleotide gated is telling us that the HCN channel is regulated by the cyclic nucleotide cyclic AMP. We will see this provides a mechanism for the autonomic nervous system to regulate the heart rate. Now moving on to the red line on the graph as the membrane potential reaches a threshold of negative 40 millivolts, the voltage gated calcium channels are triggered to open causing a rapid influx of calcium during the rising phase of the action potential. Then as the voltage gated calcium channels close voltage gated potassium channels open causing repolarization during the falling phase of the action potential shown in the blue line. The decreasing value of the membrane potential at the end of the falling phase then triggers opening of HCN channels initiating the next action potential. Here we see the structure of the HCN channel the hyperpolarization activated cyclic nucleotide gated channels that are responsible for spontaneous depolarization during the pacemaker potential phase of the action potential in auto rhythmic cells. So these sodium channels open in response to hyperpolarization at the end of the falling phase of the action potential in auto rhythmic cells but they are also gated by the cyclic nucleotide cyclic AMP enabling the autonomic nervous system to regulate the slope of the pacemaker potential to regulate the heart rate. Here we see the structure of the T type voltage gated calcium channels that T stands for transient so the transient or T type voltage gated calcium channels transient means that these channels open for a brief amount of time in contrast to L type calcium channels that open for a long period of time. These are voltage gated calcium channels triggered by depolarization so the T type voltage gated calcium channels are triggered to open at the end of the pacemaker potential in auto rhythmic cells and the influx of calcium through these channels is responsible for depolarization during the rising phase of the action potential in auto rhythmic cells. So here we see the structure of the voltage gated potassium channel these voltage gated potassium channels are essentially the same channels as we saw in the neuron or in skeletal muscle and they're responsible for repolarization during the falling phase of the action potential in the auto rhythmic cell and we'll also see that these voltage gated potassium channels are also found in the contractile cells of cardiac muscle. The auto rhythmic cell action potential is first generated in the sinoatrial node the SA node which functions as the pacemaker of the heart but the action potential quickly spreads from the SA node through the intrinsic conduction system and into the contractile cells so the action potential rapidly spreads through gap junctions into contractile cells in order to stimulate the excitation contraction mechanism. This graph shows us the action potential in contractile cells in the orange colored line we see the rising phase of the action potential which occurs when voltage gated sodium channels are triggered to open by depolarization. The depolarization is ions that spread into the contractile cells through gap junctions from the auto rhythmic cells once the membrane potential reaches threshold for opening voltage gated sodium channels sodium rapidly rushes in causing rapid depolarization during the rising phase then voltage gated sodium channels close and voltage gated calcium channels open this causes the membrane potential to become less positive or more negative but at the same time voltage gated potassium channels will open so voltage gated potassium channels are open at the same time as voltage gated calcium channels this occurs during the plateau phase of the contractile cell action potential shown with the purple line calcium is flowing in to the cell but at the same time potassium is flowing out of the cell and the inward flow of positive charges from calcium flowing in is roughly balanced by the outward flow of positive charges from potassium flowing out of the cell and that's why the membrane potential maintains a stable value during this plateau phase now during this phase we are in the absolute refractory period for the contractile cell action potential because voltage gated sodium channels are inactivated when the voltage gated calcium channels close we start to have repolarization shown with the blue line on the graph the falling phase of the action potential in the contractile cells this is a result of potassium flowing out of the cells through the voltage gated potassium channels that are still open and the voltage gated calcium channels have closed allowing repolarization to occur once the membrane potential becomes negative again that repolarization is enough to deactivate voltage gated sodium channels ending the absolute refractory period so we can see we're in a relative refractory period after about 200 milliseconds the relative refractory period is a time when it would be more difficult to trigger another action potential because voltage gated potassium channels are still open then the relative refractory period ends as the voltage gated potassium channels close returning to the resting membrane potential this illustration shows us the voltage gated sodium channels that are triggered to open at threshold causing the rapid influx of sodium during the rising phase of the action potential and then become inactivated the voltage gated sodium channels are inactivated after about a millisecond and they stay inactivated through the plateau phase of the action potential in contractile cells and they're not able to be activated again until they have been de-inactivated by repolarization here we see the structure of a voltage gated calcium channel known as an L type calcium channel so L type stands for long lasting these channels are triggered to open by depolarization and they stay open for a long period of time around 200 milliseconds so the L type calcium channels are the calcium channels that open during the contractile cell action potential and stay open through the plateau phase of the contractile cell action potential this allows a large amount of calcium to enter the cell and calcium will then trigger the contraction mechanism here we see the structure of the voltage gated potassium channels that open allowing potassium to flow out of the cell during the plateau phase of the contractile cell action potential and during the falling phase these channels are responsible for repolarization as well as the relative refractory period