Heart Rate

Heart rate
is the speed of the heartbeat measured by the number of contractions (beats) of the heart per minute (bpm). The
heart rate can vary according to the body's physical needs, including the need to absorb oxygen and excrete carbon dioxide,
but is also modulated by a myriad of factors including but not limited to genetics, physical fitness, stress or psychological
status, diet, drugs, hormonal status, environment, and disease/illness as well as the interaction between and among these
factors.[1] It is usually equal or close to the pulse measured at any peripheral point.
The American Heart Association states the normal resting adult human heart rate is 60–100 bpm.[2] Tachycardia is a high
heart rate, defined as above 100 bpm at rest.[3] Bradycardia is a low heart rate, defined as below 60 bpm at rest. During
sleep a slow heartbeat with rates around 40–50 bpm is common and is considered normal. When the heart is not beating in
a regular pattern, this is referred to as an arrhythmia. Abnormalities of heart rate sometimes indicate disease.[4]
Contents
 1Physiology
o 1.1Influences from the central nervous system
 1.1.1Cardiovascular centres
 1.1.2Input to the cardiovascular centres
o 1.2Factors influencing heart rate
 1.2.1Epinephrine and norepinephrine
 1.2.2Thyroid hormones
 1.2.3Calcium
 1.2.4Caffeine and nicotine
 1.2.5Effects of stress
 1.2.6Factors decreasing heart rate
 1.2.7Physiological control over heart rate
 2In different circumstances
o 2.1Resting heart rate
o 2.2Maximum heart rate
 2.2.1Nes, et al.
 2.2.2Tanaka, Monahan, & Seals
 2.2.3Oakland University
 2.2.4Haskell & Fox
 2.2.5Robergs & Landwehr
 2.2.6Gulati (for women)
 2.2.7Wohlfart, B. and Farazdaghi, G.R.
 2.2.8Other formulae
 2.2.9Limitations
o 2.3Heart rate reserve
o 2.4Target heart rate
 2.4.1Karvonen method
 2.4.2Zoladz method
o 2.5Heart rate recovery
o 2.6Development
 3Clinical significance
o 3.1Manual measurement
o 3.2Electronic measurement
o 3.3Optical measurements
o 3.4Tachycardia
o 3.5Bradycardia
o 3.6Arrhythmia
o 3.7Correlation with cardiovascular mortality risk
 4See also
 5Notes
 6References
 7Bibliography
 8External links
Physiology[edit]
The human heart
Normal heart sounds
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Normal heart sounds
as heard with
a stethoscope
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Auscultation of
student's racing
heart after exercise.
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Recorded heart
sounds of a 15 year
old girl reaching
maximum heart rate
immediately after
running, and the
following recovery.
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While heart rhythm is regulated entirely by the sinoatrial node under normal conditions, heart rate is regulated
by sympathetic and parasympathetic input to the sinoatrial node. The accelerans nerve provides sympathetic input to the
heart by releasing norepinephrine onto the cells of the sinoatrial node (SA node), and the vagus nerve provides
parasympathetic input to the heart by releasing acetylcholine onto sinoatrial node cells. Therefore, stimulation of
the accelerans nerve increases heart rate, while stimulation of the vagus nerve decreases it.[5]
Due to individuals having a constant blood volume,[dubious – discuss] one of the physiological ways to deliver more oxygen to an
organ is to increase heart rate to permit blood to pass by the organ more often.[4] Normal resting heart rates range from 60-
100 bpm.[6][7][8][9] Bradycardia is defined as a resting heart rate below 60 bpm. However, heart rates from 50 to 60 bpm are
common among healthy people and do not necessarily require special attention.[2] Tachycardia is defined as a resting heart
rate above 100 bpm, though persistent rest rates between 80–100 bpm, mainly if they are present during sleep, may be
signs of hyperthyroidism or anemia (see below).[4]
 Central nervous system stimulants such as substituted amphetamines increase heart rate.

 Central nervous system depressants or sedatives decrease the heart rate (apart from some particularly strange
ones with equally strange effects, such as ketamine which can cause – amongst many other things – stimulant-like
effects such as tachycardia).
There are many ways in which the heart rate speeds up or slows down. Most involve stimulant-
like endorphins and hormones being released in the brain, many of which are those that are 'forced'/'enticed' out by the
ingestion and processing of drugs.
This section discusses target heart rates for healthy persons and are inappropriately high for most persons with coronary
artery disease.[10]
Influences from the central nervous system[edit]

Cardiovascular centres[edit]
The heart rate is rhythmically generated by the sinoatrial node. It is also influenced by central factors through sympathetic
and parasympathetic nerves.[11] Nervous influence over the heart rate is centralized within the two paired cardiovascular
centres of the medulla oblongata. The cardioaccelerator regions stimulate activity via sympathetic stimulation of the
cardioaccelerator nerves, and the cardioinhibitory centers decrease heart activity via parasympathetic stimulation as one
component of the vagus nerve. During rest, both centers provide slight stimulation to the heart, contributing to autonomic
tone. This is a similar concept to tone in skeletal muscles. Normally, vagal stimulation predominates as, left unregulated, the
SA node would initiate a sinus rhythm of approximately 100 bpm.[12]
Both sympathetic and parasympathetic stimuli flow through the paired cardiac plexus near the base of the heart. The
cardioaccelerator center also sends additional fibers, forming the cardiac nerves via sympathetic ganglia (the cervical
ganglia plus superior thoracic ganglia T1–T4) to both the SA and AV nodes, plus additional fibers to the atria and ventricles.
The ventricles are more richly innervated by sympathetic fibers than parasympathetic fibers. Sympathetic stimulation causes
the release of the neurotransmitter norepinephrine (also known as noradrenaline) at the neuromuscular junction of the
cardiac nerves. This shortens the repolarization period, thus speeding the rate of depolarization and contraction, which
results in an increased heartrate. It opens chemical or ligand-gated sodium and calcium ion channels, allowing an influx of
positively charged ions.[12]
Norepinephrine binds to the beta–1 receptor. High blood pressure medications are used to block these receptors and so
reduce the heart rate.[12]
Autonomic Innervation of the Heart - Cardioaccelerator and cardioinhibitory areas are components of the paired cardiac centers located in
the medulla oblongata of the brain. They innervate the heart via sympathetic cardiac nerves that increase cardiac activity and vagus
(parasympathetic) nerves that slow cardiac activity.[12]
Parasympathetic stimulation originates from the cardioinhibitory region of the brain[13] with impulses traveling via the vagus
nerve (cranial nerve X). The vagus nerve sends branches to both the SA and AV nodes, and to portions of both the atria and
ventricles. Parasympathetic stimulation releases the neurotransmitter acetylcholine (ACh) at the neuromuscular junction.
ACh slows HR by opening chemical- or ligand-gated potassium ion channels to slow the rate of spontaneous depolarization,
which extends repolarization and increases the time before the next spontaneous depolarization occurs. Without any
nervous stimulation, the SA node would establish a sinus rhythm of approximately 100 bpm. Since resting rates are
considerably less than this, it becomes evident that parasympathetic stimulation normally slows HR. This is similar to an
individual driving a car with one foot on the brake pedal. To speed up, one need merely remove one's foot from the brake
and let the engine increase speed. In the case of the heart, decreasing parasympathetic stimulation decreases the release
of ACh, which allows HR to increase up to approximately 100 bpm. Any increases beyond this rate would require
sympathetic stimulation.[12]
Effects of Parasympathetic and Sympathetic Stimulation on Normal Sinus Rhythm - The wave of depolarization in a normal sinus rhythm
shows a stable resting HR. Following parasympathetic stimulation, HR slows. Following sympathetic stimulation, HR increases.[12]
Input to the cardiovascular centres[edit]

The cardiovascular centres receive input from a series of visceral receptors with impulses traveling through visceral sensory
fibers within the vagus and sympathetic nerves via the cardiac plexus. Among these receptors are
various proprioreceptors, baroreceptors, and chemoreceptors, plus stimuli from the limbic system which normally enable the
precise regulation of heart function, via cardiac reflexes. Increased physical activity results in increased rates of firing by
various proprioreceptors located in muscles, joint capsules, and tendons. The cardiovascular centres monitor these
increased rates of firing, suppressing parasympathetic stimulation or increasing sympathetic stimulation as needed in order
to increase blood flow.[12]
Similarly, baroreceptors are stretch receptors located in the aortic sinus, carotid bodies, the venae cavae, and other
locations, including pulmonary vessels and the right side of the heart itself. Rates of firing from the baroreceptors represent
blood pressure, level of physical activity, and the relative distribution of blood. The cardiac centers monitor baroreceptor
firing to maintain cardiac homeostasis, a mechanism called the baroreceptor reflex. With increased pressure and stretch, the
rate of baroreceptor firing increases, and the cardiac centers decrease sympathetic stimulation and increase
parasympathetic stimulation. As pressure and stretch decrease, the rate of baroreceptor firing decreases, and the cardiac
centers increase sympathetic stimulation and decrease parasympathetic stimulation.[12]
There is a similar reflex, called the atrial reflex or Bainbridge reflex, associated with varying rates of blood flow to the atria.
Increased venous return stretches the walls of the atria where specialized baroreceptors are located. However, as the atrial
baroreceptors increase their rate of firing and as they stretch due to the increased blood pressure, the cardiac center
responds by increasing sympathetic stimulation and inhibiting parasympathetic stimulation to increase HR. The opposite is
also true.[12]
Increased metabolic byproducts associated with increased activity, such as carbon dioxide, hydrogen ions, and lactic acid,
plus falling oxygen levels, are detected by a suite of chemoreceptors innervated by the glossopharyngeal and vagus nerves.
These chemoreceptors provide feedback to the cardiovascular centers about the need for increased or decreased blood
flow, based on the relative levels of these substances.[12]
The limbic system can also significantly impact HR related to emotional state. During periods of stress, it is not unusual to
identify higher than normal HRs, often accompanied by a surge in the stress hormone cortisol. Individuals experiencing
extreme anxiety may manifest panic attacks with symptoms that resemble those of heart attacks. These events are typically
transient and treatable. Meditation techniques have been developed to ease anxiety and have been shown to lower HR
effectively. Doing simple deep and slow breathing exercises with one's eyes closed can also significantly reduce this anxiety
and HR.[12]
Factors influencing heart rate[edit]

Table 1: Major factors increasing heart rate and force of contraction [12]
Factor Effect
Cardioaccelerator
Release of norepinephrine
nerves
Proprioreceptors Increased rates of firing during exercise
Chemoreceptors Decreased levels of O2; increased levels of H+, CO2, and lactic acid
Baroreceptors Decreased rates of firing, indicating falling blood volume/pressure
Limbic system Anticipation of physical exercise or strong emotions
Catecholamines Increased epinephrine and norepinephrine
Thyroid hormones Increased T3 and T4
Calcium Increased Ca2+
Potassium Decreased K+
Sodium Decreased Na+
Body temperature Increased body temperature
Nicotine and caffeine Stimulants, increasing heart rate
Table 2: Factors decreasing heart rate and force of contraction [12]
Factor Effect
Cardioinhibitor nerves
Release of acetylcholine
(vagus)
Proprioreceptors Decreased rates of firing following exercise
Chemoreceptors Increased levels of O2; decreased levels of H+ and CO2
Baroreceptors Increased rates of firing, indicating higher blood volume/pressure
Limbic system Anticipation of relaxation
Catecholamines Decreased epinephrine and norepinephrine
Thyroid hormones Decreased T3 and T4
Calcium Decreased Ca2+
Potassium Increased K+
Sodium Increased Na+
Body temperature Decrease in body temperature
Using a combination of autorhythmicity and innervation, the cardiovascular center is able to provide relatively precise control
over the heart rate, but other factors can impact on this. These include hormones, notably epinephrine, norepinephrine, and
thyroid hormones; levels of various ions including calcium, potassium, and sodium; body temperature; hypoxia; and pH
balance.[12]
Epinephrine and norepinephrine[edit]

The catecholamines, epinephrine and norepinephrine, secreted by the adrenal medulla form one component of the extended
fight-or-flight mechanism. The other component is sympathetic stimulation. Epinephrine and norepinephrine have similar
effects: binding to the beta-1 adrenergic receptors, and opening sodium and calcium ion chemical- or ligand-gated channels.
The rate of depolarization is increased by this additional influx of positively charged ions, so the threshold is reached more
quickly and the period of repolarization is shortened. However, massive releases of these hormones coupled with
sympathetic stimulation may actually lead to arrhythmias. There is no parasympathetic stimulation to the adrenal medulla.[12]
Thyroid hormones[edit]
In general, increased levels of the thyroid hormones (thyroxine(T4) and triiodothyronine (T3)), increase the heart rate;
excessive levels can trigger tachycardia. The impact of thyroid hormones is typically of a much longer duration than that of
the catecholamines. The physiologically active form of triiodothyronine, has been shown to directly enter cardiomyocytes
and alter activity at the level of the genome.[clarification needed] It also impacts the beta adrenergic response similar to epinephrine and
norepinephrine.[12]

Heart Rate

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Heart rate

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 Central nervous system stimulants such as substituted amphetamines increase heart rate.

Influences from the central nervous system[edit]

(parasympathetic) nerves that slow cardiac activity.[12]

Input to the cardiovascular centres[edit]

Factors influencing heart rate[edit]

Proprioreceptors Increased rates of firing during exercise

Baroreceptors Decreased rates of firing, indicating falling blood volume/pressure

Limbic system Anticipation of physical exercise or strong emotions

Catecholamines Increased epinephrine and norepinephrine

Thyroid hormones Increased T3 and T4

Calcium Increased Ca2+

Sodium Decreased Na+

Body temperature Increased body temperature

Nicotine and caffeine Stimulants, increasing heart rate

Table 2: Factors decreasing heart rate and force of contraction [12]

Proprioreceptors Decreased rates of firing following exercise

Chemoreceptors Increased levels of O2; decreased levels of H+ and CO2

Baroreceptors Increased rates of firing, indicating higher blood volume/pressure

Limbic system Anticipation of relaxation

Catecholamines Decreased epinephrine and norepinephrine

Thyroid hormones Decreased T3 and T4

Calcium Decreased Ca2+

Sodium Increased Na+

Body temperature Decrease in body temperature

Epinephrine and norepinephrine[edit]

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