By Tammy Petersen
The main function of this system is the internal transport of cells and dissolved materials, including nutrients, wastes, and gases.
Differences between cardiovascular functioning in older and younger persons have been extensively quantified. However, interactions between age, disease, and lifestyle are often overlooked. Whether the high prevalence of cardiovascular disorders such as hypertension, coronary artery disease, and heart failure is due to an aging process or whether these disorders merely occur more frequently in elderly persons because of a longer exposure to risk is not yet established. It is reasonable to ascertain, however, that the capabilities of the cardiovascular system gradually decline with age
Age-related changes in the blood include a decrease in the volume of packed red blood cells or constriction or blockage of peripheral veins by a blood clot. If the clot becomes detached, it might pass through the heart and become wedged in a small artery (most often in the lungs) causing a pulmonary embolism.
Age-related changes in blood vessels are often related to arteriosclerosis, a thickening and toughening of arterial walls in which the walls become less tolerant of sudden increases in pressure. This can lead to an aneurysm or rupture of the vessel causing a stroke, heart attack, or massive blood loss depending on the vessel involved. Additionally, calcium deposits can form on weakened vascular walls which increases the risk of a stroke or heart attack. Blood clots can form as plaque deposits. And, there might be pooling of blood in the veins in the legs because valves are not working effectively.
Age-related changes in the heart include a reduction in maximum cardiac output, changes in the activities of nodal and conductive fibers, a reduction in the elasticity of the heart’s fibrous tissues, progressive atherosclerosis (fatty buildup or plaques) that can restrict coronary circulation, and replacement of damaged cardiac muscle fibers by scar tissue. With age, the heart can atrophy, remain unchanged, or develop moderate or marked hypertrophy. Atrophy usually coincides with various wasting diseases and is not observed during aging in healthy persons. A modest increase in left ventricular wall thickness is normal with age; an exaggerated increase occurs in persons with hypertension. Other normal age associated changes include enlargement of the left atrium and slight enlargement of the left ventricular cavity.
Aging affects aerobic capacity and cardiovascular performance during exercise. Peak exercise capacity and peak oxygen (O2) consumption decrease with age, but there is great variation from one individual to another. Aerobic capacity decreases by 50% between ages 20 and 80, because maximum cardiac output decreases by 25% and peripheral O2 utilization decreases as muscle mass and strength decrease. Other possible disorders include inefficient redistribution of blood flow to working muscles and reduced O2 extraction and utilization per unit of muscle.
Cross-cultural studies suggest that diet, exercise habits, and smoking also affect the blood vessels and hearts of older persons. For instance, a difference in dietary sodium accounts for some of the differences in age-associated blood pressure changes. However, some changes occur because the sodium sensitivity of arterial pressure regulation increases with age. Physical conditioning appears to lessen the vascular stiffening associated with aging since stiffening is increased by only about half as much in endurance-trained seniors as compared to sedentary ones. Exercise can also improve the aerobic capacity of older persons by increasing cardiac output and O2 utilization.
The major functions of this system are locomotion, support, and heat production. When you hear the words “muscular system” we are referring to skeletal muscle only (not cardiac or smooth muscle).
As the body ages, there is generally a reduction in the size and power of all muscle tissues. In particular, skeletal muscle fibers become smaller in diameter. The overall effect of this is reduced muscular strength and endurance and a tendency to tire rapidly. Because the performance of the heart also decreases, blood flow to active muscles does not increase during exercise as rapidly as it does in younger people.
Skeletal muscles also become less elastic. Aging skeletal muscles develop increasing amounts of fibrous connective tissue, a process called fibrosis. Fibrosis makes muscle less flexible so that movement and circulation are restricted.
Tolerance for exertion decreases. A lower tolerance for exercise results partly from the tendency to fatigue rapidly and partly from the reduced ability to eliminate heat generated during muscular contraction.
Ability to recover from muscular injury decreases. The number of skeletal muscle cells/fibers is generally set before birth, and most of these fibers last a lifetime. This means that the average person does not experience an increase in the number of muscle fibers at all during a lifetime. The dramatic muscle growth that occurs after birth is achieved mainly by enlargement of existing fibers in a process called muscle hypertrophy. The body does, however, have a limited number of specialized cells called satellite cells. Satellite cells are muscle cells that retain the capacity to fuse with damaged muscle fibers and regenerate functional muscle fibers in an adult. As a result, the body has a limited ability to repair damaged tissue by replacing aged or worn out skeletal muscle fibers. Unfortunately, the number of satellite cells steadily decreases with age as the amount of fibrous tissue increases. As a result, when an injury occurs, repair capabilities are restricted, and scar tissue formation is the usual result.
Between the ages of 30 and 75, overall lean body mass decreases primarily due to reduced skeletal muscle mass. This loss is called sarcopenia and occurs as the number and size of muscle fibers progressively decrease. The pathogenesis of sarcopenia involves several age-related factors such as reduced levels of physical activity, changes in the central or peripheral nervous system that seem to affect total number of motor units, and reduced rate of skeletal muscle protein synthesis. In many elderly persons, loss of muscle mass might be accelerated as a result of greater dietary protein requirements coupled with reduced protein intake.
In healthy young persons, 30% of body weight is muscle, 20% is adipose tissue, and 10% is bone. Muscle accounts for 50% of lean body mass and about 50% of the total amount of body nitrogen. By age 75, about 15% of body weight is muscle, 40% is adipose tissue, and 8% is bone. Thus, half the muscle mass has disappeared because of sarcopenia.
The faster contracting type II muscle fibers decrease with age to a greater extent than do the slower contracting type I muscle fibers. Type II fibers participate in sudden powerful muscle contractions, whereas type I fibers function to maintain posture and to perform rhythmic, endurance-type exercises. The age-related loss of muscle fibers correlates with a loss of maximum isometric contraction force, which decreases 20% by age 60 and 50% by age 80.
The reasons for these changes in body composition and isometric contraction force are not completely understood, but contributing factors include a relative deficiency of anabolic hormones — growth hormone, insulin-like growth factor I (IGF-I), dehydroepiandrosterone (DHEA), and testosterone — and a decrease in the routine performance of vigorous muscular work. Current research indicates that exercise increases the levels of many hormones that decline with age, so it would appear that people who continue to exercise into old age would probably not experience such negative changes.
People whose mobility is restricted because of acute illness, in particular those who are bedridden, are at risk of deconditioning and an accelerated loss of muscle mass and strength. The rate of loss is anywhere from 1.5% to 3% per day. Deconditioning is greatest in the antigravity muscles which are essential for performing activities of daily living, such as sitting up, standing up, and pulling oneself up. Some geriatricians estimate that for one day of absolute bed rest, two weeks of reconditioning are necessary to return to baseline function.
Despite age-related reductions in muscle strength, muscle functional ability is similar in older and younger adults. Usually, senior persons can easily climb stairs, rise from a squatting position, walk along a straight line, hop on either foot, and perform typical activities of daily living.
Check out AAHF specialty CEC programs to learn more about exercise and nutrition for special populations!
Petersen, T. SrFit: The Personal Trainer’s Resource for Senior Fitness, Second Edition. The American Academy of Health and Fitness, 2008.
Petersen, T. SrFit: The Personal Trainer’s Resource for Senior Fitness, Third Edition. The American Academy of Health and Fitness, 2018.