The distance from the Oort cloud to the interior of the Solar System, and two of the nearest stars, is measured in astronomical units. The scale is logarithmic: each indicated distance is ten times farther out than the previous distance. The red arrow indicates the location of the space probeVoyager 1 by 2012-2013, which will reach the Oort cloud in about 300 years.
An artist's impression of the Oort cloud and the Kuiper belt (inset); the sizes of objects are over-scaled for visibility.
The Oort cloud (/ɔːrt,ʊərt/), sometimes called the Öpik–Oort cloud, is theorized to be a vast cloud of icyplanetesimals surrounding the Sun at distances ranging from 2,000 to 200,000 AU (0.03 to 3.2 light-years). The concept of such a cloud was proposed in 1950 by the Dutch astronomerJan Oort, in whose honor the idea was named. Oort proposed that the bodies in this cloud replenish and keep constant the number of long-period comets entering the inner Solar System—where they are eventually consumed and destroyed during close approaches to the Sun.
The outer limit of the Oort cloud defines the cosmographic boundary of the Solar System. This area is defined by the Sun's Hill sphere, and hence lies at the interface between solar and galactic gravitational dominion.
The outer Oort cloud is only loosely bound to the Solar System and its
constituents are easily affected by the gravitational pulls of both passing stars and the Milky Way
itself. These forces served to moderate and render more circular the
highly eccentric orbits of material ejected from the inner solar system
during its early phases of development. The circular orbits of material in the Oort disc are largely thanks to this galactic gravitational torquing. By the same token, galactic interference in the motion of Oort bodies occasionally dislodges comets from their orbits within the cloud, sending them into the inner Solar System. Based on their orbits most but not all of the short-period comets appear to have come from the Oort disc. Other short-period comets may have originated from the far larger spherical cloud.
Astronomers hypothesize that the material presently in the Oort cloud formed much closer to the Sun, in the protoplanetary disc, and was then scattered far into space through the gravitational influence of the giant planets. No direct observation of the Oort cloud is possible with present imaging technology. Nevertheless, the cloud is thought to be the source that replenishes most long-period and Halley-type
comets, which are eventually consumed by their close approaches to the
Sun after entering the inner Solar System. The cloud may also serve the
same function for many of the centaurs and Jupiter-family comets.
Development of theory
By the turn of the 20th century it was understood that there were two main classes of comet: short-period comets (also called ecliptic comets) and long-period comets (also called nearly isotropic comets). Ecliptic comets have relatively small orbits aligned near the ecliptic plane and are not found much farther than the Kuiper cliff around 50 AU from the Sun (the orbit of Neptune averages about 30 AU and 177P/Barnard
has aphelion around 48 AU). Long-period comets on the other hand travel
in very large orbits thousands of AU from the Sun and are isotropically
distributed. This means long-period comets appear from every direction
in the sky, both above and below the ecliptic plane.
The origin of these comets was not well understood and many long-period
comets were initially thought to be on assumed parabolic trajectories,
making them one-time visitors to the Sun from interstellar space.
In 1907 A. O. Leuschner
suggested that many of the comets then thought to have parabolic orbits
in fact moved along extremely large elliptical orbits that would return
them to the inner Solar System after long intervals during which they
were invisible to Earth-based astronomy. In 1932 the Estonian astronomer Ernst Öpik proposed a reservoir of long-period comets in the form of an orbiting cloud at the outermost edge of the Solar System. Dutch astronomer Jan Oort
revived this basic idea in 1950 to resolve a paradox about the origin
of comets. The following facts are not easily reconcilable with the
highly elliptical orbits in which long-period comets are always found:
Over millions and billions of years the orbits of Oort cloud comets are unstable. Celestial dynamics
will eventually dictate that a comet must be pulled away by a passing
star, collide with the Sun or a planet, or be ejected from the Solar
System through planetary perturbations.
Moreover, the volatile composition of comets means that as they repeatedly approach the Sun radiation gradually boils the volatiles off until the comet splits or develops an insulating crust that prevents further outgassing.
Oort reasoned that comets with orbits that closely approach the Sun
cannot have been doing so since the condensation of the protoplanetary
disc, more than 4.5 billion years ago. Hence long-period comets could
not have formed in the current orbits in which they are always
discovered and must have been held in an outer reservoir for nearly all
of their existence.
Oort also studied tables of ephemera
for long-period comets and discovered that there is a curious
concentration of long-period comets whose farthest retreat from the Sun
(their aphelia) cluster around 20,000 AU. This suggested a reservoir at that distance with a spherical, isotropic
distribution. He also proposed that the relatively rare comets with
orbits of about 10,000 AU probably went through one or more orbits into
the inner Solar System and there had their orbits drawn inward by the gravity of the planets.
Structure and composition
The presumed distance of the Oort cloud compared to the rest of the Solar System
The Oort cloud is thought to occupy a vast space somewhere between 2,000 and 5,000 AU (0.03 and 0.08 ly) from the Sun to as far out as 50,000 AU (0.79 ly) or even 100,000 to 200,000 AU (1.58 to 3.16 ly). The region can be subdivided into a spherical outer Oort cloud with a radius of some 20,000–50,000 AU (0.32–0.79 ly) and a torus-shaped inner Oort cloud with a radius of 2,000–20,000 AU (0.03–0.32 ly).
The inner Oort cloud is sometimes known as the Hills cloud, named for Jack G. Hills, who proposed its existence in 1981.
Models predict the inner cloud to be the much denser of the two, having
tens or hundreds of times as many cometary nuclei as the outer cloud. The Hills cloud is thought to be necessary to explain the continued existence of the Oort cloud after billions of years.
Because it lies at the interface between the dominion of Solar
and galactic gravitation, the objects composing the outer Oort cloud are
only weakly bound to the Sun. This in turn allows small perturbations
from nearby stars or the Milky Way itself to inject long-period (and
possibly Halley-type) comets inside the orbit of Neptune.
This process ought to have depleted the sparser, outer cloud and yet
long-period comets with orbits well above or below the ecliptic continue
to be observed. The Hills cloud is thought to be a secondary reservoir
of cometary nuclei and the source of replenishment for the tenuous outer
cloud as the latter's numbers are gradually depleted through losses to
the inner Solar System.
The outer Oort cloud may have trillions of objects larger than 1 km (0.62 mi), and billions with diameters of 20-kilometre (12 mi). This corresponds to an absolute magnitude of more than 11.[20]
On this analysis, "neighboring" objects in the outer cloud are
separated by a significant fraction of 1 AU, tens of millions of
kilometres. The outer cloud's total mass is not known, but assuming that Halley's Comet is a suitable proxy for the nuclei composing the outer Oort cloud, their combined mass would be roughly 3×1025 kilograms (6.6×1025 lb), or five Earth masses.
Formerly the outer cloud was thought to be more massive by two orders of magnitude, containing up to 380 Earth masses,
but improved knowledge of the size distribution of long-period comets
has led to lower estimates. No estimates of the mass of the inner Oort
cloud have been published as of 2023.
If analyses of comets are representative of the whole, the vast majority of Oort-cloud objects consist of ices such as water, methane, ethane, carbon monoxide and hydrogen cyanide.
However, the discovery of the object 1996 PW, an object whose appearance was consistent with a D-type asteroid
in an orbit typical of a long-period comet, prompted theoretical
research that suggests that the Oort cloud population consists of
roughly one to two percent asteroids. Analysis of the carbon and nitrogen isotope
ratios in both the long-period and Jupiter-family comets shows little
difference between the two, despite their presumably vastly separate
regions of origin. This suggests that both originated from the original
protosolar cloud, a conclusion also supported by studies of granular size in Oort-cloud comets and by the recent impact study of Jupiter-family comet Tempel 1.
Origin
The Oort cloud is thought to have developed after the formation of planets from the primordial protoplanetary disc approximately 4.6 billion years ago.
The most widely accepted hypothesis is that the Oort cloud's objects
initially coalesced much closer to the Sun as part of the same process
that formed the planets and minor planets.
After formation, strong gravitational interactions with young gas
giants, such as Jupiter, scattered the objects into extremely wide elliptical or parabolic orbits
that were subsequently modified by perturbations from passing stars and
giant molecular clouds into long-lived orbits detached from the gas
giant region.
Recent research has been cited by NASA hypothesizing that a large
number of Oort cloud objects are the product of an exchange of
materials between the Sun and its sibling stars as they formed and
drifted apart and it is suggested that many—possibly the majority—of
Oort cloud objects did not form in close proximity to the Sun.
Simulations of the evolution of the Oort cloud from the beginnings of
the Solar System to the present suggest that the cloud's mass peaked
around 800 million years after formation, as the pace of accretion and
collision slowed and depletion began to overtake supply.
Models by Julio Ángel Fernández suggest that the scattered disc, which is the main source for periodic comets
in the Solar System, might also be the primary source for Oort cloud
objects. According to the models, about half of the objects scattered
travel outward toward the Oort cloud, whereas a quarter are shifted
inward to Jupiter's orbit, and a quarter are ejected on hyperbolic orbits. The scattered disc might still be supplying the Oort cloud with material. A third of the scattered disc's population is likely to end up in the Oort cloud after 2.5 billion years.
Computer models suggest that collisions of cometary debris during
the formation period play a far greater role than was previously
thought. According to these models, the number of collisions early in
the Solar System's history was so great that most comets were destroyed
before they reached the Oort cloud. Therefore, the current cumulative
mass of the Oort cloud is far less than was once suspected. The estimated mass of the cloud is only a small part of the 50–100 Earth masses of ejected material.
Gravitational interaction with nearby stars and galactic tides modified cometary orbits to make them more circular. This explains the nearly spherical shape of the outer Oort cloud. On the other hand, the Hills cloud,
which is bound more strongly to the Sun, has not acquired a spherical
shape. Recent studies have shown that the formation of the Oort cloud is
broadly compatible with the hypothesis that the Solar System formed as part of an embedded cluster
of 200–400 stars. These early stars likely played a role in the cloud's
formation, since the number of close stellar passages within the
cluster was much higher than today, leading to far more frequent
perturbations.
In June 2010 Harold F. Levison
and others suggested on the basis of enhanced computer simulations that
the Sun "captured comets from other stars while it was in its birth cluster."
Their results imply that "a substantial fraction of the Oort cloud
comets, perhaps exceeding 90%, are from the protoplanetary discs of
other stars." In July 2020 Amir Siraj and Avi Loeb found that a captured origin for the Oort Cloud in the Sun's birth cluster could address the theoretical tension in explaining the observed ratio of outer Oort cloud to scattered disc objects, and in addition could increase the chances of a captured Planet Nine.
Comets
Comets
are thought to have two separate points of origin in the Solar System.
Short-period comets (those with orbits of up to 200 years) are generally
accepted to have emerged from either the Kuiper belt
or the scattered disc, which are two linked flat discs of icy debris
beyond Neptune's orbit at 30 au and jointly extending out beyond 100 au
from the Sun. Very long-period comets, such as C/1999 F1 (Catalina), whose orbits last for millions of years, are thought to originate directly from the outer Oort cloud. Other comets modeled to have come directly from the outer Oort cloud include C/2006 P1 (McNaught), C/2010 X1 (Elenin), Comet ISON, C/2013 A1 (Siding Spring), C/2017 K2, and C/2017 T2 (PANSTARRS).
The orbits within the Kuiper belt are relatively stable, and so very
few comets are thought to originate there. The scattered disc, however,
is dynamically active, and is far more likely to be the place of origin
for comets. Comets pass from the scattered disc into the realm of the outer planets, becoming what are known as centaurs. These centaurs are then sent farther inward to become the short-period comets.
There are two main varieties of short-period comet: Jupiter-family comets (those with semi-major axes of less than 5 AU) and Halley-family comets. Halley-family comets, named for their prototype, Halley's Comet,
are unusual in that although they are short-period comets, it is
hypothesized that their ultimate origin lies in the Oort cloud, not in
the scattered disc. Based on their orbits, it is suggested they were
long-period comets that were captured by the gravity of the giant
planets and sent into the inner Solar System.
This process may have also created the present orbits of a significant
fraction of the Jupiter-family comets, although the majority of such
comets are thought to have originated in the scattered disc.
Oort noted that the number of returning comets was far less than
his model predicted, and this issue, known as "cometary fading", has yet
to be resolved. No dynamical process is known to explain the smaller
number of observed comets than Oort estimated. Hypotheses for this
discrepancy include the destruction of comets due to tidal stresses,
impact or heating; the loss of all volatiles, rendering some comets invisible, or the formation of a non-volatile crust on the surface. Dynamical studies of hypothetical Oort cloud comets have estimated that their occurrence in the outer-planet
region would be several times higher than in the inner-planet region.
This discrepancy may be due to the gravitational attraction of Jupiter, which acts as a kind of barrier, trapping incoming comets and causing them to collide with it, just as it did with Comet Shoemaker–Levy 9 in 1994. An example of a typical dynamically old comet with an origin in the Oort cloud could be C/2018 F4.
Most of the comets seen close to the Sun seem to have reached their
current positions through gravitational perturbation of the Oort cloud
by the tidal force exerted by the Milky Way. Just as the Moon's
tidal force deforms Earth's oceans, causing the tides to rise and fall,
the galactic tide also distorts the orbits of bodies in the outer Solar System.
In the charted regions of the Solar System, these effects are
negligible compared to the gravity of the Sun, but in the outer reaches
of the system, the Sun's gravity is weaker and the gradient of the Milky
Way's gravitational field has substantial effects. Galactic tidal
forces stretch the cloud along an axis directed toward the galactic
center and compress it along the other two axes; these small
perturbations can shift orbits in the Oort cloud to bring objects close
to the Sun.
The point at which the Sun's gravity concedes its influence to the
galactic tide is called the tidal truncation radius. It lies at a radius
of 100,000 to 200,000 au, and marks the outer boundary of the Oort
cloud.
Some scholars theorize that the galactic tide may have contributed to the formation of the Oort cloud by increasing the perihelia (smallest distances to the Sun) of planetesimals with large aphelia (largest distances to the Sun).
The effects of the galactic tide are quite complex, and depend heavily
on the behaviour of individual objects within a planetary system.
Cumulatively, however, the effect can be quite significant: up to 90% of
all comets originating from the Oort cloud may be the result of the
galactic tide.
Statistical models of the observed orbits of long-period comets argue
that the galactic tide is the principal means by which their orbits are
perturbed toward the inner Solar System.
Stellar perturbations and stellar companion hypotheses
Besides the galactic tide,
the main trigger for sending comets into the inner Solar System is
thought to be interaction between the Sun's Oort cloud and the
gravitational fields of nearby stars or giant molecular clouds. The orbit of the Sun through the plane of the Milky Way sometimes brings it in relatively close proximity to other stellar systems. For example, it is hypothesized that 70 thousand years ago, perhaps Scholz's Star passed through the outer Oort cloud (although its low mass and high relative velocity limited its effect). During the next 10 million years the known star with the greatest possibility of perturbing the Oort cloud is Gliese 710.
This process could also scatter Oort cloud objects out of the ecliptic
plane, potentially also explaining its spherical distribution.
In 1984, physicistRichard A. Muller postulated that the Sun has an as-yet undetected companion, either a brown dwarf or a red dwarf, in an elliptical orbit within the Oort cloud. This object, known as Nemesis,
was hypothesized to pass through a portion of the Oort cloud
approximately every 26 million years, bombarding the inner Solar System
with comets. However, to date no evidence of Nemesis has been found, and
many lines of evidence (such as crater counts), have thrown its existence into doubt. Recent scientific analysis no longer supports the idea that extinctions on Earth happen at regular, repeating intervals. Thus, the Nemesis hypothesis is no longer needed to explain current assumptions.
A somewhat similar hypothesis was advanced by astronomer John J. Matese of the University of Louisiana at Lafayette
in 2002. He contends that more comets are arriving in the inner Solar
System from a particular region of the postulated Oort cloud than can be
explained by the galactic tide or stellar perturbations alone, and that
the most likely cause would be a Jupiter-mass object in a distant orbit. This hypothetical gas giant was nicknamed Tyche. The WISE mission, an all-sky survey using parallax measurements in order to clarify local star distances, was capable of proving or disproving the Tyche hypothesis. In 2014, NASA announced that the WISE survey had ruled out any object as they had defined it.
Space probes have yet to reach the area of the Oort cloud. Voyager 1, the fastest and farthestof the interplanetary space probes currently leaving the Solar System, will reach the Oort cloud in about 300 years and would take about 30,000 years to pass through it. However, around 2025, the radioisotope thermoelectric generators on Voyager 1 will no longer supply enough power to operate any of its scientific instruments, preventing any further exploration by Voyager 1. The other four probes
currently escaping the Solar System have either already stopped
functioning or are predicted to stop functioning before they reach the
Oort cloud.
In the 1980s, there was a concept for a probe that could reach 1,000 AU in 50 years, called TAU; among its missions would be to look for the Oort cloud.
In the 2014 Announcement of Opportunity for the Discovery program, an observatory to detect the objects in the Oort cloud (and Kuiper belt) called the "Whipple Mission" was proposed. It would monitor distant stars with a photometer, looking for transits up to 10,000 AU away. The observatory was proposed for halo orbiting around L2 with a suggested 5-year mission. It was also suggested that the Kepler observatory could have been capable of detecting objects in the Oort cloud.
It has been believed for some time that inputs from different
sensory organs are processed in different areas in the brain. The
communication within and among these specialized areas of the brain is
known as functional integration. Newer research has shown that these different regions of the brain may not be solely responsible for only one sensory modality, but could use multiple inputs to perceive what the body senses about its environment. Multisensory integration
is necessary for almost every activity that we perform because the
combination of multiple sensory inputs is essential for us to comprehend
our surroundings.
Overview
It
has been believed for some time that inputs from different sensory
organs are processed in different areas in the brain, relating to systems neuroscience.
Using functional neuroimaging, it can be seen that sensory-specific
cortices are activated by different inputs. For example, regions in the occipital cortex are tied to vision and those on the superior temporal gyrus
are recipients of auditory inputs. There exist studies suggesting
deeper multisensory convergences than those at the sensory-specific
cortices, which were listed earlier. This convergence of multiple
sensory modalities is known as multisensory integration.
Sensory processing deals with how the brain processes sensory
input from multiple sensory modalities. These include the five classic
senses of vision (sight), audition (hearing), tactile stimulation (touch), olfaction (smell), and gustation (taste). Other sensory modalities exist, for example the vestibular sense (balance and the sense of movement) and proprioception (the sense of knowing one's position in space) Along with Time
(The sense of knowing where one is in time or activities). It is
important that the information of these different sensory modalities
must be relatable. The sensory inputs themselves are in different
electrical signals, and in different contexts.
Through sensory processing, the brain can relate all sensory inputs
into a coherent percept, upon which our interaction with the environment
is ultimately based.
Basic structures involved
The different senses were always thought to be controlled by separate lobes of the brain, called projection areas. The lobes of the brain are the classifications that divide the brain both anatomically and functionally.
These lobes are the Frontal lobe, responsible for conscious thought,
Parietal lobe, responsible for visuospatial processing, the Occipital
lobe, responsible for the sense of sight, and the temporal lobe,
responsible for the senses of smell and sound. From the earliest times
of neurology, it has been thought that these lobes are solely
responsible for their one sensory modality input. However, newer research has shown that that may not entirely be the case.
Sometimes there can be a problem with the encoding of the sensory information. This disorder is known as Sensory processing disorder (SPD). This disorder can be further classified into three main types.
Sensory modulation disorder, in which patients seek sensory stimulation due to an over or under response to sensory stimuli.
Sensory based motor disorder. Patients have incorrect processing of motor information that leads to poor motor skills.
Sensory processing disorder or sensory discrimination disorder,
which is characterized by postural control problems, lack of
attentiveness, and disorganization.
There are several therapies used to treat SPD. Anna Jean Ayres
claimed that a child needs a healthy "sensory diet," which is all of
the activities that children engage in, that gives them the necessary
sensory inputs that they need to get their brain into improving sensory
processing.
History
In the 1930s, Wilder Penfield was conducting a very bizarre operation at the Montreal Neurological Institute. Penfield "pioneered the incorporation of neurophysiological principles in the practice of neurosurgery. Penfield was interested in determining a solution to solve the epileptic seizure
problems that his patients were having. He used an electrode to
stimulate different regions of the brain's cortex, and would ask his
still conscious patient what he or she felt. This process led to the
publication of his book, The Cerebral Cortex of Man. The "mapping" of
the sensations his patients felt led Penfield to chart out the
sensations that were triggered by stimulating different cortical
regions.
Mrs. H. P. Cantlie was the artist Penfield hired to illustrate his
findings. The result was the conception of the first sensory Homunculus.
The Homonculus
is a visual representation of the intensity of sensations derived from
different parts of the body. Wilder Penfield and his colleague Herbert Jasper developed the Montreal procedure
using an electrode to stimulate different parts of the brain to
determine which parts were the cause of the epilepsy. This part could
then be surgically removed or altered in order to regain optimal brain
performance. While performing these tests, they discovered that the functional maps
of the sensory and motor cortices were similar in all patients.
Because of their novelty at the time, these Homonculi were hailed as the
"E=mc² of Neuroscience".
Current research
There
are still no definitive answers to the questions regarding the
relationship between functional and structural asymmetries in the brain. There are a number of asymmetries in the human brain including how language is processed mainly in the left hemisphere of the brain.
There have been some cases, however, in which individuals have
comparable language skills to someone who uses his left hemisphere to
process language, yet they mainly use their right or both hemispheres.
These cases pose the possibility that function may not follow structure
in some cognitive tasks.
Current research in the fields of sensory processing and multisensory
integration is aiming to hopefully unlock the mysteries behind the
concept of brain lateralization.
Research on sensory processing has much to offer towards
understanding the function of the brain as a whole. The primary task of
multisensory integration is to figure out and sort out the vast
quantities of sensory information in the body through multiple sensory
modalities. These modalities not only are not independent, but they are
also quite complementary. Where one sensory modality may give
information on one part of a situation, another modality can pick up
other necessary information. Bringing this information together
facilitates the better understanding of the physical world around us.
It may seem redundant that we are being provided with multiple sensory inputs
about the same object, but that is not necessarily the case. This
so-called "redundant" information is in fact verification that what we
are experiencing is in fact happening. Perceptions
of the world are based on models that we build of the world. Sensory
information informs these models, but this information can also confuse
the models. Sensory illusions
occur when these models do not match up. For example, where our visual
system may fool us in one case, our auditory system can bring us back
to a ground reality. This prevents sensory misrepresentations, because
through the combination of multiple sensory modalities, the model that
we create is much more robust and gives a better assessment of the
situation. Thinking about it logically, it is far easier to fool one
sense than it is to simultaneously fool two or more senses.
Examples
One of the earliest sensations is the olfactory sensation. Evolutionary, gustation and olfaction
developed together. This multisensory integration was necessary for
early humans in order to ensure that they were receiving proper
nutrition from their food, and also to make sure that they were not
consuming poisonous materials.
There are several other sensory integrations that developed early on
in the human evolutionary time line. The integration between vision and
audition was necessary for spatial mapping. Integration between vision
and tactile sensations developed along with our finer motor skills
including better hand-eye coordination. While humans developed into bipedal organisms, balance became exponentially more essential to survival. The multisensory integration between visual inputs, vestibular (balance) inputs, and proprioception inputs played an important role in our development into upright walkers.
Audiovisual system
Perhaps one of the most studied sensory integrations is the relationship between vision and audition.
These two senses perceive the same objects in the world in different
ways, and by combining the two, they help us understand this information
better.
Vision dominates our perception of the world around us. This is
because visual spatial information is one of the most reliable sensory
modalities. Visual stimuli are recorded directly onto the retina, and
there are few, if any, external distortions that provide incorrect
information to the brain about the true location of an object.
Other spatial information is not as reliable as visual spatial
information. For example, consider auditory spatial input. The
location of an object can sometimes be determined solely on its sound,
but the sensory input can easily be modified or altered, thus giving a
less reliable spatial representation of the object.
Auditory information therefore is not spatially represented unlike
visual stimuli. But once one has the spatial mapping from the visual
information, multisensory integration helps bring the information from
both the visual and auditory stimuli together to make a more robust
mapping.
There have been studies done that show that a dynamic neural
mechanism exists for matching the auditory and visual inputs from an
event that stimulates multiple senses.
One example of this that has been observed is how the brain compensates
for target distance. When you are speaking with someone or watching
something happen, auditory and visual signals are not being processed
concurrently, but they are perceived as being simultaneous. This kind of multisensory integration can lead to slight misperceptions in the visual-auditory system in the form of the ventriloquism effect.
An example of the ventriloquism effect is when a person on the
television appears to have his voice coming from his mouth, rather than
the television's speakers. This occurs because of a pre-existing
spatial representation within the brain which is programmed to think
that voices come from another human's mouth. This then makes it so the
visual response to the audio input is spatially misrepresented, and
therefore misaligned.
Sensorimotor system
Hand
eye coordination is one example of sensory integration. In this case,
we require a tight integration of what we visually perceive about an
object, and what we tactilely perceive about that same object. If these
two senses were not combined within the brain, then one would have less
ability to manipulate an object. Eye–hand coordination
is the tactile sensation in the context of the visual system. The
visual system is very static, in that it does not move around much, but
the hands and other parts used in tactile sensory collection can freely
move around. This movement of the hands must be included in the mapping
of both the tactile and visual sensations, otherwise one would not be
able to comprehend where they were moving their hands, and what they
were touching and looking at. An example of this happening is looking
at an infant. The infant picks up objects and puts them in his mouth,
or touches them to his feet or face. All of these actions are
culminating to the formation of spatial maps in the brain and the
realization that "Hey, that thing that's moving this object is actually a
part of me." Seeing the same thing that they are feeling is a major
step in the mapping that is required for infants to begin to realize
that they can move their arms and interact with an object. This is the
earliest and most explicit way of experiencing sensory integration.
Further research
In
the future, research on sensory integration will be used to better
understand how different sensory modalities are incorporated within the
brain to help us perform even the simplest of tasks. For example, we do
not currently have the understanding needed to comprehend how neural
circuits transform sensory cues into changes in motor activities. More
research done on the sensorimotor system can help understand how these movements are controlled. This understanding can potentially be used to learn more about how to make better prosthetics,
and eventually help patients who have lost the use of a limb. Also, by
learning more about how different sensory inputs can combine can have
profound effects on new engineering approaches using robotics.
The robot's sensory devices may take in inputs of different
modalities, but if we understand multisensory integration better, we
might be able to program these robots to convey these data into a useful
output to better serve our purposes.
Heart rate (or pulse rate) is the frequency of the heartbeat measured by the number of contractions of the heart per minute (beats per minute, or 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 numerous 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. 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. Tachycardia is a high heart rate, defined as above 100 bpm at rest. 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 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.
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.
As water and blood are incompressible fluids, one of the
physiological ways to deliver more blood to an organ is to increase
heart rate. Normal resting heart rates range from 60 to 100 bpm. 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. Tachycardia
is defined as a resting heart rate above 100 bpm, though persistent
rest rates between 80 and 100 bpm, mainly if they are present during
sleep, may be signs of hyperthyroidism or anemia (see below).
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, some of which are those that are
'forced'/'enticed' out by the ingestion and processing of drugs such as cocaine or atropine.
This section discusses target heart rates for healthy persons,
which would be inappropriately high for most persons with coronary
artery disease.
Influences from the central nervous system
Cardiovascular centres
The heart rate is rhythmically generated by the sinoatrial node. It is also influenced by central factors through sympathetic and parasympathetic nerves. 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.
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.
Norepinephrine binds to the beta–1 receptor. High blood pressure medications are used to block these receptors and so reduce the heart rate.
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.
Parasympathetic stimulation originates from the cardioinhibitory region of the brain
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.
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.
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 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.
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.
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.
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.
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.
Factors influencing heart rate
Table 1: Major factors increasing heart rate and force of contraction
Factor
Effect
Cardioaccelerator nerves
Release of norepinephrine
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
Factor
Effect
Cardioinhibitor nerves (vagus)
Release of acetylcholine
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.
Epinephrine and norepinephrine
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.
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. It also impacts the beta-adrenergic response similar to epinephrine and norepinephrine.
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.
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, whereas nicotine stimulates the activity of the sympathetic neurons that deliver impulses to the heart.
Effects of stress
Both surprise and stress induce physiological response: elevate heart rate substantially.
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.
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. 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.
Factors decreasing heart rate
The heart rate can be slowed by altered sodium and potassium levels, 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, 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.
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. 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.
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 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.
Physiological control over heart rate
Dolphin heart rate graph
A study shows that bottlenose dolphins 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 only lowers the rate to a much smaller extent.
In different circumstances
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 stimulation increases and parasympathetic stimulation decreases the firing rate.
Resting heart rate
Normal pulse rates at rest, in beats per minute (BPM):
newborn (0–1 months old)
infants (1 – 11 months)
children (1 – 2 years old)
children (3 – 4 years)
children (5 – 6 years)
children (7 – 9 years)
children over 10 years & adults, including seniors
well-trained adult athletes
70-190
80–160
80-130
80-120
75–115
70–110
60–100
40–60
The basal or resting heart rate (HRrest) 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 available evidence
indicates that the normal range for resting heart rate is 50-90 beats
per minute.
This resting heart rate is often correlated with mortality. For
example, all-cause mortality is increased by 1.22 (hazard ratio) when
heart rate exceeds 90 beats per minute.
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.
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.
Finally, in one study 98% of cardiologists suggested that as a
desirable target range, 50 to 90 beats per minute is more appropriate
than 60 to 100. The normal resting heart rate is based on the at-rest firing rate of the heart's sinoatrial node, where the faster pacemaker cells driving the self-generated rhythmic firing and responsible for the heart's autorhythmicity are located. For endurance athletes at the elite level, it is not unusual to have a resting heart rate between 33 and 50 bpm.
Maximum heart rate
The maximum heart rate (HRmax) is the age-related highest number of beats per minute of the heart when reaching a point of exhaustionwithout severe problems through exercise stress.
In general it is loosely estimated as 220 minus one's age.
It generally decreases with age. Since HRmax varies by individual, the most accurate way of measuring any single person's HRmax 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]
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 tachyarrhythmia with ventricular rate of 480 beats per minute, which is comparable to the heart rate of a mouse.
For general purposes, a number of formulas are used to estimate HRmax.
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.)
Men: 208.609-0.716 × age Women: 209.273-0.804 × age
SD = 10.81 (male), 12.15 (female)
Haskell & Fox (1970)
Fox and Haskell formula; widely used.
Notwithstanding later research, the most widely cited formula for HRmax is still:
HRmax = 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.
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. It gained widespread use through being used by Polar Electro in its heart rate monitors, which Dr. Haskell has "laughed about", as the formula "was never supposed to be an absolute guide to rule people's training."
While this formula is the most common (and easy to remember and
calculate), research has consistently found that it is subject to bias.
Compared to the age-specific average HRmax, the Haskell and Fox formula overestimates HRmax in young adults, agrees with it at age 40, and underestimates HRmax in older adults. For example, in one study, the average HRmax at age 76 was about 10bpm higher than the Haskell and Fox equation. Consequently, the formula cannot be recommended for use in exercise physiology and related fields.
Yet, it is common practice to use 85% of the predicted HRmax
(Haskell & Fox) to evaluate chronotropic response to exercise. An
ongoing study has found that the 5th percentile of the study cohort
maximal heart rate correlates much better with the 85% of predicted HRmax
(Haskell & Fox) than the 5th percentile of the study cohort heart
rate reserve to the 80% of the predicted heart rate reserve.
Other formulas
The various formulae provide slightly different numbers for the maximum heart rates by age.
HRmax is strongly correlated to age, and most formulas are solely based on this.
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. The inclusion of physical activity status, maximal oxygen uptake, smoking, body mass index, body weight, or resting heart rate did not significantly improve accuracy. Nonlinear models are slightly more accurate predictors of average age-specific HRmax,
particularly above 60 years of age, but are harder to apply, and
provide statistically negligible improvement over linear models.
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. In addition, most formulas are developed for adults and are not applicable to children and adolescents.
Limitations
Maximum heart rates vary significantly between individuals. Age explains only about half of HRmax variance. For a given age, the standard deviation of HRmax from the age-specific population mean is about 12bpm, and a 95% interval for the prediction error is about 24bpm.
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. Such a variation would equate to an age range of -16 to 68 using the Wingate formula.
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 HRmax
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 HRmax are not accurate enough. Froelicher and Myers describe maximum heart formulas as "largely useless". Measurement via a maximal test is preferable whenever possible, which can be as accurate as ±2bpm.
Heart rate reserve
Heart rate reserve (HRreserve)
is the difference between a person's measured or predicted maximum
heart rate and resting heart rate. Some methods of measurement of
exercise intensity measure percentage of heart rate reserve.
Additionally, as a person increases their cardiovascular fitness, their
HRrest will drop, and the heart rate reserve will increase. Percentage of HRreserve is statistically indistinguishable from percentage of VO2 reserve.
HRreserve = HRmax − HRrest
This is often used to gauge exercise intensity (first used in 1957 by Karvonen).
Karvonen's study findings have been questioned, due to the following:
The study did not use VO2 data to develop the equation.
Only six subjects were used.
Karvonen incorrectly reported that the percentages of HRreserve and VO2 max correspond to each other, but newer evidence shows that it correlated much better with VO2 reserve as described above.
Target heart rate
For healthy people, the Target Heart Rate (THR) or Training Heart Rate Range (THRR) is a desired range of heart rate reached during aerobic exercise which enables one's heart and lungs
to receive the most benefit from a workout. This theoretical range
varies based mostly on age; however, a person's physical condition, sex,
and previous training also are used in the calculation.
By percent, Fox–Haskell-based
The THR can be calculated as a range of 65–85% intensity, with intensity defined simply as percentage of HRmax. However, it is crucial to derive an accurate HRmax to ensure these calculations are meaningful.
Example for someone with a HRmax of 180 (age 40, estimating HRmax As 220 − age):
The Karvonen method factors in resting heart rate (HRrest) to calculate target heart rate (THR), using a range of 50–85% intensity:
THR = ((HRmax − HRrest) × % intensity) + HRrest
Equivalently,
THR = (HRreserve × % intensity) + HRrest
Example for someone with a HRmax of 180 and a HRrest of 70 (and therefore a HRreserve 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. The Zoladz test zones are derived by subtracting values from HRmax:
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.
A greater reduction in heart rate after exercise during the reference
period is associated with a higher level of cardiac fitness.
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.
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.
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. A study reported that a HRR of ≤22 bpm after two minutes "best identified high-risk patients". They also found that while HRR had significant prognostic value it had no diagnostic value.
At 21 days after conception, the human heart begins beating at 70 to 80 beats per minute and accelerates linearly for the first month of beating.Fetal heart rate monitoring. 30 weeks pregnancy.
The human heart beats more than 2.8 billion times in an average lifetime.
The 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 myocytes 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.
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.
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 mm in crown-rump length or 9.2
LMP weeks is:
Clinical significance
Manual measurement
Wrist heart rate monitor (2009)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'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.
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 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.
Possible points for measuring the heart rate are:
The ventral aspect of the wrist on the side of the thumb (radial artery).
In obstetrics, heart rate can be measured by ultrasonography, such as in this embryo (at bottom left in the 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:
HR = 1000*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 monitors are also available. Some monitors, used during sport, consist of a chest strap with electrodes. The signal is transmitted to a wrist receiver for display.
Pulsatile retinal blood flow in the optic nerve head region revealed by laser Doppler imaging
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 pulses.
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:
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.
Trained athletes
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,
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.
Arrhythmias are abnormalities of the heart rate and rhythm (sometimes felt as palpitations).
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.
Correlation with cardiovascular mortality risk
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. 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.
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.
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. A faster resting heart rate is associated with shorter life expectancy and is considered a strong risk factor for heart disease and heart failure, independent of level of physical fitness.
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.
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.
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.
Given these data, heart rate should be considered in the
assessment of cardiovascular risk, even in apparently healthy
individuals. Heart rate has many advantages as a clinical parameter: It is inexpensive and quick to measure and is easily understandable.
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.
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. Exercise is one possible measure to take when an individual's heart rate is higher than 80 beats per minute.
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.
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. 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.
A very slow heart rate (bradycardia) may be associated with heart block. It may also arise from autonomous nervous system impairment.
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