View source for Heart rate

{{Short description|Speed of the heartbeat, measured in beats per minute}}
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[[File:Normal electrocardiogram.jpg|thumb|A [[medical monitoring]] device displaying a normal human heart rate]]
'''Heart rate''' is the [[frequency]] of the [[cardiac cycle|heartbeat]] measured by the number of contractions of the [[heart]] per minute (''beats per minute'', or bpm). The heart rate varies according to the body's [[Human body|physical]] needs, including the need to absorb [[oxygen]] and excrete [[carbon dioxide]]. It is also modulated by numerous factors, including (but not limited to) genetics, [[physical fitness]], [[Psychological stress|stress]] or psychological status, diet, drugs, hormonal status, environment, and disease/illness, as well as the interaction between these factors.<ref name="pmid19022405">{{cite journal |vauthors=Zhang GQ, Zhang W | title = Heart rate, lifespan, and mortality risk | journal = Ageing Research Reviews | volume = 8 | issue = 1 | pages = 52–60 | year = 2009 | pmid = 19022405 | doi = 10.1016/j.arr.2008.10.001 | s2cid = 23482241 }}</ref> It is usually equal or close to the [[pulse rate]] measured at any peripheral point.<ref>{{Cite web|url=https://www.bhf.org.uk/informationsupport/heart-matters-magazine/medical/ask-the-experts/pulse-rate|title=What is a normal pulse rate? - Heart Matters magazine - BHF}}</ref>

The [[American Heart Association]] states the normal resting adult human heart rate is 60–100 bpm. An ultra-trained athlete would have a resting heart rate of 37–38 bpm.<ref name='aha_rest'>{{Cite web|url = https://www.heart.org/HEARTORG/Conditions/HighBloodPressure/GettheFactsAboutHighBloodPressure/All-About-Heart-Rate-Pulse_UCM_438850_Article.jsp|title = All About Heart Rate (Pulse) |date = 22 Aug 2017|access-date = 25 Jan 2018|website = All About Heart Rate (Pulse)|publisher = American Heart Association}}</ref> ''[[Tachycardia]]'' is a high heart rate, defined as above 100 bpm at rest.<ref>{{Cite web|url = http://www.heart.org/HEARTORG/Conditions/Arrhythmia/AboutArrhythmia/Tachycardia_UCM_302018_Article.jsp|title = <nowiki>Tachycardia| Fast Heart Rate</nowiki>|date = 2 May 2013|access-date = 21 May 2014|website = Tachycardia|publisher = American Heart Association}}</ref> ''[[Bradycardia]]'' is a low heart rate, defined as below 60 bpm at rest. When a human sleeps, a heartbeat with rates around 40–50 bpm is common and considered normal. When the heart is not beating in a regular pattern, this is referred to as an [[Heart arrhythmia|''arrhythmia'']]. Abnormalities of heart rate sometimes indicate [[Heart disease|disease]].{{sfn|Fuster|Wayne|O'Rouke|2001|pp=78–79}}

==Physiology==
{{Main|Cardiac physiology}}
[[File:Wiki Heart Antomy Ties van Brussel.jpg|thumb|alt=Anatomy of the Human Heart, made by Ties van Brussel|350px|The [[human heart]]]]
{{listen
 | filename = HROgg.ogg
 | title = Normal heart sounds
 | description = Normal heart sounds as heard with a [[stethoscope]]
 | format = [[Ogg]]
}}
{{listen|filename=Emily's racing heartbeat.wav|title=Emily's racing heartbeat|description=Heart sounds of a 16 year old girl immediately after running, with a heart rate of 186 BPM. The S1 heart sound is intensified due to the increased cardiac output.|format=[[wav]]}}
While [[heart rhythm]] is regulated entirely by the [[sinoatrial node]] under normal conditions, ''heart rate'' is regulated by [[sympathetic nervous system|sympathetic]] and [[parasympathetic nervous system|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.<ref name="Schmidt-Nielsen 1997">{{cite book|last=Schmidt-Nielsen|first=Knut|title=Animal physiology: adaptation and environment|year=1997|publisher=Cambridge Univ. Press|location=Cambridge|isbn=978-0-521-57098-5|page=104|edition=5th}}</ref>

* [[Central nervous system]] [[stimulant]]s such as [[substituted amphetamine]]s increase heart rate.
* Central nervous system [[depressant]]s or [[sedative]]s 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 [[endorphin]]s and [[hormone]]s being released in the brain, some of which are those that are 'forced'/'enticed' out by the ingestion and processing of drugs such as [[cocaine]] or [[atropine]].<ref>{{Cite web|last=PubChem|title=Atropine|url=https://pubchem.ncbi.nlm.nih.gov/compound/174174|access-date=2021-08-08|website=pubchem.ncbi.nlm.nih.gov|language=en}}</ref><ref>{{Cite journal|last1=Richards|first1=John R.|last2=Garber|first2=Dariush|last3=Laurin|first3=Erik G.|last4=Albertson|first4=Timothy E.|last5=Derlet|first5=Robert W.|last6=Amsterdam|first6=Ezra A.|last7=Olson|first7=Kent R.|last8=Ramoska|first8=Edward A.|last9=Lange|first9=Richard A.|date=June 2016|title=Treatment of cocaine cardiovascular toxicity: a systematic review|journal=Clinical Toxicology|volume=54|issue=5|pages=345–64|doi=10.3109/15563650.2016.1142090|issn=1556-9519|pmid=26919414|s2cid=5165666}}</ref><ref>{{Cite web|title=All About Heart Rate (Pulse)|url=https://www.heart.org/en/health-topics/high-blood-pressure/the-facts-about-high-blood-pressure/all-about-heart-rate-pulse|access-date=2021-08-08|website=www.heart.org|language=en}}</ref>

This section discusses target heart rates for healthy persons, which would be inappropriately high for most persons with coronary artery disease.<ref name="pmid1866953">{{cite journal | author = Anderson JM | title = Rehabilitating elderly cardiac patients | journal = West. J. Med. | volume = 154 | issue = 5 | pages = 573–78 | year = 1991 | pmid = 1866953 | pmc = 1002834 }}</ref>

===Influences from the central nervous system===

====Cardiovascular centres====
The heart rate is rhythmically generated by the [[sinoatrial node]]. It is also influenced by [[central nervous system|central]] factors through sympathetic and parasympathetic nerves.<ref name=GUYTONHALL2005>{{cite book |author=Arthur C. Guyton |author2=John E. Hall |title=Textbook of medical physiology|date=2005|publisher=W.B. Saunders|location=Philadelphia|isbn=978-0-7216-0240-0|pages=116–22|edition=11th}}</ref> Nervous influence over the heart rate is centralized within the two paired [[cardiovascular centre]]s 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.<ref name="CNX2014">{{cite book|last1=Betts|first1=J. Gordon|title=Anatomy & physiology|date=2013|isbn=978-1-938168-13-0|url=http://cnx.org/content/m46676/latest/?collection=col11496/latest|access-date=11 August 2014|pages=787–846|publisher=OpenStax College, Rice University }}</ref>

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.<ref name="CNX2014"/>

Norepinephrine binds to the beta–1 receptor. [[High blood pressure]] medications are used to block these receptors and so reduce the heart rate.<ref name="CNX2014"/>

[[File:2032 Automatic Innervation.jpg|thumb|left|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.<ref name="CNX2014"/>]]

Parasympathetic stimulation originates from the cardioinhibitory region of the brain<ref>{{cite journal |vauthors=Garcia A, Marquez MF, Fierro EF, Baez JJ, Rockbrand LP, Gomez-Flores J |title=Cardioinhibitory syncope: from pathophysiology to treatment-should we think on cardioneuroablation? |journal=J Interv Card Electrophysiol |date=May 2020 |volume=59 |issue=2 |pages=441–61 |pmid=32377918 |doi=10.1007/s10840-020-00758-2 |s2cid=218527702 }}</ref> 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.<ref name="CNX2014"/>
[[File:2033 Depolarization in Sinus Rhythm.jpg|thumb|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.<ref name="CNX2014"/>]]

====Input to the cardiovascular centres====
The cardiovascular centre 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 [[proprioreceptor]]s, [[baroreceptor]]s, and [[chemoreceptor]]s, 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.<ref name="CNX2014"/>

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.<ref name="CNX2014"/>

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.<ref name="CNX2014"/>

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.<ref name="CNX2014"/>

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 attack]]s 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.<ref name="pmid33728595">{{cite journal | vauthors = Morais P, Quaresma C, Vigário R, Quintão C| title=Electrophysiological effects of mindfulness meditation in a concentration test | journal= [[Medical & Biological Engineering & Computing]] | volume=59 | issue=4 | pages=759–773 | year=2021 | doi= 10.1007/s11517-021-02332-y | pmid=33728595  }}</ref> Doing simple deep and slow breathing exercises with one's eyes closed can also significantly reduce this anxiety and HR.<ref name="CNX2014"/>

===Factors influencing heart rate===
{{Factors influencing heart rate}}
{{Clear}}
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.<ref name="CNX2014"/>

====Epinephrine and norepinephrine====
The [[catecholamine]]s, 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 receptor]]s, 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.<ref name="CNX2014"/>

====Thyroid hormones====
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.{{clarify|date=September 2014}} It also impacts the [[beta-adrenergic]] response similar to epinephrine and norepinephrine.<ref name="CNX2014"/>

====Calcium====
Calcium ion levels have a great impact on heart rate and [[myocardial contractility]]: increased calcium levels cause an increase in both. High levels of calcium ions result in [[hypercalcemia]] and excessive levels can induce [[cardiac arrest]]. Drugs known as calcium channel blockers slow HR by binding to these channels and blocking or slowing the inward movement of calcium ions.<ref name="CNX2014"/>

====Caffeine and nicotine====

[[Caffeine]] and [[nicotine]] are both stimulants of the nervous system and of the cardiac centres causing an increased heart rate. Caffeine works by increasing the rates of [[depolarization]] at the [[SA Node|SA node]], whereas nicotine stimulates the activity of the sympathetic neurons that deliver impulses to the heart.<ref name="CNX2014"/>

==== Effects of stress ====
Both surprise and stress induce physiological response: [[Tachycardia|elevate heart rate substantially]].<ref>{{cite journal|last1=Mustonen|first1=Veera|last2=Pantzar|first2=Mika|title=Tracking social rhythms of the heart|journal=Approaching Religion|date=2013|volume=3|issue=2|pages=16–21|doi=10.30664/ar.67512|doi-access=free}}</ref> In a study conducted on 8 female and male student actors ages 18 to 25, their reaction to an unforeseen occurrence (the cause of stress) during a performance was observed in terms of heart rate. In the data collected, there was a noticeable trend between the location of actors (onstage and offstage) and their elevation in heart rate in response to stress; the actors present offstage reacted to the stressor immediately, demonstrated by their immediate elevation in heart rate the minute the unexpected event occurred, but the actors present onstage at the time of the stressor reacted in the following 5 minute period (demonstrated by their increasingly elevated heart rate). This trend regarding stress and heart rate is supported by previous studies; [[negative emotion]]/stimulus has a prolonged effect on heart rate in individuals who are directly impacted.<ref>{{cite journal|last1=Brosschot|first1=J.F.|last2=Thayer|first2=J.F.|title=Heart rate response is longer after negative emotions than after positive emotions|journal=International Journal of Psychophysiology|date=2003|volume=50|issue=3|pages=181–87|doi=10.1016/s0167-8760(03)00146-6|pmid=14585487}}</ref>
In regard to the characters present onstage, a reduced startle response has been associated with a passive defense, and the diminished initial heart rate response has been predicted to have a greater tendency to dissociation.<ref>{{cite journal|last1=Chou|first1=C.Y.|last2=Marca|first2=R.L.|last3=Steptoe|first3=A.|last4=Brewin|first4=C.R.|title=Heart rate, startle response, and intrusive trauma memories|journal=Psychophysiology|date=2014|volume=51|issue=3|pages=236–46|doi=10.1111/psyp.12176|pmid=24397333|pmc=4283725}}</ref> Current evidence suggests that [[heart rate variability]] can be used as an accurate measure of [[psychological stress]] and may be used for an objective measurement of psychological stress.<ref>{{Cite journal|last1=Kim|first1=Hye-Geum|last2=Cheon|first2=Eun-Jin|last3=Bai|first3=Dai-Seg|last4=Lee|first4=Young Hwan|last5=Koo|first5=Bon-Hoon|date=March 2018|title=Stress and Heart Rate Variability: A Meta-Analysis and Review of the Literature|journal=Psychiatry Investigation|volume=15|issue=3|pages=235–45|doi=10.30773/pi.2017.08.17|issn=1738-3684|pmc=5900369|pmid=29486547}}</ref>

====Factors decreasing heart rate====
The heart rate can be slowed by altered sodium and potassium levels, [[hypoxia (medical)|hypoxia]], [[acidosis]], [[alkalosis]], and [[hypothermia]]. The relationship between electrolytes and HR is complex, but maintaining electrolyte balance is critical to the normal wave of depolarization. Of the two ions, potassium has the greater clinical significance. Initially, both [[hyponatremia]] (low sodium levels) and [[hypernatremia]] (high sodium levels) may lead to tachycardia. Severely high hypernatremia may lead to [[Fibrillation#Cardiology|fibrillation]], which may cause cardiac output to cease. Severe hyponatremia leads to both bradycardia and other arrhythmias. [[Hypokalemia]] (low potassium levels) also leads to arrhythmias, whereas [[hyperkalemia]] (high potassium levels) causes the heart to become weak and flaccid, and ultimately to fail.<ref name="CNX2014"/>

Heart muscle relies exclusively on [[Cellular respiration|aerobic metabolism]] for energy. Severe [[myocardial infarction]] (commonly called a heart attack) can lead to a [[Bradycardia|decreasing heart rate]], since metabolic reactions fueling heart contraction are restricted.<ref name="CNX2014"/>

[[Acidosis]] is a condition in which excess hydrogen ions are present, and the patient's blood expresses a low pH value. [[Alkalosis]] is a condition in which there are too few hydrogen ions, and the patient's blood has an elevated pH. [[Acid–base homeostasis|Normal blood pH]] falls in the range of 7.35–7.45, so a number lower than this range represents acidosis and a higher number represents alkalosis. Enzymes, being the regulators or catalysts of virtually all biochemical reactions – are sensitive to pH and will change shape slightly with values outside their normal range. These variations in pH and accompanying slight physical changes to the active site on the enzyme decrease the rate of formation of the enzyme-substrate complex, subsequently decreasing the rate of many enzymatic reactions, which can have complex effects on HR. Severe changes in pH will lead to denaturation of the enzyme.<ref name="CNX2014"/>

The last variable is body temperature. Elevated body temperature is called [[hyperthermia]], and suppressed body temperature is called [[hypothermia]]. Slight hyperthermia results in increasing HR and strength of contraction. Hypothermia slows the rate and strength of heart contractions. This distinct slowing of the heart is one component of the larger diving reflex that diverts blood to essential organs while submerged. If sufficiently chilled, the heart will stop beating, a technique that may be employed during open heart surgery. In this case, the patient's blood is normally diverted to an [[Cardiopulmonary bypass|artificial heart-lung machine]] to maintain the body's blood supply and [[gas exchange]] until the surgery is complete, and sinus rhythm can be restored. Excessive hyperthermia and hypothermia will both result in death, as enzymes drive the body systems to cease normal function, beginning with the central nervous system.<ref name="CNX2014"/>

==== Physiological control over heart rate ====
{{multiple image
| footer            = Dolphin heart rate graph
| image1            = Dolphin_Encounter-9563.jpg
| width1            = 200
| alt1              = Dolphin
| caption1          = 
| image2            = Conditioned Variation in Heart Rate During Static Breath-Holds in the Bottlenose Dolphin (Tursiops truncatus) – examples of instantaneous heart rate (ifH) responses.jpg
| width2            = 128
| alt2              = Conditioned Variation in Heart Rate During Static Breath-Holds in the Bottlenose Dolphin (Tursiops truncatus) – examples of instantaneous heart rate (ifH) responses
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A study shows that [[bottlenose dolphin]]s can learn – apparently via [[instrumental conditioning]] – to rapidly and selectively slow down their heart rate during diving for conserving oxygen depending on external signals. In humans regulating heart rate by methods such as listening to music, [[meditation]] or a [[vagal maneuver]] takes longer and lowers the rate to a much lesser extent.<ref>{{cite journal |last1=Fahlman |first1=Andreas |last2=Cozzi |first2=Bruno |last3=Manley |first3=Mercy |last4=Jabas |first4=Sandra |last5=Malik |first5=Marek |last6=Blawas |first6=Ashley |last7=Janik |first7=Vincent M. |title=Conditioned Variation in Heart Rate During Static Breath-Holds in the Bottlenose Dolphin (Tursiops truncatus) |journal=[[Frontiers in Physiology]] |date=2020 |volume=11 |article-number=604018 |doi=10.3389/fphys.2020.604018 |pmid=33329056 |pmc=7732665 |s2cid=227128277 |doi-access=free }}
*{{lay source |template = cite web|url = https://phys.org/news/2020-11-dolphins-oxygen-dive-related-problems-consciously.html|title = Dolphins conserve oxygen and prevent dive-related problems by consciously decreasing their heart rates before diving|date = November 24, 2020 |website = Phys.org }}</ref>

==In different circumstances==
[[File:VivoSenseHR vs Vt.jpg|thumb|left|Heart rate (HR) (top trace) and tidal volume (Vt) (lung volume, second trace) plotted on the same chart, showing how heart rate increases with inspiration and decreases with expiration.]]
Heart rate is not a stable value and it increases or decreases in response to the body's need in a way to maintain an equilibrium ([[basal metabolic rate]]) between requirement and delivery of oxygen and nutrients. The normal SA node firing rate is affected by [[autonomic nervous system]] activity: [[sympathetic nervous system|sympathetic stimulation]] increases and [[parasympathetic nervous system|parasympathetic stimulation]] decreases the firing rate.<ref>{{cite book|url=https://books.google.com/books?id=gOmpysGBC90C&q=When+skeletal+muscle+is+stimulated+by+somatic+motor+axons,+influx+of+Na%2B+quickly+depolarizes+the+skeletal+myocyte&pg=PT277|title=Human Physiology, From Cells to Systems|year=2008|last=Sherwood |first=L.|access-date=2013-03-10 |isbn=978-0-495-39184-5 |page=327 |publisher=Cengage Learning }}</ref>

{{anchor|Resting heart rate}}

===Resting heart rate===
Normal pulse rates at rest, in beats per minute (BPM):<ref>{{MedlinePlusEncyclopedia|003399|Pulse}}</ref>
[[File:Athletic_bradycardia_wav.wav|thumb|Resting heart rate recorded in an elite athlete demonstrating bradycardia at 42 bpm]]
{{listen |filename=Infant Heartbeat.ogg |title=Infant heartbeat |description=Infant heartbeat }}
{| class="wikitable" style="text-align: center;"
! Newborns<br />(0–1 months old)
! Infants<br />(1–11 months)
! Children<br />(1–2 years old)
! Children<br />(3–4 years)
! Children<br />(5–6 years)
! Children<br />(7–9 years)
! Children over 10 years<br />and adults, including seniors
! Well-trained<br />adult athletes

|-
|70–190
|80–160
|80–130
|80–120
|75–115
|70–110
|60–100
|40–60
|}

The basal or resting heart rate (HR<sub>rest</sub>) is defined as the heart rate when a person is awake, in a neutrally [[temperate]] environment, and has not been subject to any recent exertion or stimulation, such as stress or surprise.  The normal resting heart rate is based on the at-rest firing rate of the heart's [[sinoatrial node]], where the faster [[cardiac pacemaker|pacemaker cells]] driving the self-generated rhythmic firing and responsible for the heart's [[autorhythmicity]] are located.<ref>{{cite book|last1 = Berne| first1 = Robert |first2=Matthew |last2=Levy |first3=Bruce |last3=Koeppen |first4=Bruce |last4=Stanton | title = Physiology|url = https://archive.org/details/cardiovascularp000bern|url-access = registration| publisher = Elsevier Mosby| year = 2004| page = [https://archive.org/details/cardiovascularp000bern/page/276 276]| isbn = 978-0-8243-0348-8 }}</ref>

In one 1993 study, 98% of cardiologists suggested that as a desirable target range, 50 to 90 beats per minute is more appropriate than 60 to 100.<ref name=":3">{{Cite journal|last=Spodick|first=D. H.|date=1993-08-15|title=Survey of selected cardiologists for an operational definition of normal sinus heart rate|journal=The American Journal of Cardiology|volume=72|issue=5|pages=487–88 |pmid=8352202|doi=10.1016/0002-9149(93)91153-9}}</ref> The available evidence indicates that the normal range for resting heart rate is 50–90 beats per minute (bpm).<ref name=":0">{{Cite journal|last1=Aladin|first1=Amer I.|last2=Whelton|first2=Seamus P.|last3=Al-Mallah|first3=Mouaz H.|last4=Blaha|first4=Michael J.|last5=Keteyian|first5=Steven J.|last6=Juraschek|first6=Stephen P.|last7=Rubin|first7=Jonathan|last8=Brawner|first8=Clinton A.|last9=Michos|first9=Erin D.|date=2014-12-01|title=Relation of resting heart rate to risk for all-cause mortality by gender after considering exercise capacity (the Henry Ford exercise testing project)|journal=The American Journal of Cardiology|volume=114|issue=11|pages=1701–06|doi=10.1016/j.amjcard.2014.08.042 |pmid=25439450}}</ref><ref name=":1">{{Cite journal|last1=Hjalmarson|first1=A.|last2=Gilpin|first2=E. A.|last3=Kjekshus|first3=J.|last4=Schieman|first4=G.|last5=Nicod|first5=P.|last6=Henning|first6=H.|last7=Ross|first7=J.|date=1990-03-01|title=Influence of heart rate on mortality after acute myocardial infarction|journal=The American Journal of Cardiology|volume=65|issue=9|pages=547–53 |pmid=1968702|doi=10.1016/0002-9149(90)91029-6}}</ref><ref name=":2">{{Cite journal|last1=Mason|first1=Jay W.|last2=Ramseth|first2=Douglas J.|last3=Chanter|first3=Dennis O.|last4=Moon|first4=Thomas E.|last5=Goodman|first5=Daniel B.|last6=Mendzelevski|first6=Boaz|date=2007-07-01|title=Electrocardiographic reference ranges derived from 79,743 ambulatory subjects|journal=[[Journal of Electrocardiology]]|volume=40|issue=3|pages=228–34|doi=10.1016/j.jelectrocard.2006.09.003 |pmid=17276451}}</ref><ref name=':3' /> In a study of over 35,000 American men and women over age&nbsp;40 during the 1999–2008 period, 71&nbsp;bpm was the average for men, and 73&nbsp;bpm was the average for women.<ref name="pmid30761923">{{cite journal | author = Jensen MT | title=Resting heart rate and relation to disease and longevity: past, present and future | journal= Scandinavian Journal of Clinical and Laboratory Investigation | volume=79 | issue=1–2 | pages=108–116 | year=2019 | doi= 10.1080/00365513.2019.1566567 | pmid=30761923}}</ref>

Resting heart rate is often correlated with mortality. In the Copenhagen City Heart Study a heart rate of 65&nbsp;bpm rather than 80&nbsp;bpm was associated with 4.6&nbsp;years longer life expectancy in men and 3.6&nbsp;years in women.<ref name="pmid30761923" /> Other studies have shown all-cause mortality is increased by 1.22 (hazard ratio) when heart rate exceeds 90 beats per minute.<ref name=":0" />  ECG of 46,129 individuals with low risk for cardiovascular disease revealed that 96% had resting heart rates ranging from 48 to 98 beats per minute.<ref name=":2" /> The mortality rate of patients with myocardial infarction increased from 15% to 41% if their admission heart rate was greater than 90 beats per minute.<ref name=":1" />  For endurance athletes at the elite level, it is not unusual to have a resting heart rate between 33 and 50 bpm.{{citation needed|date=August 2014}}

=== Maximum heart rate ===
<!-- Numerous redirects, do not change title -->[[File:10_min_max_heart_rate_wav.wav|thumb|An elite athlete's heart recorded during a maximum effort workout maintaining over 180 bpm for 10 minutes.]]
The ''maximum heart rate'' (HR<sub>max</sub>) is the age-related highest number of beats per minute of the heart when reaching a point of exhaustion<ref name="MW_(mhr)">{{cite web |title=Medical Definition of MAXIMUM HEART RATE |url=https://www.merriam-webster.com/medical/maximum%20heart%20rate |website=www.merriam-webster.com |publisher=Merriam-Webster, Inc. |access-date=8 September 2022 |language=en}}</ref><ref name="NIH_(mhr)">{{cite journal |last1=Heinzmann-Filho |first1=João Paulo |last2=et |first2=al. |title=Frequência Cardíaca Máxima Medida Versus Estimada Por Diferentes Equações Durante O Teste de Exercício Cardiopulmonar Em Adolescentes Obesos |journal=Revista Paulista de Pediatria |year=2018 |volume=36 |issue=3 |pages=309–314 |doi=10.1590/1984-0462/;2018;36;3;00015 |pmid=30365812 |pmc=6202885 }}</ref> without severe problems through exercise stress.<ref name="Canadian Hockey Heart Study">{{cite journal |vauthors=Atwal S, Porter J, MacDonald P | title = Cardiovascular effects of strenuous exercise in adult recreational hockey: the Hockey Heart Study | journal = CMAJ | volume = 166 | issue = 3 | pages = 303–07 |date=February 2002  | pmid = 11868637 | pmc = 99308 }}</ref> 
In general it is loosely estimated as 220 minus one's age.<ref name="CDC_(mhr)">{{cite web |title=Target Heart Rate and Estimated Maximum Heart Rate {{!}} Physical Activity {{!}} CDC |url=https://www.cdc.gov/physicalactivity/basics/measuring/heartrate.htm |website=www.cdc.gov |publisher=U.S. Department of Health & Human Services |access-date=8 September 2022 |language=en-us |date=5 August 2022}}</ref> 
The maximum heart rate decreases with aging regardless of fitness, gender or diet.<ref name="Peters">{{cite journal |vauthors=Peters CH, Sharpe EJ, Proenza C |title=Cardiac Pacemaker Activity and Aging |journal=Annu Rev Physiol |volume=82 |issue= |pages=21–43 |date=February 2020 |pmid=31756134 |pmc=7063856 |doi=10.1146/annurev-physiol-021119-034453 |url=}}</ref><ref name="CDC_(mhr)"/> Since HR<sub>max</sub> varies by individual, the most accurate way of measuring any single person's HR<sub>max</sub> is via a [[cardiac stress test]]. In this test, a person is subjected to controlled physiologic stress (generally by [[treadmill]] or bicycle ergometer) while being monitored by an [[electrocardiogram]] (ECG). The intensity of exercise is periodically increased until certain changes in heart function are detected on the ECG monitor, at which point the subject is directed to stop. Typical duration of the test ranges ten to twenty minutes.{{citation needed|date=March 2021}} Adults who are beginning a new exercise regimen are often advised to perform this test only in the presence of medical staff due to risks associated with high heart rates.

The theoretical maximum heart rate of a human is 300 bpm; however, there have been multiple cases where this theoretical upper limit has been exceeded. The fastest human ventricular conduction rate recorded to this day is a conducted [[Tachycardia|tachyarrhythmia]] with ventricular rate of 600 beats per minute,<ref>{{cite journal |last1=Chhabra |first1=Lovely |last2=Goel |first2=Narender |last3=Prajapat |first3=Laxman |last4=Spodick |first4=David H |last5=Goyal |first5=Sanjeev |title=Mouse Heart Rate in a Human: Diagnostic Mystery of an Extreme Tachyarrhythmia |journal=Indian Pacing and Electrophysiology Journal |date=2012-01-31 |volume=12 |issue=1 |pages=32–35 |doi=10.1016/s0972-6292(16)30463-6 |pmid=22368381 |pmc=3273956 }}</ref> which is comparable to the heart rate of a [[mouse]].

For general purposes, a number of formulas are used to estimate HR<sub>max</sub>. However, these predictive formulas have been criticized as inaccurate because they only produce generalized population-averages and may deviate significantly from the actual value. (''See [[#Limitations|§ Limitations]]''.)

{| class="wikitable"
|+ Formulas for estimating HR<sub>max</sub>
|-
! Name !! Data !! HR<sub>max</sub> Formula !! Error
|- 
| Haskell & Fox (1971)<ref>{{cite journal |vauthors=Fox SM 3rd, Naughton JP, Haskell WL |title=Physical activity and the prevention of coronary heart disease. |journal=Annals of Clinical Research |date=December 1971 |volume=3 |issue=6 |pages=404–32 |pmid=4945367}}</ref><ref name="mhrt2">{{cite journal |vauthors=Robergs R, Landwehr R|title=The Surprising History of the 'HRmax=220-age' Equation |journal=Journal of Exercise Physiology |volume=5 |issue=2 |pages=1–10 |year=2002 | url = https://eprints.qut.edu.au/96880/ |citeseerx=10.1.1.526.6164 }}</ref> || 35 data points || 220 − age || SD&nbsp;= 12–15 bpm<ref>{{cite book |title=ACSM's guidelines for exercise testing and prescription |date=2010 |publisher=Lippincott Williams & Wilkins |location=Philadelphia |isbn=978-0-7817-6903-7 |page=79 |edition=8th}}</ref>
|-
| Inbar, et al. (1994)<ref name="Inbar">{{cite journal |vauthors=Inbar O, Oten A, Scheinowitz M, Rotstein A, Dlin R, Casaburi R | year = 1994 | title = Normal cardiopulmonary responses during incremental exercise in 20-70-yr-old men | journal = Med Sci Sports Exerc | volume = 26 | issue = 5| pages = 538–546 | doi = 10.1249/00005768-199405000-00003 | pmid = 8007799 }}</ref> || 1424 men || 205.8 − (0.685 × age) || SD = 6.4 bpm
|-
| Tanaka, Monahan, & Seals (2001)<ref name="pmid11153730">{{cite journal |vauthors=Tanaka H, Monahan KD, Seals DR | title = Age-predicted maximal heart rate revisited | journal = J. Am. Coll. Cardiol. | volume = 37 | issue = 1 | pages = 153–56 |date=January 2001  | pmid = 11153730 | doi =10.1016/S0735-1097(00)01054-8 | doi-access = free }}</ref> || 315 studies, 514 individuals || 208 − (0.7 × age) || SD ~10 bpm
|-
| Wohlfart, B. and Farazdaghi, G.R.<ref name="pmid11722475">{{cite journal |vauthors=Farazdaghi GR, Wohlfart B | title = Reference values for the physical work capacity on a bicycle ergometer for women between 20 and 80 years of age | journal = Clin Physiol | volume = 21 | issue = 6 | pages = 682–87 |date=November 2001  | pmid = 11722475 | doi = 10.1046/j.1365-2281.2001.00373.x }}</ref><ref name="pmid12752560">{{cite journal |vauthors=Wohlfart B, Farazdaghi GR | title = Reference values for the physical work capacity on a bicycle ergometer for men -- a comparison with a previous study on women | journal = Clin Physiol Funct Imaging | volume = 23 | issue = 3 | pages = 166–70 |date=May 2003  | pmid = 12752560 | doi = 10.1046/j.1475-097X.2003.00491.x | s2cid = 25560062 | url = http://lup.lub.lu.se/record/113907 }}</ref> || 81 men, 87 women || Men: 203.7 / ( 1 + exp( 0.033 × (age − 104.3) ) )<br /> Women: 190.2 / ( 1 + exp( 0.0453 × (age − 107.5) ) ) || SD&nbsp;= 6.5% men, 5.5% women
|-
| Oakland University (2007)<ref name=Gellish>{{cite journal |last1=Gellish |first1=Ronald L. |last2=Goslin |first2=Brian R. |last3=Olson |first3=Ronald E. |last4=McDONALD |first4=Audry |last5=Russi |first5=Gary D. |last6=Moudgil |first6=Virinder K. |title=Longitudinal Modeling of the Relationship between Age and Maximal Heart Rate |journal=Medicine & Science in Sports & Exercise |date=May 2007 |volume=39 |issue=5 |pages=822–829 |doi=10.1097/mss.0b013e31803349c6 |pmid=17468581 |s2cid=25691442 |doi-access=free }}</ref> || 100 men, 32 women, 908 longitudinal observations || Linear: 207 − (0.7 × age)<br />Nonlinear: 192 − (0.007 × age<sup>2</sup>) || 1 SD confidence interval: ±5–8 bpm (linear), ±2–5 bpm (nonlinear)
|-
| Gulati (2010)<ref name="pmid20585008">{{cite journal |vauthors=Gulati M, Shaw LJ, Thisted RA, Black HR, Bairey Merz CN, Arnsdorf MF | title = Heart rate response to exercise stress testing in asymptomatic women: the st. James women take heart project | journal = Circulation | volume = 122 | issue = 2 | pages = 130–37 | year = 2010 | pmid = 20585008 | doi = 10.1161/CIRCULATIONAHA.110.939249 | doi-access = free }}</ref>|| 5437 women || Women: 206 − (0.88 × age) || SD&nbsp;= 11.8 bpm
|-
| Nes, ''et al.'' (2013)<ref name="Nes2013">{{cite journal |last1=Nes |first1=B.M. |last2=Janszky |first2=I. |last3=Wisloff |first3=U. |last4=Stoylen |first4=A. |last5=Karlsen |first5=T. |title=Age-predicted maximal heart rate in healthy subjects: The HUNT Fitness Study |journal=Scandinavian Journal of Medicine & Science in Sports |volume=23 |issue=6 |date=December 2013 |pages=697–704 |pmid=22376273 |doi=10.1111/j.1600-0838.2012.01445.x |s2cid=2380139 }}</ref> || 1726 men, 1594 women || 211 − (0.64 × age) || SEE&nbsp;= 10.8 bpm
|-
| Wingate (2015)<ref name="Wingate">{{cite journal |last1=Shargal |first1=E |last2=Kislev-Cohen |first2=R |last3=Zigel |first3=L |last4=Epstein |first4=S |last5=Pilz-Burstein |first5=R |last6=Tenenbaum |first6=G |title=Age-related maximal heart rate: examination and refinement of prediction equations. |journal=The Journal of Sports Medicine and Physical Fitness |date=October 2015 |volume=55 |issue=10 |pages=1207–18 |doi=10.1111/j.1600-0838.2012.01445.x |pmid=25389634|s2cid=2380139 }}</ref> || 20,691 males, 7446 females || Men: 208.609–0.716 × age<br />Women: 209.273–0.804 × age || SD = 10.81 (male), 12.15 (female)
|}

==== Haskell & Fox (1970)====
[[File:Exercise zones Fox and Haskell.svg|thumb|300px|Fox and Haskell formula; widely used]]
Notwithstanding later research, the most widely cited formula for HR<sub>max</sub> is still:<ref>{{cite web|date=14 October 2020|title=Target Heart Rate and Estimated Maximum Heart Rate|url=https://www.cdc.gov/physicalactivity/basics/measuring/heartrate.htm|access-date=16 November 2021|website=U.S. [[Centers for Disease Control and Prevention]] (CDC)}}</ref>

:HR<sub>max</sub> = 220 − age

Although attributed to various sources, it is widely thought to have been devised in 1970 by Dr. William Haskell and Dr. Samuel Fox.<ref name="mhrt" /> They did not develop this formula from original research, but rather by plotting data from approximately 11 references consisting of published research or unpublished scientific compilations.<ref name="mhrt2"/> It gained widespread use through being used by [[Polar Electro]] in its heart rate monitors,<ref name="mhrt" /> which Dr. Haskell has "laughed about",<ref name="mhrt" /> as the formula "was never supposed to be an absolute guide to rule people's training."<ref name="mhrt" />

While this formula is commonly used (and easy to remember and calculate), research has consistently found that it is subject to bias, particularly in older adults.<ref>{{cite journal |last1=Tanaka |first1=Hirofumi |last2=Monahan |first2=Kevin D |last3=Seals |first3=Douglas R |title=Age-predicted maximal heart rate revisited |journal=Journal of the American College of Cardiology |date=January 2001 |volume=37 |issue=1 |pages=153–156 |doi=10.1016/S0735-1097(00)01054-8|pmid=11153730 |doi-access=free }}</ref> Compared to the age-specific average HR<sub>max</sub>, the Haskell and Fox formula overestimates HR<sub>max</sub> in young adults, agrees with it at age 40, and underestimates HR<sub>max</sub> in older adults.<ref name="Nes2013"/><ref name=Wingate/> For example, in one study, the average HR<sub>max</sub> at age 76 was about 10bpm higher than the Haskell and Fox equation.<ref name=Wingate/> Consequently, the formula cannot be recommended for use in exercise physiology and related fields.<ref name="mhrt2"/>

==== Other formulas ====

[[File:MaximumHeartRateByAgeVariousFormulae.png|thumb|300px|The various formulae provide slightly different numbers for the maximum heart rates by age.]]

HR<sub>max</sub> is strongly correlated to age, and most formulas are solely based on this.<ref name="pmid11153730"/> Studies have been mixed on the effect of gender, with some finding that gender is statistically significant, although small when considering overall equation error, while others finding negligible effect.<ref name="Wingate"/> The inclusion of physical activity status, maximal oxygen uptake, smoking, body mass index,<ref name="Nes2013"/> body weight, or resting heart rate<ref name=Gellish/> did not significantly improve accuracy. Nonlinear models are slightly more accurate predictors of average age-specific HR<sub>max</sub>, particularly above 60 years of age, but are harder to apply, and provide statistically negligible improvement over linear models.<ref name=Gellish/><ref name="Wingate"/> The Wingate formula is the most recent, had the largest data set, and performed best on a fresh data set when compared with other formulas, although it had only a small amount of data for ages 60 and older so those estimates should be viewed with caution.<ref name="Wingate"/> In addition, most formulas are developed for adults and are not applicable to children and adolescents.<ref>{{cite journal |last1=Cicone |first1=Zackary S. |last2=Holmes |first2=Clifton J. |last3=Fedewa |first3=Michael V. |last4=MacDonald |first4=Hayley V. |last5=Esco |first5=Michael R. |title=Age-Based Prediction of Maximal Heart Rate in Children and Adolescents: A Systematic Review and Meta-Analysis |journal=Research Quarterly for Exercise and Sport |date=3 July 2019 |volume=90 |issue=3 |pages=417–428 |doi=10.1080/02701367.2019.1615605|pmid=31157608 |s2cid=173993682 }}</ref>

====<!-- internal anchor --> Limitations ====

Maximum heart rates vary significantly between individuals.<ref name="mhrt">{{Cite news
|title='Maximum' Heart Rate Theory Is Challenged
|last=Kolata
|first=Gina
|date=2001-04-24
|newspaper=New York Times
|url=https://www.nytimes.com/2001/04/24/health/maximum-heart-rate-theory-is-challenged.html}}</ref> Age explains only about half of HR<sub>max</sub> variance.<ref name="Wingate"/> For a given age, the standard deviation of HR<sub>max</sub> from the age-specific population mean is about 12bpm, and a 95% interval for the prediction error is about 24bpm.<ref>{{cite journal |last1=Arena |first1=R |last2=Myers |first2=J |last3=Kaminsky |first3=LA |title=Revisiting age-predicted maximal heart rate: Can it be used as a valid measure of effort? |journal=American Heart Journal |date=March 2016 |volume=173 |pages=49–56 |doi=10.1016/j.ahj.2015.12.006 |pmid=26920596|pmc=4919019 }}</ref> For example, Dr. Fritz Hagerman observed that the maximum heart rates of men in their 20s on Olympic rowing teams vary from 160 to 220.<ref name="mhrt" /> Such a variation would equate to an age range of -16 to 68 using the Wingate formula.<ref>calculation, (208.609-HR<sub>max</sub>)/0.716</ref> The formulas are quite accurate at predicting the average heart rate of a group of similarly-aged individuals, but relatively poor for a given individual.

Robergs and Landwehr opine that for [[VO2 max]], prediction errors in HR<sub>max</sub> need to be less than ±3 bpm. No current formula meets this accuracy. For prescribing exercise training heart rate ranges, the errors in the more accurate formulas may be acceptable, but again it is likely that, for a significant fraction of the population, current equations used to estimate HR<sub>max</sub> are not accurate enough.<ref name="mhrt2"/> Froelicher and Myers describe maximum heart formulas as "largely useless".<ref name="froelicher pp.ix,108-12">{{cite book
 | last1 = Froelicher | first1 = Victor
 | first2 = Jonathan | last2 = Myers
 | title = Exercise and the Heart (fifth ed.)
 | location = Philadelphia
 | publisher = [[Elsevier]]
 | year = 2006
 | isbn = 978-1-4160-0311-3
 | pages=ix, 108–12 }}</ref> Measurement via a maximal test is preferable whenever possible,<ref name="Nes2013"/> which can be as accurate as ±2bpm.<ref name="mhrt2"/>

=== Heart rate reserve ===
''Heart rate reserve'' (HR<sub>reserve</sub>) is the difference between a person's measured or predicted maximum heart rate and resting heart rate, HR<sub>max</sub> − HR<sub>rest</sub>. As a person increases their cardiovascular fitness, their HR<sub>rest</sub> will drop, and the heart rate reserve will increase.

===Target heart rate===
For healthy people, the ''Target Heart Rate'' (THR) or ''Training Heart Rate Range'' (THRR) is a desired heart rate reached during [[aerobic exercise]] which enables one's [[heart]] and [[lung]]s to receive the most benefit from a workout. In practice metrics such as heart rate and VO<sub>2</sub> have significant individual variations in their relationship to exercise physiology, meaning a broad range is given for exercise prescription.<ref>{{cite journal |last1=Jamnick |first1=Nicholas A. |last2=Pettitt |first2=Robert W. |last3=Granata |first3=Cesare |last4=Pyne |first4=David B. |last5=Bishop |first5=David J. |title=An Examination and Critique of Current Methods to Determine Exercise Intensity |journal=Sports Medicine |date=October 2020 |volume=50 |issue=10 |pages=1729–1756 |doi=10.1007/s40279-020-01322-8 |pmid=32729096 }}</ref>

==== By percent, Fox–Haskell-based  ====
The THR can be calculated as a range of 65–85% intensity, with intensity defined simply as percentage of HR<sub>max</sub>.

''Example for someone with a HR<sub>max</sub> of 180 (age 40, estimating HR<sub>max</sub> As 220 − age): ''

: 65% Intensity: (220 − (age = 40)) × 0.65 → 117 bpm
: 85% Intensity: (220 − (age = 40)) × 0.85 → 154 bpm

==== Karvonen method ====

The '''Karvonen method''' gauges exercise intensity as the percentage of heart rate reserve. It is named after Karvonen, author of the initial 1957 study.<ref name="pmid13470504">{{cite journal |vauthors=Karvonen MJ, Kentala E, Mustala O | title = The effects of training on heart rate; a longitudinal study | journal = Ann Med Exp Biol Fenn | volume = 35 | issue = 3 | pages = 307–15 | year = 1957 | pmid = 13470504 }}</ref> Karvonen's study used only six subjects, and Karvonen did not connect his recommendations to VO<sub>2</sub> data,<ref name="pmid9502363">{{cite journal |vauthors=Swain DP, Leutholtz BC, King ME, Haas LA, Branch JD | title = Relationship between % heart rate reserve and % VO2 reserve in treadmill exercise | journal = Med Sci Sports Exerc | volume = 30 | issue = 2 | pages = 318–21 | year = 1998 | pmid = 9502363 | doi = 10.1097/00005768-199802000-00022 | doi-access = free }}</ref> but later studies identified a connection.<ref>{{cite journal |vauthors=Karvonen J, Vuorimaa T |title=Heart rate and exercise intensity during sports activities. Practical application |journal=Sports Medicine |volume=5 |issue=5 |pages=303–11 | date=May 1988 |pmid=3387734 |doi=10.2165/00007256-198805050-00002|s2cid=42982362 }}</ref> The percentage of heart rate reserve is strongly correlated with the percentage of [[VO2 max]] and the percentage of VO<sub>2</sub> in reserve,<ref>{{cite journal |last1=Ferri Marini |first1=C |last2=Sisti |first2=D |last3=Leon |first3=AS |last4=Skinner |first4=JS |last5=Sarzynski |first5=MA |last6=Bouchard |first6=C |last7=Rocchi |first7=MBL |last8=Piccoli |first8=G |last9=Stocchi |first9=V |last10=Federici |first10=A |last11=Lucertini |first11=F |title=HRR and V˙O2R Fractions Are Not Equivalent: Is It Time to Rethink Aerobic Exercise Prescription Methods? |journal=Medicine and Science in Sports and Exercise |date=January 2021 |volume=53 |issue=1 |pages=174–182 |doi=10.1249/MSS.0000000000002434|doi-access=free |pmid=32694364}}</ref> but the correlation is not perfect.<ref>{{cite journal |last1=Vehrs |first1=Pat R. |last2=Tafunai |first2=Nicole D. |last3=Fellingham |first3=Gilbert W. |title=Bayesian Analysis of the HR–VO2 Relationship during Cycling and Running in Males and Females |journal=International Journal of Environmental Research and Public Health |date=16 December 2022 |volume=19 |issue=24 |article-number=16914 |doi=10.3390/ijerph192416914|pmid=36554797 |doi-access=free|pmc=9779181 }}</ref><ref>{{cite journal |last1=Wynne |first1=Jaison L. |last2=Swain |first2=David P. |last3=Harden |first3=Joel E. |last4=Wilson |first4=Patrick B. |title=Heart Rate Reserve and VO2 Reserve Are Not Interchangeable During Prolonged Exercise |journal=Journal of Clinical Exercise Physiology |date=September 2023 |volume=12 |issue=3 |pages=65–71 |doi=10.31189/2165-6193-12.3.65|doi-access=free}}</ref>

As formulas:
: % intensity = (THR - HR<sub>rest</sub>) / (HR<sub>max</sub> − HR<sub>rest</sub>)
: THR = ((HR<sub>max</sub> − HR<sub>rest</sub>) × % intensity) + HR<sub>rest</sub>
Equivalently,
: % intensity = (THR - HR<sub>rest</sub>) / HR<sub>reserve</sub>
: THR = (HR<sub>reserve</sub> × % intensity) + HR<sub>rest</sub>

''Example for someone with a HR<sub>max</sub> of 180 and a HR<sub>rest</sub> of 70 (and therefore a HR<sub>reserve</sub> of 110):''

: 50% Intensity: ((180 − 70) × 0.50) + 70 = 125 bpm
: 85% Intensity: ((180 − 70) × 0.85) + 70 = 163 bpm

==== Zoladz method ====

An alternative to the Karvonen method is the ''Zoladz method'', which is used to test an athlete's capabilities at specific heart rates. These are not intended to be used as exercise zones, although they are often used as such.<ref name="zoladz">{{cite book
 | last1 = Zoladz | first1 = Jerzy A.
 | title = Muscle and Exercise Physiology (first ed.)
 | publisher = [[Elsevier]]
 | year = 2018
 | isbn = 978-0-12-814593-7 }}</ref> The Zoladz test zones are derived by subtracting values from HR<sub>max</sub>:

: THR = HR<sub>max</sub> − Adjuster ± 5&nbsp;bpm
:: Zone 1 Adjuster = 50&nbsp;bpm
:: Zone 2 Adjuster = 40&nbsp;bpm
:: Zone 3 Adjuster = 30&nbsp;bpm
:: Zone 4 Adjuster = 20&nbsp;bpm
:: Zone 5 Adjuster = 10&nbsp;bpm

''Example for someone with a HR<sub>max</sub> of 180:''

: Zone 1 (easy exercise): 180 − 50 ± 5 → 125 − 135 bpm
: Zone 4 (tough exercise): 180 − 20 ± 5 → 155 − 165 bpm

=== Heart rate recovery ===
Heart rate recovery (HRR) is the reduction in heart rate at peak exercise and the rate as measured after a cool-down period of fixed duration.<ref name="mort" /> A greater reduction in heart rate after exercise during the reference period is associated with a higher level of cardiac fitness.<ref name="froelicher p114">{{cite book | last1=Froelicher | first1=Victor | first2=Jonathan |last2=Myers | title=Exercise and the Heart (fifth ed.) |location=Philadelphia |publisher=Elsevier |year=2006 |isbn = 978-1-4160-0311-3 |page=114 }}</ref>

Heart rates assessed during treadmill stress test that do not drop by more than 12 bpm one minute after stopping exercise (if cool-down period after exercise) or by more than 18 bpm one minute after stopping exercise (if no cool-down period and supine position as soon as possible) are associated with an increased risk of death.<ref>{{Cite journal |last1=Watanabe |first1=Junko |last2=Thamilarasan |first2=Maran |last3=Blackstone |first3=Eugene H. |last4=Thomas |first4=James D. |last5=Lauer |first5=Michael S. |date=2001-10-16 |title=Heart Rate Recovery Immediately After Treadmill Exercise and Left Ventricular Systolic Dysfunction as Predictors of Mortality |journal=Circulation |volume=104 |issue=16 |pages=1911–1916 |doi=10.1161/circ.104.16.1911 |s2cid=10587811 |issn=0009-7322|doi-access=free }}</ref><ref name="mort">{{cite journal |vauthors=Cole CR, Blackstone EH, Pashkow FJ, Snader CE, Lauer MS | title=Heart-rate recovery immediately after exercise as a predictor of mortality | journal= N Engl J Med |volume=341|issue=18| pages=1351–57 | year=1999 | pmid=10536127 | doi=10.1056/NEJM199910283411804 | doi-access=free }}</ref> People with an abnormal HRR defined as a decrease of 42 beats per minutes or less at two minutes post-exercise had a mortality rate 2.5 times greater than patients with a normal recovery.<ref name="froelicher p114"/> Another study reported a four-fold increase in mortality in subjects with an abnormal HRR defined as ≤12 bpm reduction one minute after the cessation of exercise.<ref name="froelicher p114"/> A study reported that a HRR of ≤22 bpm after two minutes "best identified high-risk patients".<ref name="froelicher p114"/> They also found that while HRR had significant [[prognosis|prognostic]] value it had no [[diagnosis|diagnostic]] value.<ref name="froelicher p114"/><ref>{{Cite journal|last1=Emren|first1=SV|last2=Gediz|first2=RB|last3=Şenöz|first3=O |last4=Karagöz|first4=U |last5=Şimşek|first5=EÇ|last6=Levent|first6=F|last7=Özdemir|first7=E |last8=Gürsoy|first8=MO|last9=Nazli|first9=C|date=February 2019|title=Decreased heart rate recovery may predict a high SYNTAX score in patients with stable coronary artery disease|journal=Bosnian Journal of Basic Medical Sciences|volume=19|issue=1|pages=109–15 |doi=10.17305/bjbms.2019.3725 |pmc=6387669|pmid=30599115}}</ref>

=== Heart rate prediction ===
Heart rate prediction using machine learning has gained significant attention in health monitoring and sports performance research. Namazi et.al., 2025 study evaluated various models including Long Short-Term Memory (LSTM), Physics-Informed Neural Networks (PINNs), and 1D Convolutional Neural Networks (1D CNNs), using physiological data such as heart rate (HR), breathing rate (BR), and RR intervals collected from wearable sensors during sports activities. The study introduced a hybrid approach combining Singular Spectrum Analysis (SSA) with these models to enhance predictive performance. Among the tested models, the SSA-LSTM method yielded the lowest prediction error, particularly when multivariate inputs (HR + BR + RR) were used. These findings support the use of AI-driven, multivariate prediction models for real-time cardiovascular monitoring in athletic and healthcare settings.<ref>{{Cite journal |last1=Namazi |first1=Asieh |last2=Modiri |first2=Ehsan |last3=Blesić |first3=Suzana |last4=Knežević |first4=Olivera M. |last5=Mirkov |first5=Dragan M. |date=2025-03-13 |title=Comparative Analysis of Machine Learning Techniques for Heart Rate Prediction Employing Wearable Sensor Data |journal=Sports |volume=13 |issue=3 |page=87 |doi=10.3390/sports13030087 |doi-access=free |pmid=40137811 |pmc=11946376 }}</ref>

===Development===
{{See also|Heart development}}
[[Image:EHR-BBII.jpg|thumb|left|300px|At 21 days after [[Fertilization|conception]], the human heart begins beating at 70 to 80 beats per minute and accelerates linearly for the first month of beating.]]
[[File:Fetal heart rate monitoring.jpg|thumb|left|Fetal heart rate monitoring. 30 weeks pregnancy.]]
The human heart beats more than 2.8 billion times in an average lifetime.<ref>{{Cite web|date=2015-06-02|title=Human Heart Trivia|url=https://www.fi.edu/heart/human-heart-trivia|archive-url=https://web.archive.org/web/20150908160310/https://www.fi.edu/heart/human-heart-trivia|archive-date=September 8, 2015|access-date=2021-08-08|website=The Franklin Institute|language=en}}</ref>
The [[fetal heartbeat|heartbeat]] of a human [[embryo]] begins at approximately 21 days after conception, or five weeks after the last normal [[menstrual period]] (LMP), which is the date normally used to date pregnancy in the medical community. The electrical depolarizations that trigger cardiac [[myocyte]]s to contract arise spontaneously within the [[myocyte]] itself. The heartbeat is initiated in the pacemaker regions and spreads to the rest of the heart through a conduction pathway. Pacemaker cells develop in the primitive atrium and the sinus venosus to form the [[sinoatrial node]] and the [[atrioventricular node]] respectively. Conductive cells develop the [[bundle of His]] and carry the [[depolarization]] into the lower heart.{{citation needed|date=March 2021}}

The human heart begins beating at a rate near the mother's, about 75–80 beats per minute (bpm). The embryonic heart rate then accelerates linearly for the first month of beating, peaking at 165–185 bpm during the early 7th week, (early 9th week after the LMP). This acceleration is approximately 3.3 bpm per day, or about 10 bpm every three days, an increase of 100 bpm in the first month.<ref>{{cite web |title=Embryonic Heart Rates Compared in Assisted and Non-Assisted Pregnancies |url=https://www.contemporaryobgyn.net/view/embryonic-heart-rates-compared-assisted-and-non-assisted-pregnancies |website=Contemporary OB/GYN |date=14 July 2011 }}</ref>

After peaking at about 9.2 weeks after the LMP, it decelerates to about 150 bpm (+/-25 bpm) during the 15th week after the LMP. After the 15th week the deceleration slows reaching an average rate of about 145 (+/-25 bpm) bpm at term. The regression formula which describes this acceleration before the embryo reaches 25&nbsp;mm in crown-rump length or 9.2 LMP weeks is:

<math>\mathrm{Age\ in\ days} =\ \mathrm{EHR} (0.3)+6 </math>

==Clinical significance==

=== Manual measurement ===
[[File:Suunto t6c rannetietokone.JPG|thumb|250px|Wrist heart rate monitor (2009)]]
[[File:Polar Heart Rate Monitor.jpg|thumb|250px|Heart rate monitor with a wrist receiver]]
Heart rate is measured by finding the [[pulse]] of the heart. This pulse rate can be found at any point on the body where the [[artery|artery's]] pulsation is transmitted to the surface by pressuring it with the index and middle fingers; often it is compressed against an underlying structure like bone. The thumb should not be used for measuring another person's heart rate, as its strong pulse may interfere with the correct perception of the target pulse.{{citation needed|date=March 2021}}

The [[radial artery]] is the easiest to use to check the heart rate. However, in emergency situations the most reliable arteries to measure heart rate are [[carotid artery|carotid arteries]]. This is important mainly in patients with [[atrial fibrillation]], in whom heart beats are irregular and [[stroke volume]] is largely different from one beat to another. In those beats following a shorter diastolic interval left ventricle does not fill properly, stroke volume is lower and pulse wave is not strong enough to be detected by palpation on a distal artery like the radial artery. It can be detected, however, by doppler.{{sfn|Fuster|Wayne|O'Rouke|2001|pp=824–29}}<ref>[http://serendip.brynmawr.edu/sci_edu/waldron/heartrate.html Regulation of Human Heart Rate] {{Webarchive|url=https://web.archive.org/web/20070514225223/http://serendip.brynmawr.edu/sci_edu/waldron/heartrate.html |date=2007-05-14 }}. Serendip. Retrieved on June 27, 2007.</ref>

Possible points for measuring the heart rate are:{{citation needed|date=March 2021}}
# The ventral aspect of the [[wrist]] on the side of the thumb ([[radial artery]]).
# The [[ulnar artery]].
# The inside of the [[elbow]], or under the biceps muscle ([[brachial artery]]).
# The [[groin]] ([[femoral artery]]).
# Behind the medial [[malleolus]] on the feet ([[posterior tibial artery]]).
# Middle of [[Dorsum (anatomy)|dorsum]] of the foot ([[dorsalis pedis]]).
# Behind the knee ([[popliteal artery]]).
# Over the [[abdomen]] ([[abdominal aorta]]).
# The chest ([[apex of the heart]]), which can be felt with one's hand or fingers. It is also possible to [[auscultate]] the heart using a [[stethoscope]].
# In the neck, lateral of the [[larynx]] ([[carotid artery]])
# The [[Temple (anatomy)|temple]] ([[superficial temporal artery]]).
# The lateral edge of the mandible ([[facial artery]]).
# The side of the head near the ear ([[posterior auricular artery]]).
[[File:ECG-RRinterval.svg|thumb|250px|ECG-RRinterval]]

=== Electronic measurement ===
[[File:Embryo at 5 weeks 5 days with heartbeat.gif|thumb|150px|In [[obstetrics]], heart rate can be measured by [[obstetric ultrasonography|ultrasonography]], such as in this embryo (at bottom left in the [[gestational sac|sac]]) of 6 weeks with a heart rate of approximately 90 per minute.]]
A more precise method of determining heart rate involves the use of an [[electrocardiograph]], or ECG (also abbreviated [[EKG]]). An ECG generates a pattern based on electrical activity of the heart, which closely follows heart function. Continuous ECG monitoring is routinely done in many clinical settings, especially in [[critical care medicine]]. On the ECG, instantaneous heart rate is calculated using the R wave-to-R wave (RR) interval and multiplying/dividing in order to derive heart rate in heartbeats/min. Multiple methods exist:{{citation needed|date=March 2021}}
* HR = 1000&nbsp;·&nbsp;60/(RR interval in milliseconds)
* HR = 60/(RR interval in seconds)
* HR = 300/number of "large" squares between successive R waves.
* HR = 1,500 number of large blocks
Heart rate monitors allow measurements to be taken continuously and can be used during exercise when manual measurement would be difficult or impossible (such as when the hands are being used). Various commercial [[heart rate monitor]]s are also available. Some monitors, used during sport, consist of a chest strap with [[electrode]]s. The signal is transmitted to a wrist receiver for display.{{citation needed|date=March 2021}}

Alternative methods of measurement include [[wikt:seismocardiography|seismocardiography]].<ref name="pmid1914618">{{cite journal |vauthors=Salerno DM, Zanetti J | title = Seismocardiography for monitoring changes in left ventricular function during ischemia | journal = Chest | volume = 100 | issue = 4 | pages = 991–93 | year = 1991 | doi = 10.1378/chest.100.4.991 | pmid = 1914618 | s2cid = 40190244 }}</ref>

=== Optical measurements ===
[[File:Retinal blood flow in the optic nerve head region revealed by laser Doppler imaging by digital holography.gif|thumb|left|Pulsatile retinal blood flow in the optic nerve head region revealed by [[laser Doppler imaging]]<ref>{{cite journal |last1=Puyo |first1=Léo |last2=Paques |first2=Michel |last3=Fink |first3=Mathias |last4=Sahel |first4=José-Alain |last5=Atlan |first5=Michael |title=Waveform analysis of human retinal and choroidal blood flow with laser Doppler holography |journal=Biomedical Optics Express |date=2019-09-05 |volume=10 |issue=10 |pages=4942–4963 |doi=10.1364/BOE.10.004942|arxiv=2106.00634 |pmid=31646021 |pmc=6788604 }}</ref>]]
[[Pulse oximetry]] of the finger and [[laser Doppler imaging]] of the eye fundus are often used in the clinics. Those techniques can assess the heart rate by measuring the delay between [[pulse]]s.{{citation needed|date=April 2021}}

===Tachycardia===
{{Main|Tachycardia}}
Tachycardia is a resting heart rate more than 100 beats per minute. This number can vary as smaller people and children have faster heart rates than average adults.

Physiological conditions where tachycardia occurs:
# Pregnancy
# Emotional conditions such as anxiety or stress.
# Exercise
{{clear}}
Pathological conditions where tachycardia occurs:
# Sepsis
# Fever
# Anemia
# Hypoxia
# Hyperthyroidism
# Hypersecretion of catecholamines
# Cardiomyopathy
# Valvular heart diseases
# Acute Radiation Syndrome
# Dehydration
# [[Metabolic myopathy|Metabolic myopathies]] (At rest, tachycardia is commonly seen in fatty acid oxidation disorders. An inappropriate rapid heart rate response to exercise is seen in muscle glycogenoses and mitochondrial myopathies, where the tachycardia is faster than would be expected during exercise).

===Bradycardia===
{{Main|Bradycardia|Athletic heart syndrome}}
Bradycardia was defined as a heart rate less than 60 beats per minute when textbooks asserted that the normal range for heart rates was 60–100 bpm. The normal range has since been revised in textbooks to 50–90 bpm for a human at total rest. Setting a lower threshold for bradycardia prevents misclassification of fit individuals as having a pathologic heart rate. The normal heart rate number can vary as children and adolescents tend to have faster heart rates than average adults. Bradycardia may be associated with medical conditions such as [[hypothyroidism]], heart disease, or inflammatory disease.<ref>{{Cite web|title=Bradycardia - Symptoms and causes|url=https://www.mayoclinic.org/diseases-conditions/bradycardia/symptoms-causes/syc-20355474|access-date=2021-08-08|website=Mayo Clinic|language=en}}</ref> At rest, although tachycardia is more commonly seen in [[Fatty-acid metabolism disorder|fatty acid oxidation disorders]], more rarely acute bradycardia can occur.<ref>{{Cite journal |last1=Bonnet |first1=D. |last2=Martin |first2=D. |last3=Pascale De Lonlay |first3=null |last4=Villain |first4=E. |last5=Jouvet |first5=P. |last6=Rabier |first6=D. |last7=Brivet |first7=M. |last8=Saudubray |first8=J. M. |date=1999-11-30 |title=Arrhythmias and conduction defects as presenting symptoms of fatty acid oxidation disorders in children |journal=Circulation |volume=100 |issue=22 |pages=2248–2253 |doi=10.1161/01.cir.100.22.2248 |issn=1524-4539 |pmid=10577999|doi-access=free }}</ref>

Trained [[sportsperson|athlete]]s tend to have slow resting heart rates, and resting bradycardia in athletes should not be considered abnormal if the individual has no symptoms associated with it. For example, [[Miguel Indurain]], a Spanish cyclist and five time [[Tour de France]] winner, had a resting heart rate of 28 beats per minute,<ref name=GuinessWR2004>{{cite book|title=Guinness World Records 2004 |url=https://archive.org/details/guinnessworldrec2004guin |url-access=registration |date=2004|publisher=Bantam Books|location=New York|isbn=978-0-553-58712-8|edition=Bantam|pages=[https://archive.org/details/guinnessworldrec2004guin/page/10 10–11]}}</ref> one of the lowest ever recorded in a healthy human. Daniel Green achieved the world record for the slowest heartbeat in a healthy human with a heart rate of just 26 bpm in 2014.<ref>{{cite web |title=Slowest heart rate: Daniel Green breaks Guinness World Records record |date=29 November 2014 |website=World Record Academy |url=http://www.worldrecordacademy.com/medical/slowest_heart_rate_Daniel_Green_breaks_Guinness_World_Records_record_214157.html }}</ref>

===Arrhythmia===
{{Main|Cardiac dysrhythmia}}
Arrhythmias are abnormalities of the heart rate and rhythm (sometimes felt as [[palpitation]]s). They can be divided into two broad categories: fast and slow heart rates. Some cause few or minimal symptoms. Others produce more serious symptoms of lightheadedness, dizziness and fainting.<ref>{{Cite web|title=Heart arrhythmia - Symptoms and causes|url=https://www.mayoclinic.org/diseases-conditions/heart-arrhythmia/symptoms-causes/syc-20350668|access-date=2021-08-08|website=Mayo Clinic|language=en}}</ref>

=== Hypertension ===
{{Main|Hypertension}}

Elevated heart rate is a powerful predictor of morbidity and mortality in patients with hypertension.<ref name="pmid29232971">{{cite journal | vauthors = Kouvas N, Dimitriadis K, Kakosaiou Z, Tousoulis D | title=Heart Rate and Blood Pressure: "Connecting the Dots" in Epidemiology and Pathophysiology | journal= [[Angiology (journal)|Angiology]] | volume=69 | issue=8 | pages=660–665 | year=2018 | doi= 10.1177/0003319717746524 | pmid=29232971 }}</ref> [[Atherosclerosis]] and [[dysautonomia]] are major contributors to the pathogenesis.<ref name="pmid29232971" />

===Correlation with cardiovascular mortality risk===

{{More medical citations needed|section|date=July 2015}}

A number of investigations indicate that faster resting heart rate has emerged as a new risk factor for mortality in [[homeothermic]] mammals, particularly cardiovascular mortality in human beings. High heart rate is associated with [[endothelial dysfunction]] and increased [[Atheroma|atheromatous plaque]] formation leading to [[atherosclerosis]].<ref name="pmid25447617">{{cite journal | vauthors = Böhm M, Reil J, Borer JS | title=Resting heart rate: risk indicator and emerging risk factor in cardiovascular disease | journal= [[The American Journal of Medicine]] | volume=128 | issue=3 | pages=219–228 | year=2015 | doi= 10.1016/j.amjmed.2014.09.016 | pmid=25447617}}</ref> Faster heart rate may accompany increased production of inflammation molecules and increased production of reactive oxygen species in cardiovascular system, in addition to increased mechanical stress to the heart. There is a correlation between increased resting rate and cardiovascular risk. This is not seen to be "using an allotment of heart beats" but rather an increased risk to the system from the increased rate.<ref name="pmid19022405"/>

An Australian-led international study of patients with cardiovascular disease has shown that heart beat rate is a key indicator for the risk of heart attack. The study, published in ''The Lancet'' (September 2008) studied 11,000 people, across 33 countries, who were being treated for heart problems. Those patients whose heart rate was above 70 beats per minute had significantly higher incidence of heart attacks, hospital admissions and the need for surgery. Higher heart rate is thought to be correlated with an increase in heart attack and about a 46 percent increase in hospitalizations for non-fatal or fatal heart attack.<ref name="pmid18757091">{{cite journal |vauthors=Fox K, Ford I | title = Heart rate as a prognostic risk factor in patients with coronary artery disease and left-ventricular systolic dysfunction (BEAUTIFUL): a subgroup analysis of a randomised controlled trial | journal = Lancet | volume = 372 | issue = 6 | year = 2008 | pmid = 18757091 | doi = 10.1016/S0140-6736(08)61171-X | pages=817–21| s2cid = 6481363 }}</ref>

Other studies have shown that a high resting heart rate is associated with an increase in cardiovascular and all-cause mortality in the general population and in patients with chronic diseases.<ref name="Metabolic syndrome is associated wi">{{cite journal | vauthors = Jiang X, Liu X, Wu S, Zhang GQ, Peng M, Wu Y, Zheng X, Ruan C, Zhang W | title = Metabolic syndrome is associated with and predicted by resting heart rate: a cross-sectional and longitudinal study | journal = Heart | volume = 101 | issue = 1 | pages = 44–9 | date = Jan 2015 | pmid = 25179964 | doi = 10.1136/heartjnl-2014-305685 | doi-access = free }}</ref><ref>{{Cite journal|last1=Cook|first1=Stéphane|last2=Hess|first2=Otto M.|date=2010-03-01|title=Resting heart rate and cardiovascular events: time for a new crusade?|journal=European Heart Journal|volume=31|issue=5|pages=517–19|doi=10.1093/eurheartj/ehp484 |pmid=19933283|doi-access=free}}</ref> A faster resting heart rate is associated with shorter life expectancy <ref name="pmid19022405"/><ref name=":4">{{Cite journal|last1=Cooney|first1=Marie Therese|last2=Vartiainen|first2=Erkki|last3=Laatikainen|first3=Tiina|last4=Laakitainen|first4=Tinna|last5=Juolevi|first5=Anne|last6=Dudina|first6=Alexandra|last7=Graham|first7=Ian M.|date=2010-04-01|title=Elevated resting heart rate is an independent risk factor for cardiovascular disease in healthy men and women|journal=American Heart Journal|volume=159|issue=4|pages=612–19.e3|doi=10.1016/j.ahj.2009.12.029 |pmid=20362720}}</ref> and is considered a strong risk factor for heart disease and heart failure,<ref name=":5">{{Cite journal|last1=Teodorescu|first1=Carmen|last2=Reinier|first2=Kyndaron|last3=Uy-Evanado|first3=Audrey|last4=Gunson|first4=Karen|last5=Jui|first5=Jonathan|last6=Chugh|first6=Sumeet S.|date=2013-08-01|title=Resting heart rate and risk of sudden cardiac death in the general population: influence of left ventricular systolic dysfunction and heart rate-modulating drugs|journal=Heart Rhythm |volume=10|issue=8|pages=1153–58|doi=10.1016/j.hrthm.2013.05.009 |pmc=3765077|pmid=23680897}}</ref> independent of level of physical fitness.<ref>{{Cite journal|last1=Jensen|first1=Magnus Thorsten|last2=Suadicani|first2=Poul|last3=Hein|first3=Hans Ole|last4=Gyntelberg|first4=Finn|date=2013-06-01|title=Elevated resting heart rate, physical fitness and all-cause mortality: a 16-year follow-up in the Copenhagen Male Study|journal=Heart|volume=99|issue=12|pages=882–87|doi=10.1136/heartjnl-2012-303375 |pmc=3664385|pmid=23595657}}</ref> Specifically, a resting heart rate above 65 beats per minute has been shown to have a strong independent effect on premature mortality; every 10 beats per minute increase in resting heart rate has been shown to be associated with a 10–20% increase in risk of death.<ref name=":6">{{Cite journal|last1=Woodward|first1=Mark|last2=Webster|first2=Ruth|last3=Murakami|first3=Yoshitaka|last4=Barzi|first4=Federica|last5=Lam|first5=Tai-Hing|last6=Fang|first6=Xianghua|last7=Suh|first7=Il|last8=Batty|first8=G. David|last9=Huxley|first9=Rachel|date=2014-06-01|title=The association between resting heart rate, cardiovascular disease and mortality: evidence from 112,680 men and women in 12 cohorts|journal=European Journal of Preventive Cardiology|volume=21|issue=6|pages=719–26|doi=10.1177/2047487312452501 |pmid=22718796|s2cid=31791634|doi-access=free|hdl=20.500.11937/23854|hdl-access=free}}</ref> In one study, men with no evidence of heart disease and a resting heart rate of more than 90 beats per minute had a five times higher risk of sudden cardiac death.<ref name=":5" /> Similarly, another study found that men with resting heart rates of over 90 beats per minute had an almost two-fold increase in risk for cardiovascular disease mortality; in women it was associated with a three-fold increase.<ref name=":4" /> In patients having heart rates of 70 beats/minute or above, each additional beat/minute was associated with increased rate of cardiovascular death and heart failure hospitalization.<ref name="pmid25447617" />

Given these data, heart rate should be considered in the assessment of cardiovascular risk, even in apparently healthy individuals.<ref>{{Cite journal|last1=Arnold|first1=J. Malcolm|last2=Fitchett|first2=David H.|last3=Howlett|first3=Jonathan G.|last4=Lonn|first4=Eva M.|last5=Tardif|first5=Jean-Claude|date=2008-05-01|title=Resting heart rate: a modifiable prognostic indicator of cardiovascular risk and outcomes?|journal=The Canadian Journal of Cardiology|volume=24 Suppl A|issue=Suppl A |pages=3A–8A |pmc=2787005|pmid=18437251|doi=10.1016/s0828-282x(08)71019-5}}</ref> Heart rate has many advantages as a clinical parameter: It is inexpensive and quick to measure and is easily understandable.<ref name=":7">{{Cite journal|last=Nauman|first=Javaid|date=2012-06-12|title=Why measure resting heart rate?|journal=Tidsskrift for den Norske Lægeforening |volume=132|issue=11|page=1314|doi=10.4045/tidsskr.12.0553 |pmid=22717845|doi-access=free}}</ref> Although the accepted limits of heart rate are between 60 and 100 beats per minute, this was based for convenience on the scale of the squares on electrocardiogram paper; a better definition of normal sinus heart rate may be between 50 and 90 beats per minute.<ref>{{Cite journal|last=Spodick|first=DH|date=1992|title=Operational definition of normal sinus heart rate|journal=Am J Cardiol|volume=69|issue=14|doi=10.1016/0002-9149(92)90947-W|pmid=1575201|pages=1245–46}}</ref><ref name="Metabolic syndrome is associated wi"/>

Standard textbooks of physiology and medicine mention that heart rate (HR) is readily calculated from the ECG as follows: HR = 1000*60/RR interval in milliseconds, HR = 60/RR interval in seconds, or HR = 300/number of large squares between successive R waves. In each case, the authors are actually referring to instantaneous HR, which is the number of times the heart would beat if successive RR intervals were constant.

Lifestyle and pharmacological regimens may be beneficial to those with high resting heart rates.<ref name=":6" /> Exercise is one possible measure to take when an individual's heart rate is higher than 80 beats per minute.<ref name=":7" /><ref>{{Cite journal|last1=Sloan|first1=Richard P.|last2=Shapiro|first2=Peter A.|last3=DeMeersman|first3=Ronald E.|last4=Bagiella|first4=Emilia|last5=Brondolo|first5=Elizabeth N.|last6=McKinley|first6=Paula S.|last7=Slavov|first7=Iordan|last8=Fang|first8=Yixin|last9=Myers|first9=Michael M.|date=2009-05-01|title=The effect of aerobic training and cardiac autonomic regulation in young adults|journal=American Journal of Public Health|volume=99|issue=5|pages=921–28|doi=10.2105/AJPH.2007.133165 |pmc=2667843|pmid=19299682}}</ref> Diet has also been found to be beneficial in lowering resting heart rate: In studies of resting heart rate and risk of death and cardiac complications on patients with type 2 diabetes, legumes were found to lower resting heart rate.<ref name=":8">{{Cite journal|last1=Jenkins|first1=David J. A.|last2=Kendall|first2=Cyril W. C.|last3=Augustin|first3=Livia S. A.|last4=Mitchell|first4=Sandra|last5=Sahye-Pudaruth|first5=Sandhya|last6=Blanco Mejia|first6=Sonia|last7=Chiavaroli|first7=Laura|last8=Mirrahimi|first8=Arash|last9=Ireland|first9=Christopher|date=2012-11-26|title=Effect of legumes as part of a low glycemic index diet on glycemic control and cardiovascular risk factors in type 2 diabetes mellitus: a randomized controlled trial|journal=Archives of Internal Medicine|volume=172|issue=21|pages=1653–60|doi=10.1001/2013.jamainternmed.70 |pmid=23089999|doi-access=}}</ref> This is thought to occur because in addition to the direct beneficial effects of legumes, they also displace animal proteins in the diet, which are higher in saturated fat and cholesterol.<ref name=":8" /> Another nutrient is omega-3 long chain polyunsaturated fatty acids ([[omega-3 fatty acid]] or LC-[[PUFA]]). In a meta-analysis with a total of 51 randomized controlled trials ([[RCTs]]) involving 3,000 participants, the supplement mildly but significantly reduced heart rate (-2.23 bpm; 95% CI: -3.07, -1.40 bpm). When [[docosahexaenoic acid]] (DHA) and [[eicosapentaenoic acid]] (EPA) were compared, modest heart rate reduction was observed in trials that supplemented with DHA (-2.47 bpm; 95% CI: -3.47, -1.46 bpm), but not in those received EPA.<ref>{{cite journal | vauthors = Hidayat K, Yang J, Zhang Z, Chen GC, Qin LQ, Eggersdorfer M, Zhang W | title = Effect of omega-3 long-chain polyunsaturated fatty acid supplementation on heart rate: a meta-analysis of randomized controlled trials | journal = European Journal of Clinical Nutrition | volume = 72 | issue = 6 | pages = 805–817 | date = Jun 2018 | pmid = 29284786 | doi = 10.1038/s41430-017-0052-3 | pmc = 5988646 | doi-access = free }}</ref>

A very slow heart rate ([[bradycardia]]) may be associated with [[heart block]].<ref>{{EMedicine|article|151597|Atrioventricular Block}}</ref> It may also arise from autonomous nervous system impairment.{{Medical citation needed|Reason=The original reference was to a New Scientist book review, not to a published study or meta-study in an accredited medical journal.|date=July 2015}}

==See also==
* [[Heart rate monitor]]
* [[Cardiac cycle]]
* [[Electrocardiography]]
* [[Sinus rhythm]]
* [[Second wind#Pathology|Second wind]] (heart rate is measured during 12 Minute Walk Test)
* [[Bainbridge reflex]]

==Notes==
{{Reflist}}

==References==
* {{CNX A&P}}

==Bibliography==
{{Refbegin|50em}}
* {{cite book|title=Hurst's The Heart|edition=10th International|year=2001|last1=Fuster |first1=Valentin |last2=Wayne |first2=Alexander R. |last3=O'Rouke |first3=Robert A. |isbn=978-0-07-116296-8 |location=New York |publisher=McGraw-Hill |oclc=49034333 }}
* {{cite book|title=Physical Examination and Health Assessment|edition=6|year=2011|last=Jarvis, C.|isbn=978-1-4377-0151-7|publisher=Saunders Elsevier}}
{{Refend}}

==External links==
* [http://www.tapheartrate.com/ Online Heart Beats Per Minute Calculator] ''Tap along with your heart rate''
* [https://sourceforge.net/projects/pulsecapture/ An application (open-source) for contactless real time heart rate measurements by means of an ordinary web cam]

{{Cardiovascular physiology}}
{{Portal bar|Medicine}}
{{Authority control}}

{{DEFAULTSORT:Heart Rate}}
[[Category:Cardiovascular physiology]]
[[Category:Medical signs]]
[[Category:Mathematics in medicine]]
[[Category:Temporal rates]]