Normal Structural Changes
Left Ventricle and Myocardial Remodeling
With advancing age, the heart undergoes several key structural changes. One of the most notable is a modest increase in the thickness of the left ventricular (LV) wall, often without a significant change in the overall size of the chamber. This process is known as concentric hypertrophy and is caused by the enlargement of individual heart muscle cells, or cardiomyocytes, which compensate for a natural decline in the total number of cells over time. The deposition of new, non-elastic collagen fibers, a process known as fibrosis, also stiffens the heart muscle, particularly the left ventricle. This remodeling makes the heart less flexible and less compliant.
Atrial Enlargement
The heart's upper chambers, or atria, are also affected by aging. Due to slower and less efficient filling of the stiffening ventricles, the left atrium must work harder to pump blood into the ventricle. This increased workload can cause the left atrial chamber to enlarge over time. While this can be a compensatory mechanism, it also increases the risk of atrial fibrillation, a common age-related arrhythmia.
Heart Valve Stiffening
Within the heart, the valves regulate blood flow. With age, the valves, especially the aortic valve, can thicken and become stiffer and less flexible due to increased collagen and calcium deposits. This can lead to the development of a heart murmur and, in some cases, significant valve disease like aortic stenosis, which impairs the valve's ability to open fully.
Conduction System
The heart's electrical system, which controls the heartbeat, also changes. The natural pacemaker of the heart, the sinoatrial node, loses some of its cells and becomes surrounded by fat and fibrous tissue. This degeneration of the conduction pathways can lead to a slightly slower heart rate at rest and a significantly blunted maximum heart rate during exercise, a condition known as chronotropic incompetence.
Functional Alterations in the Cardiovascular System
Diastolic vs. Systolic Function
Perhaps the most defining functional change with age is the alteration in diastolic function, the phase when the heart relaxes and fills with blood. The thickened, stiffer ventricles fill more slowly in early diastole, forcing the left atrium to contract more forcefully to complete filling in late diastole. This reliance on atrial contraction makes older adults more susceptible to issues if they develop atrial fibrillation. In contrast, resting systolic function, the heart's pumping action, is remarkably well-preserved in healthy older individuals, though it may become impaired under high-demand situations like vigorous exercise.
Blunted Response to Exercise
An aging heart's capacity to respond to physical stress decreases considerably. This is primarily due to a lower maximal heart rate and reduced contractility reserve, meaning the heart cannot pump as much extra blood per beat when pushed to its limits. The lower aerobic capacity that accompanies aging is a direct result of this reduced ability to increase cardiac output during strenuous activity.
Vascular Stiffening and Blood Pressure
Changes outside the heart also affect its function. The large arteries, particularly the aorta, become thicker, stiffer, and less flexible with age due to changes in connective tissue. This arterial stiffening increases the workload on the heart, contributing to the LV wall thickening. This also causes systolic blood pressure to rise with age, while diastolic pressure may flatten or decrease, leading to a wider pulse pressure.
Comparison of Aging Heart to Younger Heart
| Feature | Younger Heart | Aging Heart |
|---|---|---|
| Left Ventricular Wall | Normal Thickness | Modestly Thicker |
| Heart Muscle Elasticity | High | Reduced/Stiffer |
| Left Atrial Size | Normal | Modestly Enlarged |
| Diastolic Function (Filling) | Predominantly Early | Delayed Early, Increased Late |
| Resting Systolic Function | Preserved | Preserved |
| Maximal Heart Rate | High | Reduced (Chronotropic Incompetence) |
| Response to Stress/Exercise | High Reserve | Diminished Reserve |
| Heart Valves | Flexible, Pliable | Thicker, Stiffer, More Fibrosis/Calcification |
| Arterial Stiffness | Low | Increased |
The Role of Exercise in Mitigating Age-Related Changes
While the aging process is natural, lifestyle choices, particularly exercise, can significantly influence the extent and rate of cardiac changes. Regular, consistent physical activity can combat the stiffening of the heart muscle and blood vessels, maintain better heart reserve, and improve endothelial function. Studies have shown that a long-term, supervised aerobic exercise program can reverse some of the damage caused by a sedentary lifestyle, particularly if started before age 65 when the heart retains more plasticity.
Cellular and Molecular Factors
Underpinning these physiological changes are complex molecular mechanisms. These include increased oxidative stress and mitochondrial dysfunction, which reduce the energy available to heart cells and promote damage. There is also an alteration in the balance of collagen synthesis and degradation, favoring the build-up of stiffer collagen fibers, which promotes fibrosis. Senescence, or the aging of cells, also impacts cardiomyocytes and cardiac progenitor cells, contributing to their loss and functional decline.
Conclusion
Understanding what are the changes in cardiac structure and function with aging? is key to appreciating that many age-related shifts are part of a normal, adaptive process rather than an immediate sign of disease. While resting heart function remains stable in healthy individuals, challenges appear under stress. These changes, such as diastolic stiffening, reduced maximal heart rate, and arterial rigidity, do increase vulnerability to common cardiovascular diseases. However, consistent physical activity and a healthy lifestyle can powerfully counteract these effects, promoting better heart health and an improved quality of life in older age. For more information, please consult resources from the American Heart Association.
