mindful that physiological aging is an extremely individual process and that how the body ages is greatly affected by a person’s genetic makeup, health behaviors, and availability of resources.
The Cardiovascular System
The heart and associated vasculature connects to every organ system in the body, maintaining oxygen levels, supplying nutrients, and filtering toxins. The structural and functional abilities of
the cardiovascular system are crucial to sustain- ing the human body. Age-related changes to the cardiovascular structure and function will be evaluated in this section.
Overview of the Cardiovascular Structure and Function
The heart contains four chambers consisting of the two upper atria and the two lower ventricles (Digiovanna, 2000). Blood from the venous sys- tem enters the two atria. Oxygenated blood from the lungs enters the left atrium and deoxygenated blood from the body enters the right atrium.
Blood then flows into the ventricles, from which it is pumped into the aorta and connected arter- ies (Digiovanna, 2000). The left ventricle expels oxygen-rich blood into the aorta for delivery to the entire body, excluding the lungs. The right ven- tricle expels oxygen-poor blood into pulmonary arteries that carry the blood to the lungs for reoxy- genation (Digiovanna, 2000; Moore et al., 2003).
When ventricles contract, blood fills and stores in the arteries during systole, or peak blood pressure.
Once the ventricles relax during diastole, or low rate blood pressure, blood is propelled into the capillaries (Digiovanna, 2000; Pugh & Wei, 2001; Moore, Mangoni, Lyons, & Jackson, 2003).
Larger arteries are associated with the struc- ture and function of the heart whereas smaller arteries and arterioles are associated with sys- temic structure and function. The arterial sys- tem as a whole is responsible for the qualities of pressure and resistance that are characteristic of the cardiovascular system (Moore et al., 2003).
The veins carry over half of the total blood in the cardiovascular system and are associated with the qualities of volume and conformity (Moore et al., 2003). Figure 6-1 illustrates the arterial and venous systems within the body and organ systems while Figure 6-2 demonstrates the
Figure 6-1 The cardiovascular system.
Source: Robert L. Clark, Anatomy and physiology: Understanding the human body. Sudbury, MA: Jones and Bartlett Publishers, 2005.
Jugular veins Superior vena cava Pulmonary veins
Renal vein
Inferior vena cava
Femoral vein
Carotid arteries
Ascending aorta Pulmonary arteries
Brachial artery Coronary arteries
Renal artery
Abdominal aorta Capillary beds
Femoral artery
Superior vena cava (from head) Right
pulmonary artery
Right pulmonary vein
Right atrium
Inferior vena cava (from body)
Right ventricle
Aorta
Left pulmonary artery
Left pulmonary vein
Left atrium
Left ventricle Interventricular septum
Endocardium
Myocardium
Pericardium
Figure 6-2 Blood flow through the heart.
Source: Daniel D. Chiras, Human biology (5th ed.). Sudbury, MA: Jones and Bartlett Publishers, 2005.
structural overview of the heart and the path of blood flow into and out of the heart.
The main function of the cardiovascular sys- tem is to maintain homeostasis by transferring oxygen, nutrients, and hormones to other organ systems. The cardiovascular system also provides defense mechanisms through lymph nodes and white blood cells. In addition, this physiologi- cal system regulates body temperature as well as acid-base balance within the range of pH 7.35 to 7.45 (Digiovanna, 2000). Figure 6-3 illus- trates the pathway of oxygen-rich and oxygen-
depleted blood circulation to corresponding organs and body areas.
Aging Changes in
Cardiovascular Structure
Cardiac Aging
Enlargement of heart chambers and coronary cells occurs with age, as does increased thickening of heart walls, especially in the left ventricle (Priebe, 2000; Pugh & Wei, 2001; Weisfeldt, 1998). This enlargement and thickening causes a decline in
ventricle flexibility (Pugh & Wei, 2001) and an overall increase in heart weight of about 1.5 grams/year in women and 1.0 gram/year in men measured from age 30 to age 90 years (Ferrari et al., 2003; Lakatta, 1996). Ventricles in
the heart also begin to thicken and stiffen in cor- relation with continued steady production of col- lagen. In addition, there is a decline in the number of myocardial cells and subsequent enlargement of the remaining cells (Ferrari et al., Figure 6-3 The circulatory system.
Source: Daniel D. Chiras, Human biology (5th ed.). Sudbury, MA: Jones and Bartlett Publishers, 2005.
Venules Vena
cavae Aorta and
branches
Right ventricle
Left ventricle
Arterioles Systemic circuit
Pulmonary circuit Pulmonary
arteries
Pulmonary veins
Pulmonary circulationSystemic circulation Capillary beds of lungs where gas exchange occurs
Capillary beds of all body tissues where gas exchange occurs
Oxygen-rich, CO2-poor blood Oxygen-poor,
CO2-rich blood
2003; Olivetti, Melessari, Capasso, & Anversa, 1991; Pugh & Wei, 2001). Early studies found that the total number of myocardial cells declines by approximately 40% to 50% between the ages of 20 and 90 (Olivetti et al., 1991). However, recent investigations have concluded that women maintain myocardial cell numbers with age (Olivetti et al., 2000).
Vascular Aging
Aged arteries become extended and twisted.
Alterations also occur in endothelial cells, and arterial walls thicken due to increased levels of collagen and decreased levels of elastin (Ferrari et al., 2003; Lakatta, 1999b; Virmani et al., 1991). With age, large arteries begin to stiffen, leading to hypertension pathophysiology char- acterized by increased blood velocity from the aorta to the systemic arterial system (Moore et al., 2003; Weisfeldt, 1998). Variable levels of arterial stiffness occur depending on differential changes in elastin and collagen levels. The level of arterial stiffness also depends on whether the affected arteries are central elastic arteries or peripheral muscular arteries (Pugh & Wei, 2001; Robert, 1999). Peripheral arteries can show increased stiffness due to accumulating mineral (calcium), lipid, and collagen residues (Lakatta, 1993a; Richardson, 1994; Robert, 1999). Although arteries stiffen due to alter- ations in elastin and collagen, arterioles undergo atrophy, affecting their ability to expand with pressure alterations (Richardson, 1994).
Although the aorta and other arteries begin to stiffen with age, the left ventricle pumps the same amount of blood. This combination of arterial stiffening and stable blood flow results in increased wave velocity of blood traveling toward the arterial system and toward the aorta.
If blood returns to the aorta before the aortic valve can shut there is a resultant increase in sys-
tolic and arterial blood pressure and a decrease in diastolic pressure (Carroll, Shroff, Wirth, Halsted, & Rajfer, 1991; Lakatta, 1993a;
Schulman, 1999; Weisfeldt, 1998). The flexi- bility of the aorta remains greater in women than in men until menopause, at which time aortic flexibility declines. However, estrogen replacement recovers some of the lost aortic expandability (Hayward, Kelly, & Collins, 2000; Rajkumar et al., 1997).
Overall vascular tone tends to decline with age due to deterioration in endothelium regula- tion of vascular relaxation (Pugh & Wei, 2001;
Quyyumi, 1998). All four cardiac valves increase in circumference in older adults with the great- est increase occurring in the aortic valve. In addi- tion, calcium deposits accrue in the valves and may lead to stenosis (Pugh & Wei, 2001; Roffe, 1998; Tresch & Jamali, 1998).
In the cardiac conduction system, the sino- atrial (SA) node demonstrates some fibrosis as well as loss of pacemaker cells to approximately 10% of those observed at age 20 (Lakatta, 1993a; Wei, 1992). Also with age, the atroven- tricular (AV) node may be affected by nearby calcification of cardiac muscle (Pugh & Wei, 2001). In contrast to those of the arterial system, age-related changes to the venous system have not been well described in the literature (Moore et al., 2003). Table 6-1 summarizes cardiovas- cular age-related structural changes.
Cardiovascular Aging Mechanisms Finding the mechanism responsible for the aging of the cardiovascular system could lead to inter- ventions and therapies aimed at reducing the age-associated physiological factors that alter cardiovascular structure and functioning. Some potential mechanisms include free radicals, apoptosis, inflammatory processes, advanced gly- cation end products, and gene expression (Pugh
& Wei, 2001). Free radicals have been implicated in the overall aging process of the body, as described in Chapter 3 and also mentioned in this chapter under “The Aging Brain.” The pres- ence of lipofuscin, a brown pigment found in aging cells, relates to oxidative mechanisms. In combination with mitochondrial dysfunction, lipofuscin may result in the increased production of free radicals (Roffe, 1998; Wei, 1992).
Increased levels of free radicals can foster apoptosis, or cell death. Due to the very limited regenerative properties of cardiomyocytes, or heart cells, apoptosis can have detrimental effects on cardiovascular structure and functioning (Pugh & Wei, 2001). The proposed triggers for induction of apoptosis include elevated levels of noradrenaline and initiation of the renin- angiotensin system with age (Sabbah, 2000).
Another possible trigger for apoptosis is gene expression, which causes changes in the messen-
ger RNA (mRNA) associated with the sar- coplasmic reticulum and related enzyme ATPase (Lakatta, 1993a). These mRNA changes lead to both qualitative and quantitative alterations in the sarcoplasmic reticulum and ATPase. These alterations, in turn, lead to functional changes in relaxation of the heart and diastolic filling (Lakatta, 1993a; Lompre, 1998; Pugh & Wei, 2001). Aging mechanisms associated with the heart continue to be researched in depth, hope- fully leading to new insights in the near future.
Aging Changes in
Cardiovascular Function
Cardiac Aging
According to several studies, the ability of the heart to exert force or to contract does not change with age (Gerstenblith et al., 1997; Rodeheffer et al., 1984; Weisfeldt, 1998). At rest, the aging Table 6-1 Summarization of Cardiovascular Structural and
Functional Changes that Occur with Age
Structural changes with age
Functional changes with age
No change with age
Decreased myocardial cells, decreased aortic distensibility, decreased vascular tone
Increased heart weight, increased myocardial cell size, increased left ventricle wall thickness, increased artery stiffness, increased elastin levels, increased collagen levels, increased left atrium size
Decreased diastolic pressure (during initial filling), decreased diastolic filling, decreased reaction to -adrenergic stimulus
Increased systolic pressure, increased arterial pressure, increased wave velocity, increased left ventricular end-diastolic pressure, elongation of muscle contraction phase, elongation of muscle relaxation phase, elongation of ventricle relaxation
Ejection fraction, stroke volume, cardiac output, overall systolic function
heart adapts and maintains necessary function- ing quite efficiently (Pugh & Wei, 2001).
Although the ability of the cardiac muscle to exert force does not change with age, the actual muscle contraction as well as the relaxation phase does elongate with age (Lakatta, 1993a; Lakatta, Gerstenblith, Angell, Shock, & Weisfeldt, 1975;
Roffe, 1998; Schulman, 1999). The prolonged contraction and relaxation phases with age cor- relate with extended release of calcium as well as decline in calcium reuptake (Roffe, 1998).
Ventricles also experience prolonged relaxation due to age-related declines in the sarcoplasmic reticulum pump and associated enzyme ATPase, which produces energy for the cardiovascular sys- tem (Lompre, 1998; Pugh & Wei, 2001). The left atrium in the heart enlarges, contributing to functional changes in the filling rate. Further- more, research has demonstrated that increased arterial stiffness along with the extended relax- ation period leads to increased left ventricular end-diastolic pressure. This is demonstrated by a decline in pressure at the beginning of diastolic filling and an increase in pressure during late diastolic filling (Kane, Ouslander, & Abrass, 1999; Lakatta, 1993a; Miller et al., 1986; Pugh
& Wei, 2001; Roffe, 1998). With age, diastolic filling declines at a rate of approximately 6% to 7% each decade both during exercise and at rest, but diastolic heart failure rarely occurs (Schulman, 1999). Increased left ventricle mass has been cor- related with age-related declines in initial dias- tolic filling (Salmasi, Alino, Jepson, & Dancy, 2003). The increase in left ventricular mass cor- relates with increased total blood flow and ele- vated systolic blood pressure (Weisfeldt, 1998).
However, no age-related change occurs in ejec- tion fracture, stroke volume, or cardiac output (Ferrari, Radaelli, & Centola, 2003; Gerstenblith et al., 1997; Rodeheffer et al., 1984).
Vascular Aging
Aging does not appear to change the overall max- imum capacity, the maximum vasodilation, or the perfusion of coronary vessels (Weisfeldt, 1998).
However, resistance increases with age in the aorta, arterial wall, and vascular periphery. In addition, blood viscosity increases between the ages of 20 and 70 years (Morley & Reese, 1989).
Cardiovascular symptoms of hypertension paral- lel the usual aging changes seen in older adults.
Such symptoms, however, are exhibited at younger ages as well and are sometimes exagger- ated. These differences have led to use of the term muted hypertension to describe cardiovascular aging changes (Lakatta, 1999b). Other changes such as moderate accumulation of cardiac amyloid and lipofuscin do not appear to alter functional abili- ties, but they are present in approximately half of individuals over age 70, and elevated levels could produce degenerative changes (Pugh & Wei, 2001). No age-related changes occur in blood- tissue exchange via the capillaries, suggesting a possible compensatory mechanism such as capil- lary thickening (Richardson, 1994).
Autonomic Nervous System Aging Effects
A few of the age-related changes in the cardio- vascular system occur in the autonomic ner- vous system. These changes include decreased reaction of the entire system, myocardial and vascular, to -adrenergic stimulus as well as reduced baroreflex activity relating to an imbal- ance in neuroendocrine control (Lakatta, 1999b;
Philips, Hodsman, & Johnston, 1991; Pugh &
Wei, 2001; Weisfeldt, 1998). Norepinephrine concentrations increase with age, causing over- activation of the sympathetic nervous system.
This overactivation subsequently leads to over- stimulation of -adrenoceptors, even to the
point of desensitization (Esler, Kaye, et al., 1995; Lakatta, 1993b, 1999a; Moore et al., 2003). With usual functional abilities, however, stimulation of the -adrenoceptors triggers ves- sel dilation. In contrast, ␣-adrenoceptors that control vessel constriction remain stable with age (Priebe, 2000; Weisfeldt, 1998). Reduced arterial baroreflex activity, which controls peripheral vessels, has been correlated with sev- eral changes including arterial stiffening, neu- ral modifications, and decreased stimulation of baroreceptors (Hunt, Farquar, & Taylor, 2001).
These changes in baroreflex activity can lead to impaired sympathetic nerve response and resis- tance in peripheral vessels. As a result, blood pressure becomes unstable and hypotension may result (Ferrari et al., 2003). Table 6-1 summa- rizes age-associated changes in the functional abilities of the cardiovascular system.
Exercise and Aging
When older adults exercise, the cardiovascular response is different than the response of younger individuals. Cardiovascular condition during exercise is usually measured using maximum oxygen consumption (VO2max), which equals the sum of cardiac output and systemic oxygen reserve. VO2max shows age-related declines of around 10% per decade beginning in the second decade of life and reductions of around 50% by age 80 (Aronow, 1998; Maharam, Bauman, Karlman, Skolnick, & Perle, 1999). Cardio- vascular reserve is best measured using maxi- mum cardiac output, which is equal to heart rate multiplied by stroke volume during exercise (Fleg, 1986). For example, with age the increased heart rate and contractility usually associated with exercise become less pronounced;
however, opposition to blood flow increases (Weisfeldt, 1998). With these changes an over-
all decline in cardiac function and cardiac output is observed with initiation of exercise (Pugh &
Wei, 2001; Weisfeldt, 1998).
A number of individuals from the Baltimore Longitudinal Study, aged 20 to 80 years and without heart disease, participated in an exercise program so that their cardiovascular function- ing could be assessed (Rodeheffer et al., 1984).
The researchers conducting this study observed and concluded that when older adults began to exercise their heart rate did not respond as well, a greater end systolic volume existed, and heart contractility declined. However, as these older adults continued to exercise, the end diastolic volume increased, producing greater stroke volume and ending with an unchanged cardiac output. Other research has shown similar con- clusions with exercise including decreased heart rate and contractility, decreased peak heart rate and ejection fraction, decreased end-systolic vol- ume, increased end-diastolic volume, and pre- served stroke volume, further supporting the findings of increased left ventricle end-diastolic volume and maintained cardiac output during exercise (Fleg et al., 1995; Kane et al., 1999;
Lakatta, 1993a, 1999a; Roffe, 1998; Wei, 1992).
Exercise also increases vascular resistance and ele- vates both systolic and diastolic pressure (Lind &
McNicol, 1986). Salmasi and colleagues (2003) conducted a research study involving 55 patients less than 50 years of age and 45 patients greater than 50 years of age and evaluated them for left ventricle diastolic function at rest and during iso- metric exercise. These researchers concluded that degeneration in left ventricle diastolic function- ing occurred in the 50 year and older group both at rest and during isometric exercise due to ven- tricle stiffening leading to decreased diastolic fill- ing initially (Salmasi et al., 2003). Conclusions on cardiovascular change with exercise must be
Table 6-2 Lifestyle Interventions to Maintain or Improve Physiological Functioning in Aging
Physical activity 1. Do some type of exercise at least 30 minutes a day and more involved exercise 3–5 days per week.
2. Include cardio training, weight-bearing exercise, resistance, balance training, and flexibility exercise.
Nutrition 1. Low calorie diet
2. Low fat diet 3. Low cholesterol diet 4. Low sodium diet
5. At least five fruits and vegetables per day 6. Plenty of whole grains
7. Eight glasses of water a day
Vitamins and minerals 1. Vitamins: B6, B12, D, K, A, C, E, beta carotene, and folic acid 2. Minerals: selenium, calcium, and iron
Examples of self-report 1. The Physical Activity Scale for the Elderly (PASE) (Washburn et al., assessment measures of 1993)
physical activity and 2. Nutritional Risk Index (Wolinsky et al., 1990)
nutrition status 3. The DETERMINE Screen (Nutrition Screening Initiative, 1992) Prevalence rates of weight, 1. Obese: Men—27%, Women—32%
dietary intake, and physical Age 65–74: Men—32%, Women—39%
activity in individuals Age 75 and over: Men—18%, Women—24%
age 65 and over Overweight: Men—73%, Women—66%
Underweight: Men—1%, Women—3%
2. Diet (Healthy Eating Index):
19% good diet, 67% needed improvement, 14% poor diet
*low score on daily fruit and dairy servings
*high score on variety of food and cholesterol intake 3. Nonstrenuous physical activity: 21% total for 65 and over;
Regular strenuous physical activity:
Age 65–74: 26%
Age 75–84: 18%
Age 85 and over: 9%
Source: Drewnowski & Evans, 2001; Federal Interagency Forum on Aging-Related Statistics, 2004; McReynolds & Rossen, 2004; Topp et al., 2004)
Although structural and functional changes occur in the cardiovascular system with age, some changes remain variable across time and across evaluated carefully in order to discern age-
associated alterations across time and across indi- viduals (Table 6-2).
individuals. Some research studies comparing cardiovascular function across different age cohorts do not take into account nutrition prac- tices, exercise regimens or lack thereof, and other effects such as the lifestyle of older adults across time and space compared to younger individuals (Lakatta, 1999b). For example, older adults today often will say they grew up on a farm with large meals and a lack of concern for fat content; how- ever, younger individuals today are very health conscience with tremendous focus on fat and calo- ries. Nutrition and exercise habits as well as other health-related practices continually change over time, which brings up the question of how com- parable younger individuals are to older individ- uals in terms of cardiovascular functioning.