Organ Systems Physiological Changes: Cardiovascular
Reserve Capacity Of The Heart
At rest, the heart of an average person pumps approximately five liters of blood per minute (cardiac output). The cardiac output can increase dramatically when demand for blood flow increases during physical activity. During maximal exercise, the cardiac output can be as high as thirty-five liters per minute. This tremendous capacity of the heart to increase its pumping ability is accomplished by increasing the heart rate and stroke volume and is termed the reserve capacity of the heart. The heart rate and stroke volume can be measured during exercise to assess the reserve capacity of the heart, and the overall capacity of the body to exercise is assessed by measuring the maximal rate of oxygen consumption (VO 2 max). The reserve capacity of the body is important for two reasons. First, it allows an individual to meet the needs required by physical work and play. Second, the reserve capacity of the heart provides a margin of safety that allows one to survive the effects of cardiovascular diseases.
Exercise response. The peak work rate and oxygen consumption of healthy, sedentary men and women during upright, seated, bicycle exercise, declines by approximately 50 percent with advancing age between twenty and eighty years of age. This is attributable to approximate declines of 25 percent in cardiac output and 25 percent in oxygen utilization (the ability of the skeletal muscles to extract oxygen from the blood and the ability of the vascular system to deliver blood [(A-V)O 2 difference, see Table 2]). The age-associated decrease in cardiac output is during peak exercise is due entirely to a reduction in maximal heart rate, as the stroke volume index does not decline with age in either men or women. However, the manner in which stroke volume is achieved during exercise varies dramatically with aging. The EDV increases during vigorous exercise in older, but not younger, men and women (see Figure 4). But, because the end-systolic volume (ESV) in older persons fails to become reduced to the same extent as in a younger individual, the percentage of the total blood ejected per beat (EF) decreases, and the SV is not greater, in older persons. In other words, while the Frank-Starling mechanism (a unique property of the heart that results in a stronger heartbeat when more blood is present in the heart at the beginning of a contraction) is utilized in older persons during exercise, its effectiveness is reduced because the LV of an older person does not empty to the extent to which it does in younger individual. Thus, the older heart, while contracting from a larger preload (amount of blood in the ventricle at beginning of contraction) than the younger heart at all levels of exercise, delivers a stroke volume that equals that of the younger heart.
The deficiency in the ability of the old heart to "squeeze down" and reduce LV end-systolic volume during exercise in healthy older individuals likely results from increased stiffness of the arteries, from decreased contractility of the heart muscle, and from a decline in the response of the heart to the sympathetic nervous system (β-adrenergic responsiveness).
β-Adrenergic modulation of cardiovascular performance. During exercise, excitement or stress, the sympathetic nervous system becomes activated and releases norepinephrine and epinephrine (commonly referred to as adrenaline). Norepinephrine and epinephrine act in the heart by binding to β-adrenergic receptors and increases both the heart rate and the strength of contraction. β-adrenergic receptors mediate the effects of the hormones/neuro-transmitters norepinephrine and epinephrine (commonly referred to as adrenaline). They are important in regulating the heart rate and strength of each beat. Without β-adrenergic receptors, the adrenaline produced by the nerves and adrenal gland, would have no effect on the heart. One of the most prominent changes in the cardiovascular response to exercise stress that occurs with aging in healthy individuals, is a reduction in the ability of norepinephrine and epinephrine to activate the β-adrenergic system of the heart, thereby limiting the maximum heart rate and the strength of contraction in the aging heart. Resting sympathetic nervous activity increases progressively with aging, as does the sympathetic response to any perturbation from the resting state. Plasma levels of epinephrine and norepinephrine increase with age, due to enhanced spillover into the circulation and to reduced clearance. The increased spillover does not occur from all body organs, but is increased within the heart, and is thought to be due, in part at least, to a reduced reuptake by the nerve endings following release. The net result is likely an enhanced post-synaptic receptor occupancy by neurotransmitter, leading to β-adrenergic receptor desensitization. Deficits in β-adrenergic signaling with aging are attributable, in large part, to changes in enzymes and proteins that relay the signals from the β-adrenergic receptor to the molecules inside the heart muscle cell that control the rate and force of contraction.
- Organ Systems Physiological Changes: Cardiovascular - Vascular Structure And Function At Rest
- Organ Systems Physiological Changes: Cardiovascular - Heart Structure And Function At Rest
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Medicine EncyclopediaAging Healthy - Part 3Organ Systems Physiological Changes: Cardiovascular - Heart Structure And Function At Rest, Reserve Capacity Of The Heart, Vascular Structure And Function At Rest