With advanced age, cells of the myocardium show microscopical signs of degeneration including increases in myocardial fat content (i.e., storage of triglyceride droplets within cardiomyocytes); however, the relationship between the quantity of fat and disease severity remains unclear.11 Unlike aging skeletal muscle cells, there is minimal atrophy of cardiac smooth muscle cells. More typically, there is hypertrophy of the left ventricular myocardium, increasing the diameter of the left atrium.^12–14 These changes have been attributed to cardiac tissue responses to an increased systolic blood pressure (SBP) and to reduced compliance of the left ventricle and are associated with an increase in weight and size of the heart.^13–17

The four valves of the aged heart often become fibrous and thickened at their margins, as well as somewhat calcified.18 Calcification of the aorta at the base of the cusps of the aortic valve (aortic stenosis) is clinically associated with the slowed exit of blood from the left ventricle into the aorta.¹⁹ Such aortic stenosis contributes to a functional reduction in CO. A baroreflex-mediated increase in SBP attempts to compensate for this reduced CO.^20,21 Over time, the larger residual of blood in the left ventricle after each beat (increased end systolic volume, or ESV) begins to weaken the left ventricular muscle.²² The left ventricular muscle must work harder to pump the blood out of the ventricle into a more resistant peripheral vascular system.^23,24

Calcification of the annulus of the mitral valve can restrict blood flow from the left atrium into the left ventricle during diastole. As a result, end diastolic volume (EDV) of blood in the left ventricle is decreased because the left atrium does not completely empty. Over time, this residual blood in the left atrium elongates the muscle of the atrial walls and increases the diameter of the atrium of the heart.^23–25

Age-related changes of the coronary arteries are similar to those in any aged arterial vessel: an increase in thickness of vessel walls and tortuosity of its path.26 These changes tend to occur earlier in the left coronary artery than in the right.²⁷ When coupled with atherosclerosis, these changes may compromise the muscular contraction and pumping efficiency and effectiveness of the left ventricle during exercise or activity of high physiological demand.^2,3,28

Age-related changes in the conduction system of the heart can have a substantial impact on cardiac function. The typical 75-year-old has less than 10% of the original number of pacemaker cells of the sinoatrial node.29,³⁰ Fibrous tissue builds within the internodal tracts as well as within the atrioventricular node, including the bundle of His and its main bundle branches.^29,30 As a consequence, the ability of the heart to coordinate the actions of all four of its chambers may be compromised.²⁹ Arrhythmias are pathological conditions that become more common in later life; they are managed pharmacologically or with implantation of a pacemaker/defibrillator.³¹ Rehabilitation professionals must be aware of the impact of medications or pacemaker settings on an individual’s ability to physiologically respond to exercise and to adapt to the intervention, whether it be a conditioning program or early mobility after a medical/surgical event, accordingly.³²

Age-related changes in the arterial vascular tree, demonstrated most notably by the thoracic aorta and eventually the more distal vessels, can disrupt the smooth or streamline flow (i.e., laminar flow) of blood from the heart toward the periphery.31,³³ Altered alignment of endothelial cells of the intima creates rough or turbulence flow (i.e., nonlaminar flow), which increases the likelihood of deposition of collagen and lipid.³⁴ Fragmentation of elastic fibers in the intima and media of larger arterioles and arteries further compromises the functionally important “rebound” characteristic of arterial vessels.³⁵ Rebound normally assists directional blood flow through the system, preventing the backward reflection of fluid pressure waves of blood. This loss of elasticity increases vulnerability of the aorta, which, distended and stiffened, cannot effectively resist the tensile force of left ventricular ejection. Not surprisingly, the incidence of abdominal aortic aneurysms rises sharply among older adults, and stiffness (distensibility) of the ascending aorta is associated with severity of coronary artery disease.^36,37

One of the most marked age-related changes in cardiovascular function is the reduced sensitivity of the heart to sympathetic stimulation, specifically to the stimulation of beta-adrenergic receptors.40,⁴¹ Age-related reduction in beta-adrenergic sensitivity includes a decreased response to norepinephrine and epinephrine released from sympathetic nerve endings in the heart, as well as a decreased sensitivity to any of these catecholamines circulating in the blood.^41,42 Normally, norepinephrine and epinephrine are potent stimulators of ventricular contraction.

An important functional consequence of the change in receptor sensitivity is less efficient cardioacceleratory response, which leads to a lower HR at submaximal and maximal levels of exercise or activity.⁴³ The time for HR rise to the peak rate is prolonged, so more time is necessary to reach the appropriate HR level for physically demanding activities. A further consequence of this reduced beta-adrenergic sensitivity is less than optimal vasodilation of the coronary arteries with increasing activity.^41,44 In peripheral arterial vessels, beta-adrenergic receptors do not appear to play a primary role in mediating vasodilation in the working muscles.⁴⁵

Age-related change in the cardiovascular baroreceptor reflex also contributes to prolongation of cardiovascular response time in the face of an increase in activity (physiological demand).40 The baroreceptors in the proximal aorta appear to become less sensitive to changes in blood volume (pressure) within the vessel. Normally, any drop in proximal aortic pressure triggers the hypothalamus to begin a sequence of events that leads to increased sympathetic stimulation of the heart. Decreased baroreceptor responsiveness may increase an older individual’s susceptibility to orthostatic (postural) and postprandial (after eating) hypotension, or compromise their tolerance of the physiological stress of a Valsalva maneuver associated with breath holding during strenuous activity.^46,47 Clinically, this is evidenced by lightheadedness when rising from lying or sitting, especially after a meal, or if one tends to hold one’s breath during effortful activity.

The consequences of age-related physiological changes on the cardiovascular system can often be managed effectively by routinely using simple lower extremity warmup exercises before position changes. Several repetitions of ankle and knee exercises before standing up, especially after a prolonged time sitting (including for meals) or lying down (after a night’s rest), help maximize blood return to the heart (preload), assisting cardiovascular function for the impending demand. In addition, taking a bit more time in initiating and progressing difficulty of activities may help the slowed cardiovascular response time reach an effective level of performance. Scheduling physical therapy or physical activity remote from mealtimes might also be beneficial for patients who are particularly vulnerable to postprandial hypotension.

Cardiac filling/preload determines the volume of blood in the left ventricle at the end of diastole. The most effective ventricular filling occurs when pressure is low within the heart and relaxation of the muscular walls of the ventricle is maximal.1,⁵ Mitral valve calcification, decreased compliance of the left ventricle, and the prolonged relaxation of myocardial contraction can contribute to a less effective filling of the left ventricle in early diastole.⁴⁸ Doppler studies of the flow of blood into the left ventricle in aging adults demonstrate decreased rates of early filling, an increased rate of late atrial filling, and an overall decrease in the peak filling rate.^5,22,48 When compared with healthy 45- to 50-year-old adults, the early diastolic filling of a healthy 65- to 80-year-old is 50% less.^5,22,49 This reduced volume of blood in the ventricle at the end of diastole does not effectively stretch the ventricular muscle of the heart, compromising the Frank-Starling mechanism and the myocontractility of the left ventricle.⁵⁰ The functional outcome of decreased early diastolic filling and the reduced EDV is a proportional decrease in SV, one of the determinants of CO and, subsequently, work capacity (VO_2max).^5,21,40

High vascular impedance and increased afterload disrupts flow of blood as it leaves the heart toward the peripheral vasculature. Increased afterload is, in part, a function of age-related stiffness of the proximal aorta, an increase in systemic vascular resistance (elevation of SBP, hypertension), or a combination of both factors.40,⁵¹ Ventricular contraction that forces blood flow into a resistant peripheral vascular system produces pressure waves in the blood. These pressure waves reflect back toward the heart, unrestricted by the stiffened walls of the proximal aorta. The reflected pressure waves, aortic stiffness, and increased systemic vascular resistance collectively contribute to an increased afterload in the aging heart.^39,51 Increased afterload is thought to be a major factor in the age-associated decrease in maximum SV, hypertrophy of the left ventricle, and prolongation of myocardial relaxation (e.g., slowed relaxation in the presence of a persisting load on the heart).^6,7,9

An unfortunate long-term consequence of increased afterload is weakening of the heart muscle itself, particularly of the left ventricle. Restricted blood flow out of the heart results in a large residual volume (RV) of blood in the heart at the end of systole when ventricular contraction is complete. Large ESVs gradually increase the resting length of ventricular cardiac muscle, effectively weakening the force of contraction.^{2,6,7,9,22,52}

Left Ventricular Ejection Fraction

Left ventricular ejection fraction (LVEF) is the proportion of blood pumped out of the heart with each contraction of the left ventricle, which is expressed by the following equation:

LVEF=(EDV−ESV)  ÷  EDV

At rest the LVEF does not appear to be reduced in older adults. Under conditions of maximum exercise, however, the rise in LVEF is much less than in younger adults.21,^53,54 This reduced rise in the LVEF with maximal exercise clearly illustrates the impact that preload and afterload functional cardiovascular age-related changes have on performance.

A substantial reduction in EDV, an expansion of ESV, or a more modest change in both components may account for the decreased LVEF of the exercising older adult:

↓EDV  =  ↓LVEF↑ESV  =  ↓LVEF

When going from resting to maximal exercise conditions, the amount of blood pumped with each beat for young healthy adults increases 20% to 30% from a resting LVEF of 55% to an exercise LVEF of 80%. For a healthy older adult, in contrast, LVEF typically increases less than 5% from rest to maximal exercise.^53,55 The LVEF may actually decrease in adults who are 60 years of age and older.^53,56 As LVEF and CO decrease with aging, so does the ability to work over prolonged periods (functional cardiopulmonary reserve capacity) because the volume of blood delivered to active tissue decreases (Figure 2-3). Functional reserve capacity is further compromised by the long-term effects of inactivity and by cardiopulmonary pathology.^21,28,57,58 The contribution of habitual exercise to achieving effective maximum exercise LVEF is not well understood but the decline may not be as substantial for highly fit older adults.²¹

One of the readily measurable consequences of the reduced response of the heart to sympathetic stimulation in later life is a reduction in the maximal attainable HR.39,^69,75 This reduction in maximal HR also signals that an older person’s HR reserve, the difference between the rate for any given level of activity and the maximal attainable HR, is limited as well. For older patients involved in rehabilitation programs, the difference between resting and maximal HR is narrowed. One method of estimating maximal (max) attainable HR is the following⁵:

Max HR  =  220  −  age

For healthy individuals, the recommended target HR for aerobic conditioning exercise is between 60% and 80% of maximal attainable HR. For many older adults, especially those who are habitually inactive, resting HR may be close to the recommended range for exercise exertion.⁷⁶ Consider an 80-year-old individual with a resting HR of 72 beats per minute. His maximal attainable HR is approximately 140 beats per minute (220 − 80 years). A target HR for an aerobic training level of exertion of 60% of maximal HR would be 84 beats per minute. His resting HR is within 12 beats of the HR for aerobic training. Functionally, this means that an activity as routine as rising from a chair or walking a short distance on a level surface may represent physical work of a level of exertion equated with moderate- to high-intensity exercise. Because of the reduction in maximal attainable HR with age, older adults may be working close to their VO_2max range even in usual activities of daily living.^76,77

Because HR essentially signals the work of the heart, with each beat representing ventricular contraction, increased HR relates closely to increased heart work and increased oxygen consumption by the myocardium.⁷⁵ Given that afterload on the heart increases with age, the overall work of the heart for each beat is likely greater as well.^21,38,39,40 A more representative way to estimate the work of the heart during activity for older adults is the rate pressure product (RPP),^78–80 using HR and SBP as follows:

RPP=HR  ×  SBP

The linear relationship between VO_2max and HR for younger adults actually levels off for older adults.⁸¹ Because of this, HR alone cannot accurately reflect the physiological work that the older patient experiences; the RPP provides a clearer impression of relative work.⁸⁰ For older individuals with HR reserve limited by age, adjusting activity to keep the rise in HR within the lower end of the HR reserve is wise, especially for those with known coronary artery compromise.

An older person’s blood pressure (BP) must also be considered. Hypertension, particularly increased SBP, is common in older adults. SBP also provides a relative indication of the level of afterload on the heart.40,^82,83 Resting BP can be used to indicate whether an older person can safely tolerate increased physiological work. Persons with resting BPs of more than 180/95 mm Hg may have difficulty with increased activity. A conservative estimate of the safe range of exercise suggests that exercise should be stopped if and when BP exceeds 220/110 mm Hg, although some consider 220 mm Hg too conservative a limit for older adults.⁷⁵ SBP should rise with increasing activity or exercise.⁸⁴

The older adult with limited HR reserve must increase SV to achieve the required CO.^21,39,53 SBP rises as SV increases and blood volume in the peripheral vasculature rises.⁴⁰ If SBP fails to rise or actually decreases during activity, this is a significant concern.⁷⁵ The drop or lack of change in SBP indicates that the heart is an ineffective pump, unable to contract and force a reasonable volume of blood out of the left ventricle. Continuing exercise or activity in the presence of a dropping SBP returns more blood to a heart that is incapable of pumping it back out to the body. Elevated diastolic blood pressure (DBP) suggests that the left ventricle is maintaining a higher pressure during the filling period.^39,40,69 Early diastolic filling during preload will be compromised,^40,49 and the heart will be unable to capitalize on the Frank-Starling mechanism to enhance the force of ventricular contraction.^21,53

Dyspnea, or shortness of breath, is an important warning sign as well. Age-related changes in the pulmonary system increase the work of breathing, and breathing becomes less efficient as work increases.72 Because an older person is prone to shortness of breath, recovering from shortness of breath during exercise may be difficult. Breathing more deeply requires a disproportionately greater amount of respiratory muscle work, which further increases the cost of ventilation.^73,74 The use of supplemental oxygen by nasal cannula for the postoperative or medically ill older adult who is beginning rehabilitation may be quite beneficial.

Oxygen supplementation may prevent or minimize shortness of breath, enabling an older person to tolerate increased activity better and to participate in rehabilitation more fully. During this oxygen-assisted time, any conditioning exercise to improve muscular performance (especially if combined with nutritional support) delivers blood to the working tissues and improves tissue oxygenation, ultimately aiding pulmonary function. Improved muscular conditioning and cardiovascular function may prevent or delay onset of lactic acidemia and the resultant increased desire to breathe that would trigger shortness of breath.^72,85