To read this article with accompanying illustrations, as well as all the articles in the series, you can go to the mini-site: "Aging of Your Heart and Blood Vessels is Risky" by clicking here.

Introduction

You're watching an episode of ER. Suddenly one of the actors yells, "CODE BLUE", meaning in this case that a patient's heart has stopped beating. The ER staff runs for emergency equipment. Two paddles are whipped from a red cart; they are applied to the unfortunate person's chest. A doctor shouts, "stand back", and the patient is given an electric shock through his chest wall. The patient's heart is restarted!

Sounds electrifying, doesn't it? You sure wouldn't want that to happen to you! Well guess what? It is happening to you with every beat of your heart. Every one of your heartbeats starts with an electrical impulse along the membrane (or outer skin) of all the individual cells, which make up the heart. So, in essence this scene from ER is played out in your heart on a cellular level millions of times throughout your lifetime.

The heart ...an excitable organ

Previously we learned that the heart cells within the wall of the ventricle must "relax" between heart beats, so that the pressure inside the ventricle can decrease and allow it to fill with blood. This blood is then pumped out with the next heartbeat. This sixth article in our series explains to you how exquisitely timed electrical impulses that shock your heart cells are responsible for this ability of the heart to contract and relax, and how this process changes with aging.

Unlike the ER situation described above, normally, it is not necessary for us to supply an electrical shock to our chests to excite our heart cells. Our hearts have an internal clock or pacemaker mechanism to repeatedly send an electrical signal to shock each cell, by causing an "action potential" to occur. An action potential is a transient alteration in electrical charge along a heart muscle cell membrane. It is one of several steps leading to the cell's contraction. Following this shock or action potential, Calcium, the "actor" who plays the staring role in the drama of the heartbeat, comes onstage.

Introducing calcium in the staring role

Most of us are familiar with the element, Calcium. In its mineralized form (hard form) calcium is what makes our teeth and bones strong. In the heart's cells calcium appears in its soft form, meaning that it is dissolved in liquid or bound to various proteins. Because it is in dissolved form it is able to move freely through microscopic channels (holes that open and close repetitively) in the cell membranes (or "skins") of the heart's cells.

The myocyte or muscle cell

Lets look at a single cardiac muscle cell, called a myocyte, to see how this works. Think of a myocyte as a porous elastic-like balloon. A membrane, or outer skin, surrounds the myocyte. Inside, the myocyte is filled with fluid and proteins, and it contains structures (or organelles), one of which is called the sarcoplasmic reticulum.

This organelle (a small "organ" within a cell) functions as a storage bin for calcium. As we said, the outer membrane of the myocyte is not watertight at all times. It has tiny openings, called channels, which open and close in response to a stimulus, namely, a change in electrical charge across the cell membrane during the action potential. Calcium enters and leaves the myocyte through these tiny calcium-channels. It's similar to flipping an electrical switch to open a door. An electrical wave spreads from your heart's pacemaker (a group of specialized cells that start the electrical impulse) to the heart's ventricular wall. This produces an action potential that results in a change in the electrical charge. Essentially, this "flips the switch" on the membrane of the myocyte, to open these calcium-channels (doors). The open channels then allow the movement of a small amount of calcium to enter the cell. This calcium then binds to another calcium channel on the sarcoplasmic reticulum, the storage bin for calcium. This causes it to release a large amount of calcium within the cell. The increased calcium flows into the vicinity of the cell's myofilaments or the "contractile machinery" of the heart muscle. The calcium bound to the myofilaments causes them to shorten (or tighten). Because these myofilaments are connected to the surface of the cell their shortening causes the heart cell to shorten (shrink its length and fatten its width). This process occurs nearly simultaneously among all the cells in the heart wall, causing the entire heart wall to squeeze the blood within it, and to eject blood. Thus, the heartbeat is the cumulative effect of all the cells making up the heart muscle contracting in unison.

Then, the scene plays in rewind and the reverse takes place. Calcium disengages from the myofilaments. A special "calcium pump" pumps most of it back into the storage bin, and some is extruded, or forced from the cell through specialized calcium exit-channels in the cell membrane. The show is over for now." Elvis has left the building!" The environment becomes calmer. Similarly, this decrease in calcium around the contractile filaments of the cell permits them to relax and thus causes the cell to lengthen.

The essence of a heartbeat

From what you have learned about how the heart cell, or myocyte, works you now know that the essence of a heartbeat is a change in the calcium level within your heart cells. When the heart completes its filling period the calcium dissolved in the fluid inside the cell and surrounding the contractile filaments is very low, at least 10,000 times lower than the calcium levels in your blood and in the other fluids between your cells, called the intercellular spaces. "The Director of the heartbeat" (or pacemaker) gives the signal to increase the calcium level around the contractile machinery (myofilaments). At this point the stage hands (positive and negative charges) on both sides of the cell membrane are called upon to set up the scene and the Director calls for "ACTION". This mechanism is thus called "the action potential". This action or change in electrical charge on the myocytes' membranes, called depolarization, starts the scene by opening the small channels on the cells membrane and letting some calcium enter the cell. Then the process of contraction and relaxation of the heart cells occurs. Our director, the pacemaker, is not satisfied with just one take. The pacemaker calls for a retake of this same scene over and over. The result is an Oscar-winning and long-standing production called "The Beating Heart". We'll learn more about this famous Director, Pacemaker, in a future article. If this system fails for some reason, and the temporary increase in calcium inside the cell doesn't happen, the next heartbeat doesn't occur and you experience a skipped heartbeat. (We will also discuss this in a future article.) If the system fails altogether and does not generate another electrical impulse, this can lead to a scene similar to the emergency room situation in the Introduction to this article.

The calcium pump becomes less efficient with aging

From our individual experiences we know the strength of the heartbeat can vary from a given situation to the next. For example, during vigorous exercise our body's cells need extra oxygen. In order to supply this extra oxygen the volume of blood pumped during each beat must increase. To pump more blood heart rate increases and the strength of the heartbeat increases. Article How Good a Pump is Your Older Heart?. From what we have learned so far about our lead actor, Calcium, it is easy to see that heart cells are able to increase the strength of their contraction by increasing the amount of calcium released from their intracellular calcium storage bins during beats. In other words, the amplitude (or range of size) of the calcium oscillation (flow) that drives the contractile machinery (myofilaments) varies with the amount of calcium delivered to the contractile protein inside the heart cell. But, this mechanism is obviously dependent upon how much calcium can be released from these storage bins. And further, how much can be released is determined by how much is pumped in during the period between heartbeats. These calcium pumps generally work very efficiently in the young heart, but this changes as the heart ages.

Lets compare the calcium storage bin pump to a factory with machinery that uses a new millennium fuel, called "CalCoal". This fuel doesn't burn up, but instead, recycles. Electrical release channel switches are flipped when the machines need fuel. Fuel then flows from storage bins to the machinery and then back to the same bins to wait for the next signal to repeat the action. During periods when the fuel has to be cycled faster, the pumps and switches cycle the fuel at a faster rate. All goes well when the electrical switches and pumps are working efficiently. But, consider this! The pumps and switches used in this factory are from when it was originally built in the thirties. Some of these older pumps stopped working and were removed. The management chose not to replace them. When the switches are flipped on, the machinery is delivered a lot less fuel than if all pumps were in operation, particularly when the rate of cycling must increase. Just like the machinery at the factory needs the right number and efficiently working switches and pumps, the heart cells need a certain number of operating calcium pumps and efficient switches (signals) to push calcium back into its storage bin (the sarcoplasmic reticulum) and have fuel ready for the next signal (electrical impulse) to start another heart contraction. Obviously, the amount of calcium that can be released from the storage area is dependent on how much can be pumped in and stored there in the first place. If the pump isn't working, the bin will not fill with calcium and calcium will not be available for the next release signal, particularly at higher cycling rates or during exercise. With aging, and with many types of cardiac diseases that lead to heart failure, these calcium pumps fail. Like our factory problem there are two similar reasons for this. One, the number of pumps decreases, because fewer pumps are produced within the cell. This is because the genes that make this pump protein become partially silenced with advancing age. Because there are fewer pumps, the second reason the calcium pumps falter is that the collective maximum pumping capacity of all the storage bins, which is regulated via brain-heart communication (or switches) is reduced with aging. (We will learn more about this brain-heart communication in a future article.) These two deficits cause the maximum amount of calcium that can be released by the intracellular or Ca2+ storage site to decline particularly during exercise. The end result is a decrease in the maximum strength of the heartbeat, during vigorous exercise, with aging. This reduced overall calcium pumping function also results in a prolonged time for cell calcium to return to its resting level, and a prolonged contraction or delayed relaxation of the heart's cells, essentially a delay in the heart's ability to relax. This makes it more difficult for the heart to fill with blood during the diastolic period and prepare for the next heartbeat. See Article The Older Heart Has Trouble Pumping Blood During ExerciseThis impaired relaxation on a cellular level reduces the ability of the older heart to fill during the period between heartbeats, and thus plays a role in causing shortness of breath in older persons during vigorous exercise. As discussed in Article Your Older Heart May Cause You to Feel Short of Breath.

Dr. Ed is a physician/scientist, who is internationally recognized for studies that range from humans to molecules on how the heart and blood vessels work in health and disease as the body ages.