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Life System: Anatomy and physiology of ageing 1: the cardiovascular system

The normal ageing process brings about
changes to the cardiovascular system that
mean the heart works less efficiently. What
exactly happens and why?
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In this article…
How age affects the normal functioning of
the cardiovascular system
Age-related changes to vasculature,
chemicals, heart muscles and blood
Conditions experienced by older people as
a result of declining heart function
John Knight is senior lecturer in biomedical
science; Yamni Nigam is associate professor in
biomedical science; both at the College of Human
Health and Science, Swansea University.
The cardiovascular system is the body’s main
transport system, and its efficiency is
essential for health and longevity. As it ages,
it becomes less efficient, which has a negative
impact on all other organ systems. This
article explores the normal age-related
changes occurring in the cardiovascular
system. This is the first of an updated article
series on how age affects the main organ
Knight J, Nigam Y (2017) Anatomy and
physiology of ageing 1: the cardiovascular
system. Nursing Times [online]; 113: 2,
This article has been double-blind peer
Download a print-friendly PDF file of this
article here
Key points
1. An efficient cardiovascular system is
essential for health and longevity,
but age brings about changes that reduce
its efficiency
2. Blood vessels, particularly arteries, lose
their elasticity with age, and the arterial
walls become stiffer and thicker
3. Age-related changes in the chemical
signals produced by the body
contribute to restricting blood flow
4. As the heart ages, it undergoes a
redistribution of its muscle mass, which
negatively affects its function
5. Older people should be encouraged to
take regular exercise, which will support
their cardiovascular function well into old
The average lifespan of people in the UK is rising
– mainly due to advances in healthcare – and
many 60-year-olds can expect a further 25 years
of healthy life. However, knowledge of the ageing
process remains limited. This is the first article in
an updated and expanded series examining the
anatomy and physiology of ageing.
The ageing process is largely determined by
genetic factors but it is also heavily influenced by
environmental factors such as diet, exercise and
exposure to micro-organisms, pollutants and
ionising radiation. That is why people of the same
age vary both in physical appearance and
physiology. Gender also plays a part; in most
developed countries, women typically outlive men
by 7-10 years.
The cardiovascular system
The cardiovascular system is the body’s main
transport system. Its most important role is to
deliver oxygenated blood, nutrients and chemical
signals, such as hormones, to the organs and
tissues. It also transports carbon dioxide to the
lungs and waste products, such as urea and uric
acid, to the kidneys for elimination. It plays a
major role in thermoregulation – distributing and
dissipating heat throughout the body (Marieb and
Hoehn, 2015). An efficient cardiovascular system
is essential for health and longevity, but its
efficiency reduces with age, which has a negative
impact on all other organ systems.
Vascular changes
We are born with arteries that are elastic, flexible
and compliant, allowing optimal cardiac function
and blood flow. During ventricular systole
(contraction), blood is ejected into the pulmonary
and systemic circuits and the larger elastic
arteries stretch, reducing the resistance to blood
flow. As the body ages, blood vessels, particularly
arteries, lose their elasticity and the arterial walls
become stiffer and thicker.
The tunica intima is the innermost layer of a
blood vessel, and consists of two main regions:
Endothelium – a single layer of cells;
Lamina – a thin layer of connective tissue that
anchors the endothelium to the tunica media
(muscle layer) above. This mainly comprises
elastin (elastic fibres) and collagen, and
undergoes significant changes with age.
The larger arteries have a high elastin content as
they need to stretch in harmony with the powerful
ventricular contractions of the heart to cushion
the force of the pulse wave, smoothing out the
flow of blood entering the smaller arteries. These
smaller arteries have much less elasticity and a
greater proportion of collagen fibres in their vessel
walls (Steppan et al, 2011).
The tunica media, which lies underneath the
tunica intima, is made up of layers of smooth
muscle cells. It is controlled by the vasomotor
centre within the medulla oblongata (the lower
part of the brain stem). The vasomotor centre
plays an important role in regulating blood
pressure by controlling vasodilation and
vasoconstriction (Marieb and Hoehn, 2015).
With age comes a gradual thickening of the tunica
intima and tunica media of large and medium-
sized arteries (Fig 1). This is associated with an
increase in the number and density of collagen
fibres in the vessel walls (Ferrari et al, 2003).
Collagen fibres also undergo a process of cross-
linking, which makes them less compliant. With
age and repeated stretching, elastin – which
partly gives arterial walls their elasticity –
undergoes fracture and fatigue (Greenwald, 2007).
Ageing blood vessels may also display varying
degrees of calcification. These events
cumulatively result in a gradual loss of elasticity
and stiffening of the arteries, which is often
reflected by increased blood pressure (Bolton and
Rajkumar, 2011).
Fig 1. Age-induced arterial thickening
The endothelium, the most delicate part of a blood
vessel, is in direct contact with the circulating
blood (Marieb and Hoehn, 2015). It is composed
of a single layer of squamous epithelial cells that,
in children and young adults, are regular and
smooth, minimising resistance to blood flow.
As it ages, the endothelium develops irregularly
shaped cells and is often thickened due to the
presence of smooth muscle fibres that have
migrated from the tunica media. This thickening
contributes to a reduction in arterial elasticity and
compliance, and reduces the lumen size (Fig 1),
further increasing resistance to blood flow.
Atherosclerosis, the most common form of blood
vessel disease, is triggered by injury to the
endothelium, which can have a wide variety of
causes including:
Toxins (for example, cigarette smoke);
The mechanism of atherosclerotic occlusion (fatty
deposits) following endothelial damage involves
monocytes (white blood cells) attaching to the
damaged or irritated endothelium and crossing
into the tunica media. These monocytes gradually
grow and mature into much bigger cells called
macrophages (Galkina and Ley, 2009). The
macrophages absorb fat (including cholesterol)
from the blood and ‘puff up’ to form foam cells.
These foam cells form ‘fatty plaque’ that occludes
blood vessels (Libby et al, 2011).
Atherosclerosis of the coronary arteries may
result in coronary artery disease. The fatty plaque
often ruptures, resulting in clot formation and
heart attack (myocardial infarction). Similarly,
atherosclerosis of the carotid or cerebral arteries
dramatically increases the risk of stroke.
Chemical changes
Reduced nitric oxide production
Endothelial cells release various chemical signals
that help to regulate blood flow by controlling the
internal diameter of blood vessels. One of the
most important of these chemicals is nitric oxide,
which is produced by endothelial cells from the
amino acid L-arginine. This diffuses into the
smooth muscle layer of the blood vessels, where
it acts as a powerful vasodilator, expanding the
vessels and ensuring good blood flow.
Damage to the endothelium – be it age-related or
due to other causes – results in reduced nitric
oxide generation and therefore blood flow
(Greenwald, 2007; Bode-Böger et al, 2003). This
contributes to, and may exacerbate, age-related
blood vessel pathologies including peripheral
vascular disease and angina pectoris.
Increased pro-inflammatory
The concentration of pro-inflammatory chemical
mediators circulating in the blood increases with
age. Many are implicated in blood vessel
pathology, including atherosclerotic occlusion and
blood vessel wall calcification (Harvey et al,
Delayed angiogenesis
After an injury or infection, new blood vessels can
be rapidly produced in a process known as
angiogenesis. This is orchestrated by a variety of
chemical signals and growth factors.
Angiogenesis slows with age, and is often
significantly delayed (Sadoun and Reed, 2003),
which may help to explain why wound healing
generally occurs more slowly in older people.
Cardiac changes
To overcome reduced elasticity and increased
resistance to blood flow of aged and occluded
arteries, the heart’s ventricles have to pump with
greater force. The myocardium (muscular layer of
the heart) responds by becoming hypertrophied.
Earlier ultrasound studies suggested the thickness
of the left ventricle increases by around 30%
between the ages of 20 and 80 years, with an
associated gradual increase in cardiac weight
(Pearson et al, 1991). However, the validity of
some of these studies has recently been
Examination of hearts removed during autopsy
revealed little evidence of age-related ventricular
thickening in women, while in men, there was
often an apparent reduction in muscle mass. The
hypertrophy observed on ultrasound scans seems
to result primarily from a thickening of the
intraventricular septum, rather than the left
ventricle; a remodelling and redistribution of
cardiac muscle tissue seems to occur with age
(Strait and Lakatta, 2012).
The number of cardiac myocytes (muscle cells) in
the myocardium decreases progressively through
apoptosis (programmed cell death); the remaining
myocytes undergo morphological changes, often
becoming enlarged (cellular hypertrophy) or
irregular in shape. The amount of collagen
deposited in the myocardium also increases with
age. Together with the redistribution of cardiac
muscle mass, this typically results in an
observable change in the shape of the heart from
the classic elliptical shape to a slightly more
spherical appearance (Strait and Lakatta, 2012;
Ferrari et al, 2003).
Wear and tear to the heart’s internal structure
(which occurs more rapidly in patients with
hypertension) can also lead to calcification and
fibrous scar tissue on the heart valves. This
commonly results in stenosis (a narrowing in the
aperture of the valve), which restricts blood flow
and reduces the heart’s efficiency. Stenosed
valves typically produce a turbulent blood flow,
which may be detected through a stethoscope as
a heart murmur (Bolton and Rajkumar, 2011).
Cardiac function
The changes to both the vasculature and the heart
itself lead to a general reduction in the efficiency
of the heart. The resting heart rate when a person
is lying flat remains fairly constant as we age but,
in a sitting position, this generally decreases
(Bolton and Rajkumar, 2011).
One of the most striking age-related changes in
cardiac function is a linear decrease in the
maximal heart rate achievable during exercise. In
young healthy children, a maximal heart rate of
around 220 beats per minute (bpm) is normal
following vigorous exercise. With age, this falls,
roughly in line with the formula ‘220 minus age in
years’ so, by the age of 60, it is around 160bpm.
It is thought this reduction is primarily due to
changes in the heart’s conductive system. The
filling of the ventricles also slows with age, as the
increased collagen content in the ventricle walls
leads to slower ventricular relaxation (Strait and
Lakatta, 2012).
In addition to the age-related decline in cardiac
function, the heart’s ability to repair itself
following injury or infection also declines (Strait
and Lakatta, 2012).
Cardiac conductive system
By the age of 50, the sinoatrial node (the heart’s
natural pacemaker) has lost 50-75% of its cells.
While the number of cells in the atrioventricular
node remains relatively constant, there is fibrosis
and cellular death in the atrioventricular bundle,
also called the bundle of His (heart muscle cells
specialised in electrical conduction).
These changes may reduce the efficiency of
cardiac conduction and contribute to the decline
in maximal heart rate (Ferrari et al, 2003). The
reduction in pacemaker cells makes atrial and
ventricular arrhythmias much more likely; an
example of this is atrial fibrillation in older people.
Blood pressure
Systolic blood pressure gradually increases with
age – the average in men is around 126mmHg at
25 years and 140mmHg at 60. This is thought to
reflect the decrease in elasticity and lumen
diameter within the arterial tree, and the
associated structural changes to the heart. In
addition, small arteries and arterioles become less
responsive to vasodilators such as nitric oxide,
further increasing peripheral resistance. Recent
research has also demonstrated a general age-
related up-regulation of the renin-angiotensin
mechanism. This results in increased levels of the
powerful vasoconstrictor angiotensin II, which
elevates blood pressure (Harvey et al, 2015).
In the absence of any pathology, diastolic
pressure (when the ventricles are relaxed)
changes very little with age and may even be
reduced (Steppan et al, 2011).
Reduced baroreceptor response
After a change in posture, such as moving from a
sitting to a standing position, blood drains into
the lower extremities and blood pressure falls.
This hypotension is immediately detected by the
baroreceptors (blood pressure sensors) in the
aortic arch and carotid sinus, causing the cardiac
in the medulla oblongata to increase the heart
rate. The vasomotor centre, also in the medulla
oblongata, initiates vasoconstriction to restore
normal blood pressure, ensuring adequate blood
flow to the brain and preventing postural
hypotension and fainting (Marieb and Hoehn,
In older people, baroreceptor reflexes are blunted,
which often results in an increased variability of
blood pressure throughout the day and may
reduce the ability to maintain blood pressure after
blood loss (Monahan, 2007). It is thought that
age-related thickening of the arterial walls may
interfere with the ability of baroreceptors to
accurately measure the degree of stretch (blood
pressure) within the vessel. This can increase the
risk of postural hypotension, increasing the risk of
Ageing is often associated with a general
reduction in activity and fitness but exercise can
be beneficial at any age. It is a good idea to
encourage older people to remain active and take
regular exercise, as this will support their
cardiovascular function well into their old age
(Montague et al, 2005).
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