Changes in the Heart as We Age

group of scientists working at the laboratory

Rather than declining with age; research suggests that our heart adjusts itself as we age.  The National Institute on Aging (NIA) has scientific information that will change our views on an aging heart.

There are no magic pills to stop human aging. The molecular buildup and cellular damage is ongoing, leaving our bodies vulnerable to disease and debilities as we grow older. Heart disease and strokes rises steeply after the age of 65, and 40% of all deaths for ages 65-74 and almost 60% at the age of 85 and older.

Scientists at the National Institute on Aging (NIA) have been researching new areas on the link between aging and the development and course of heart disease.  Dr. Edward Lakatta, Md, Chief of the Laboratory of Cardiovascular Science, NIA stated that “Fortunately, in the past few years, we have uncovered some remarkable new clues that have clarified how and why these changes occur. At the same time, however, we have detected some intriguing evidence that transforms much of what we once thought of as normal cardiovascular aging.”

Structural Change

High quality images of the aging heart provided by the MRI, revealed that the heart might be adjusting rather than declining with age. Researchers believe that the increased thickness of the left ventricular walls during aging, allows the walls to compensate for the extra stress imposed by pumping blood into stiffer blood vessels. The thickened walls allow stress to spread out over a larger area of the heart muscle.

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Dr. Gary Gerstenblith and his colleagues found that in addition to the left ventricular wall growing thicker, the cavity of the left atrium increased. The mitral valve-the gateway between the left atrium and ventricle-appeared to close more slowly in older people. Indicating perhaps the ventricle was filling with blood more slowly. This suggests, perhaps that the ventricle wall was not relaxing between heart beats as quickly as it did when it was young. Another adjustment the heart makes with age, the NIA researchers found that the heart compensates for the slower, early filling rate by filling more quickly in the late diastolic period.

Pumping at Rest

The difference between a healthy young, resting heart and an old one is the heart rate. The sympathetic nervous system signals to the heart’s pacemaker. With age, the pathways in this system may develop fibrous tissue and fat deposits, causing the heart’s natural pacemaker to lose some of its cells. In men, the heart compensates partly for this decline in two ways. First, the increase in end diastolic volume that comes with age means there is more blood to pump; and second, the greater volume stretches the ventricular walls and brings into play a peculiar property of muscle cells-the more they are stretched, the more they contract. This phenomenon is called the Frank-Starling mechanism. With the greater volume of blood pumped, it helps to make up for lower heart rate. Encouraging findings, but even though the resting older heart can keep pace with the younger heart, the older heart is still no match even at peak condition, to the younger one during exercise or stress.

Active senior couple out for a jog on a sunny day

The body’s capacity to perform vigorous exercise declines by approximately 50% between the ages of 20 and 80, half of this is attributed to the aging heart. A 20 year-old can increase his cardiac output during exercise to 31/2-4 times over resting levels. An 80 year old can only do about 2 times as much cardiac output as at rest. Surprisingly, the aging heart still must respond to some of the same demands as the younger heart. To do so, it has the amazing ability to use its natural flexibility. The elastic-like material can alter shape and size depending on the amount of blood within its chambers.

The older heart beats less during exercise than its younger counterpart; therefore, it has more time to fill with blood between beats. However, when the heart works harder the left ventricular walls become harder and stiffer, causing increased end diastolic left ventricular pressure, which in turn prevents the oxygenated blood from the lungs to reach the left side of your heart, thereby preventing it from pumping it out to the body. Aerobic exercise can help to decrease many of these age-related affects

Communication Between the Brain and the Heart

 

ILLUSTRATIVE EDITORIAL.Vintage illustration - BRAIN AND NERVOUS 

The brain talks to the heart through the autonomic nervous system.  As we get older, the communication lines are worn and the messages from the brain aren’t as clear in its coaching ability with the heart.

The sympathetic nervous system, part of the autonomic nervous system, helps regulate the heart beat through a series of signals passed from neurotransmitters to receptors on the membranes of heart cells. The older heart doesn’t respond to these neurotransmitters, thereby it doesn’t react to stress as well as a younger heart.

Research found, that the number of beta adrenergic receptors on heart cells diminishes slightly. New studies suggest that the adrenergic receptors are capable of binding with catecholamine’s, I.e., those in a “high affinity state,” seem to decline with age. The cascade of events in the heart muscle cell that occurs after catecholamine binds to the receptors could explain why there is a reduced response to messages sent from the brain to the heart.

Calcium Pump

Calcium plays an important role in the functioning of our heart.   Research at the National Institute of Aging found that between heart beats, calcium levels diminish in a myocyte’s inner fluid or cytosol, allowing it to relax. During contraction, a large amount of calcium surges out of the myocyte’s sarcoplasmic reticulum, triggering tightening or shortening of the cell’s muscle fibers. This process occurs almost simultaneously in every cell in the heart wall, causing them to contract and pump blood out of the heart.”

If this system fails, the heart can’t relax to fill with blood and diastolic pressure in the heart increases. Individual cells may fire off rapidly and independently, causing arrhythmia, irregular heartbeats and fibrillation. Older hearts are more susceptible to spontaneous calcium oscillations and it takes fewer oscillations to bring on fibrillation which if in the left ventricle can lead to acute heart failure and death if not treated.

Age Lengthens Action Potential

As we age, the pores on the myocyte’s membrane stays open longer to allow more calcium to enter between beats. Proteins that transport calcium from the cell and sodium back into the heart work more slowly. This allows more calcium availability within the cell. This prolonged action potentially helps older hearts to work better in most situations.

Contractile Proteins

When we age chemicals that interact to shorten or contract the myocyte change. Because slower and longer contractions don’t need much energy, it helps the older heart to work more efficiently. Prolonged contractions allow the older heart to eject blood into arteries later in the heart beat, thereby improving the blood flow through the stiff arteries of the aged.

Free Radical Damage

Free radicals damage proteins, membranes, and calcium pumps on the sarcoplasmic reticulum that myocytes need to produce contractions. The result is cellular damage, where myocytes can’t process calcium as efficiently. The consequence of this deficiency is a calcium buildup in the cell, which will contract erratically, causing arrhythmia. Arrhythmia could spread to other cells, eventually disrupting the beating throughout the heart, in turn causing serious problems.
Bigger Heart Cells

As the heart cells get older, there are fewer cells to do their work, and those that remain get bigger. Enlargement of the myocyte seems to be a way the heart adapts to increased loads, but as it gets to its oldest stage, it adapts much less. This slowing in adaptive response is the reason why 80-year-old are much more likely to have heart failure following a heart attack than a 60-year-old.

Untapped Promise of an Aging Heart

Cardiovascular scientists studying apoptosis, are interested in the process called cardiac stretch. Chemicals called growth factors, such as epinephrine and angiotensin are released when the myocytes are stretched. These growth factors may play an important role to what once was thought to be impossible; the replication and regeneration of heart cells.

Hope

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There are new scientific breakthroughs every day. The pieces to the puzzle are coming together. Today there is a greater understanding to the complexities of the human body. Tomorrow the unattainable will be attainable. But we have to do our part. Live a healthy lifestyle. Eat healthy, exercise, don’t pollute your body with toxins, (cigarettes, alcohol, etc.) have a good attitude. Get regular checkups, socialize, and follow your dreams no matter what your age. If we die before we’re 100, we died a premature death.

Always check with your doctor before starting a new diet or exercise regime.

This is just an overview of the aging heart. For more in depth reading go to;   Htt://www.nia.nih.gov/HealthInformation/Publications/AgingHeartsandArteries/default.htm

source; Htt://www.nia.nih.gov/HealthInformation/Publicati ons/AgingHeartsandArteries/default.htm

 

 

 

 

 

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