As seen from the orbiting Earth, the Sunappears to move with respect to the fixed stars, and the ecliptic is the yearly path the Sun follows on the celestial sphere. This process repeats itself in a cycle lasting a little over 365 days.
The ecliptic is the apparent path of the Sun throughout the course of a year.
Because Earth takes one year to orbit the Sun, the apparent
position of the Sun takes one year to make a complete circuit of the
ecliptic. With slightly more than 365 days in one year, the Sun moves a
little less than 1° eastward
every day. This small difference in the Sun's position against the
stars causes any particular spot on Earth's surface to catch up with
(and stand directly north or south of) the Sun about four minutes later
each day than it would if Earth did not orbit; a day on Earth is
therefore 24 hours long rather than the approximately 23-hour 56-minute sidereal day.
Again, this is a simplification, based on a hypothetical Earth that
orbits at uniform speed around the Sun. The actual speed with which
Earth orbits the Sun varies slightly during the year, so the speed with
which the Sun seems to move along the ecliptic also varies. For example,
the Sun is north of the celestial equator for about 185 days of each
year, and south of it for about 180 days. The variation of orbital speed accounts for part of the equation of time.
Because of the movement of Earth around the Earth–Moon center of mass, the apparent path of the Sun wobbles slightly, with a period of about one month. Because of further perturbations by the other planets of the Solar System, the Earth–Moon barycenter wobbles slightly around a mean position in a complex fashion.
The plane of Earth's orbit projected in all directions forms the reference plane known as the ecliptic. Here, it is shown projected outward (gray) to the celestial sphere, along with Earth's equator and polar axis (green). The plane of the ecliptic intersects the celestial sphere along a great circle
(black), the same circle on which the Sun seems to move as Earth orbits
it. The intersections of the ecliptic and the equator on the celestial
sphere are the vernal and autumnal equinoxes (red), where the Sun seems to cross the celestial equator.
The orientation of Earth's axis and equator are not fixed in space, but rotate about the poles of the ecliptic with a period of about 26,000 years, a process known as lunisolar precession, as it is due mostly to the gravitational effect of the Moon and Sun on Earth's equatorial bulge.
Likewise, the ecliptic itself is not fixed. The gravitational
perturbations of the other bodies of the Solar System cause a much
smaller motion of the plane of Earth's orbit, and hence of the ecliptic,
known as planetary precession. The combined action of these two motions is called general precession, and changes the position of the equinoxes by about 50 arc seconds (about 0.014°) per year.
Once again, this is a simplification. Periodic motions of the Moon and apparent periodic motions of the Sun
(actually of Earth in its orbit) cause short-term small-amplitude
periodic oscillations of Earth's axis, and hence the celestial equator,
known as nutation.
This adds a periodic component to the position of the equinoxes; the
positions of the celestial equator and (vernal) equinox with fully
updated precession and nutation are called the true equator and equinox; the positions without nutation are the mean equator and equinox.
Obliquity of the ecliptic is the term used by astronomers for
the inclination of Earth's equator with respect to the ecliptic, or of
Earth's rotation axis to a perpendicular to the ecliptic. It is about
23.4° and is currently decreasing 0.013 degrees (47 arcseconds) per
hundred years because of planetary perturbations.
The angular value of the obliquity is found by observation of the
motions of Earth and other planets over many years. Astronomers produce
new fundamental ephemerides as the accuracy of observation improves and as the understanding of the dynamics increases, and from these ephemerides various astronomical values, including the obliquity, are derived.
Obliquity of the ecliptic for 20,000 years, from Laskar (1986). Note that the obliquity varies only from 24.2° to 22.5° during this time. The red point represents the year 2000.
Until 1983 the obliquity for any date was calculated from work of Newcomb, who analyzed positions of the planets until about 1895:
ε = 23°27′08.26″ − 46.845″ T − 0.0059″ T2 + 0.00181″ T3
From 1984, the Jet Propulsion Laboratory's DE series of computer-generated ephemerides took over as the fundamental ephemeris of the Astronomical Almanac. Obliquity based on DE200, which analyzed observations from 1911 to 1979, was calculated:
ε = 23°26′21.45″ − 46.815″ T − 0.0006″ T2 + 0.00181″ T3
JPL's fundamental ephemerides have been continually updated. The Astronomical Almanac for 2010 specifies:
ε = 23°26′21.406″ − 46.836769″ T − 0.0001831″ T2 + 0.00200340″ T3 − 0.576×10−6″ T4 − 4.34×10−8″ T5
These expressions for the obliquity are intended for high
precision over a relatively short time span, perhaps several centuries. J. Laskar computed an expression to order T10 good to 0.04″/1000 years over 10,000 years.
All of these expressions are for the mean obliquity, that is, without the nutation of the equator included. The true or instantaneous obliquity includes the nutation.
Top and side views of the plane of the ecliptic, showing planets Mercury, Venus, Earth, and Mars. Most of the planets orbit the Sun very nearly in the same plane in which Earth orbits, the ecliptic.
Five planets (Earth included) lined up along the
ecliptic in July 2010, illustrating how the planets orbit the Sun in
nearly the same plane. Photo taken at sunset, looking west over
Surakarta, Java, Indonesia.
Most of the major bodies of the Solar System orbit the Sun in nearly
the same plane. This is likely due to the way in which the Solar System
formed from a protoplanetary disk. Probably the closest current representation of the disk is known as the invariable plane of the Solar System.
Earth's orbit, and hence, the ecliptic, is inclined a little more than
1° to the invariable plane, Jupiter's orbit is within a little more than
½° of it, and the other major planets are all within about 6°. Because
of this, most Solar System bodies appear very close to the ecliptic in
the sky.
The invariable plane is defined by the angular momentum of the entire Solar System, essentially the vector sum of all of the orbital and rotational angular momenta of all the bodies of the system; more than 60% of the total comes from the orbit of Jupiter.
That sum requires precise knowledge of every object in the system,
making it a somewhat uncertain value. Because of the uncertainty
regarding the exact location of the invariable plane, and because the
ecliptic is well defined by the apparent motion of the Sun, the ecliptic
is used as the reference plane of the Solar System both for precision
and convenience. The only drawback of using the ecliptic instead of the
invariable plane is that over geologic time scales, it will move against
fixed reference points in the sky's distant background.
The ecliptic forms one of the two fundamental planes used as reference for positions on the celestial sphere, the other being the celestial equator. Perpendicular to the ecliptic are the ecliptic poles,
the north ecliptic pole being the pole north of the equator. Of the two
fundamental planes, the ecliptic is closer to unmoving against the
background stars, its motion due to planetary precession being roughly 1/100 that of the celestial equator.
Spherical coordinates,
known as ecliptic longitude and latitude or celestial longitude and
latitude, are used to specify positions of bodies on the celestial
sphere with respect to the ecliptic. Longitude is measured positively
eastward
0° to 360° along the ecliptic from the vernal equinox, the same
direction in which the Sun appears to move. Latitude is measured
perpendicular to the ecliptic, to +90° northward or −90° southward to
the poles of the ecliptic, the ecliptic itself being 0° latitude. For a
complete spherical position, a distance parameter is also necessary.
Different distance units are used for different objects. Within the
Solar System, astronomical units are used, and for objects near Earth, Earth radii or kilometers are used. A corresponding right-handed rectangular coordinate system is also used occasionally; the x-axis is directed toward the vernal equinox, the y-axis 90° to the east, and the z-axis
toward the north ecliptic pole; the astronomical unit is the unit of
measure. Symbols for ecliptic coordinates are somewhat standardized; see
the table.
Ecliptic coordinates are convenient for specifying positions of Solar System objects, as most of the planets' orbits have small inclinations
to the ecliptic, and therefore always appear relatively close to it on
the sky. Because Earth's orbit, and hence the ecliptic, moves very
little, it is a relatively fixed reference with respect to the stars.
Inclination of the ecliptic over 200,000 years, from Dziobek (1892).
This is the inclination to the ecliptic of 101,800 CE. Note that the
ecliptic rotates by only about 7° during this time, whereas the celestial equator
makes several complete cycles around the ecliptic. The ecliptic is a
relatively stable reference compared to the celestial equator.
Because of the precessional motion of the equinox,
the ecliptic coordinates of objects on the celestial sphere are
continuously changing. Specifying a position in ecliptic coordinates
requires specifying a particular equinox, that is, the equinox of a
particular date, known as an epoch; the coordinates are referred to the direction of the equinox at that date. For instance, the Astronomical Almanac lists the heliocentric position of Mars at 0h Terrestrial Time,
4 January 2010 as: longitude 118°09′15.8″, latitude +1°43′16.7″, true
heliocentric distance 1.6302454 AU, mean equinox and ecliptic of date.
This specifies the mean equinox of 4 January 2010 0h TT as above, without the addition of nutation.
As the Earth revolves around the Sun, approximate axial parallelism of the Moon's orbital plane (tilted five degrees to the ecliptic) results in the revolution of the lunar nodes relative to the Earth. This causes an eclipse season approximately every six months, in which a solar eclipse can occur at the new moon phase and a lunar eclipse can occur at the full moon phase.
Because the orbit of the Moon is inclined only about 5.145° to the ecliptic and the Sun is always very near the ecliptic, eclipses always occur on or near it. Because of the inclination of the Moon's orbit, eclipses do not occur at every conjunction and opposition of the Sun and Moon, but only when the Moon is near an ascending or descending node at the same time it is at conjunction (new) or opposition (full). The ecliptic is so named because the ancients noted that eclipses only occur when the Moon is crossing it.
Equirectangular
plot of declination vs right ascension of the modern constellations
with a dotted line denoting the ecliptic. Constellations are
colour-coded by family and year established.
The ecliptic currently passes through the following constellations:
The ecliptic forms the center of the zodiac, a celestial belt about 20° wide in latitude through which the Sun, Moon, and planets always appear to move.
Traditionally, this region is divided into 12 signs of 30° longitude, each of which approximates the Sun's motion in one month. In ancient times, the signs corresponded roughly to 12 of the constellations that straddle the ecliptic.
These signs are sometimes still used in modern terminology. The "First Point of Aries" was named when the March equinox Sun was actually in the constellation Aries; it has since moved into Pisces because of precession of the equinoxes.
The neurobiological effects of physical exercise are numerous and involve a wide range of interrelated effects on brain structure, brain function, and cognition. A large body of research in humans has demonstrated that consistent aerobic exercise (e.g., 30 minutes every day) induces persistent improvements in certain cognitive functions, healthy alterations in gene expression in the brain, and beneficial forms of neuroplasticity and behavioral plasticity; some of these long-term effects include: increased neuron growth, increased neurological activity (e.g., c-Fos and BDNF signaling), improved stress coping, enhanced cognitive control of behavior, improved declarative, spatial, and working memory, and structural and functional improvements in brain structures and pathways associated with cognitive control and memory. The effects of exercise on cognition have important implications for improving academic performance in children and college students, improving adult productivity, preserving cognitive function in old age, preventing or treating certain neurological disorders, and improving overall quality of life.
In healthy adults, aerobic exercise has been shown to induce
transient effects on cognition after a single exercise session and
persistent effects on cognition following regular exercise over the
course of several months.People who regularly perform an aerobic exercise (e.g., running, jogging, brisk walking, swimming, and cycling) have greater scores on neuropsychological function and performance tests that measure certain cognitive functions, such as attentional control, inhibitory control, cognitive flexibility, working memory updating and capacity, declarative memory, spatial memory, and information processing speed. The transient effects of exercise on cognition include improvements in most executive functions
(e.g., attention, working memory, cognitive flexibility, inhibitory
control, problem solving, and decision making) and information
processing speed for a period of up to 2 hours after exercising.
Aerobic exercise induces short- and long-term effects on mood and emotional states by promoting positive affect, inhibiting negative affect, and decreasing the biological response to acute psychological stress. Over the short-term, aerobic exercise functions as both an antidepressant and euphoriant,whereas consistent exercise produces general improvements in mood and self-esteem.
Neuroplasticity is the process by which neurons adapt to a disturbance over time, and most often occurs in response to repeated exposure to stimuli. Aerobic exercise increases the production of neurotrophic factors (e.g., BDNF, IGF-1, VEGF) which mediate improvements in cognitive functions and various forms of memory by promoting blood vessel formation in the brain, adult neurogenesis, and other forms of neuroplasticity. Consistent aerobic exercise over a period of several months induces clinically significant improvements in executive functions and increased gray matter volume in nearly all regions of the brain, with the most marked increases occurring in brain regions that give rise to executive functions. The brain structures that show the greatest improvements in gray matter volume in response to aerobic exercise are the prefrontal cortex, caudate nucleus, and hippocampus; less significant increases in gray matter volume occur in the anterior cingulate cortex, parietal cortex, cerebellum, and nucleus accumbens. The prefrontal cortex, caudate nucleus, and anterior cingulate cortex are among the most significant brain structures in the dopamine and norepinephrine systems that give rise to cognitive control.
Exercise-induced neurogenesis (i.e., the increases in gray matter
volume) in the hippocampus is associated with measurable improvements in
spatial memory. Higher physical fitness scores, as measured by VO2 max, are associated with better executive function, faster information processing speed, and greater gray matter volume of the hippocampus, caudate nucleus, and nucleus accumbens. Long-term aerobic exercise is also associated with persistent beneficial epigenetic changes that result in improved stress coping, improved cognitive function, and increased neuronal activity (c-Fos and BDNF signaling).
Structural growth
Reviews of neuroimaging studies indicate that consistent aerobic exercise increases gray matter volume in nearly all regions of the brain, with more pronounced increases occurring in brain regions associated with memory processing, cognitive control, motor function, and reward;
the most prominent gains in gray matter volume are seen in the
prefrontal cortex, caudate nucleus, and hippocampus, which support
cognitive control and memory processing, among other cognitive
functions. Moreover, the left and right halves of the prefrontal cortex, the hippocampus, and the cingulate cortex appear to become more functionally interconnected in response to consistent aerobic exercise.
Three reviews indicate that marked improvements in prefrontal and
hippocampal gray matter volume occur in healthy adults that regularly
engage in medium intensity exercise for several months.
Other regions of the brain that demonstrate moderate or less
significant gains in gray matter volume during neuroimaging include the anterior cingulate cortex, parietal cortex, cerebellum, and nucleus accumbens.
Regular exercise has been shown to counter the shrinking of the
hippocampus and memory impairment that naturally occurs in late
adulthood. Sedentary adults over age 55 show a 1–2% decline in hippocampal volume annually.
A neuroimaging study with a sample of 120 adults revealed that
participating in regular aerobic exercise increased the volume of the
left hippocampus by 2.12% and the right hippocampus by 1.97% over a
one-year period.
Subjects in the low intensity stretching group who had higher fitness
levels at baseline showed less hippocampal volume loss, providing
evidence for exercise being protective against age-related cognitive
decline. In general, individuals that exercise more over a given period have greater hippocampal volumes and better memory function. Aerobic exercise has also been shown to induce growth in the white matter tracts in the anterior corpus callosum, which normally shrink with age.
The various functions of the brain structures that show exercise-induced increases in gray matter volume include:
Concordant with the functional roles of the brain structures that
exhibit increased gray matter volumes, regular exercise over a period of
several months has been shown to persistently improve numerous
executive functions and several forms of memory. In particular, consistent aerobic exercise has been shown to improve attentional control, information processing speed, cognitive flexibility (e.g., task switching), inhibitory control, working memory updating and capacity, declarative memory, and spatial memory.In healthy young and middle-aged adults, the effect sizes
of improvements in cognitive function are largest for indices of
executive functions and small to moderate for aspects of memory and
information processing speed.
It may be that in older adults, individuals benefit cognitively by
taking part in both aerobic and resistance type exercise of at least
moderate intensity.
Individuals who have a sedentary lifestyle tend to have impaired
executive functions relative to other more physically active
non-exercisers.
A reciprocal relationship between exercise and executive functions has
also been noted: improvements in executive control processes, such as
attentional control and inhibitory control, increase an individual's
tendency to exercise.
One of the most significant effects of exercise on the brain is increased synthesis and expression of BDNF, a neuropeptide and hormone, resulting in increased signaling through its receptor tyrosine kinase, tropomyosin receptor kinase B (TrkB). Since BDNF is capable of crossing the blood–brain barrier, higher peripheral BDNF synthesis also increases BDNF signaling in the brain. Exercise-induced increases in BDNF signaling are associated with beneficial epigenetic changes, improved cognitive function, improved mood, and improved memory.
Furthermore, research has provided a great deal of support for the role
of BDNF in hippocampal neurogenesis, synaptic plasticity, and neural
repair.Engaging in moderate-high intensity aerobic exercise such as running, swimming, and cycling increases BDNF biosynthesis through myokine signaling, resulting in up to a threefold increase in blood plasma and BDNF levels; exercise intensity is positively correlated with the magnitude of increased BDNF biosynthesis and expression.
A meta-analysis of studies involving the effect of exercise on BDNF
levels found that consistent exercise modestly increases resting BDNF
levels as well.
This has important implications for exercise as a mechanism to reduce
stress since stress is closely linked with decreased levels of BDNF in
the hippocampus. In fact, studies suggest that BDNF contributes to the
anxiety-reducing effects of antidepressants. The increase in BDNF levels
caused by exercise helps reverse the stress-induced decrease in BDNF
which mediates stress in the short term and buffers against
stress-related diseases in the long term.
IGF-1 is a peptide and neurotrophic factor that mediates some of the effects of growth hormone; IGF-1 elicits its physiological effects by binding to a specific receptor tyrosine kinase, the IGF-1 receptor, to control tissue growth and remodeling. In the brain, IGF-1 functions as a neurotrophic factor that, like BDNF, plays a significant role in cognition, neurogenesis, and neuronal survival. Physical activity is associated with increased levels of IGF-1 in blood serum, which is known to contribute to neuroplasticity in the brain due to its capacity to cross the blood–brain barrier and blood–cerebrospinal fluid barrier;
consequently, one review noted that IGF-1 is a key mediator of
exercise-induced adult neurogenesis, while a second review characterized
it as a factor which links "body fitness" with "brain fitness". The amount of IGF-1 released into blood plasma during exercise is positively correlated with exercise intensity and duration.
VEGF is a neurotrophic and angiogenic (i.e., blood vessel growth-promoting) signaling protein that binds to two receptor tyrosine kinases, VEGFR1 and VEGFR2, which are expressed in neurons and glial cells in the brain. Hypoxia,
or inadequate cellular oxygen supply, strongly upregulates VEGF
expression and VEGF exerts a neuroprotective effect in hypoxic neurons. Like BDNF and IGF-1,
aerobic exercise has been shown to increase VEGF biosynthesis in
peripheral tissue which subsequently crosses the blood–brain barrier and
promotes neurogenesis and blood vessel formation in the central nervous system.
Exercise-induced increases in VEGF signaling have been shown to improve
cerebral blood volume and contribute to exercise-induced neurogenesis
in the hippocampus.
GPLD1
In July 2020 scientists reported that after mice exercise their livers secrete the protein GPLD1,
which is also elevated in elderly humans who exercise regularly, that
this is associated with improved cognitive function in aged mice and
that increasing the amount of GPLD1 produced by the mouse liver in old
mice via genetic engineering
could yield many benefits of regular exercise for their brains – such
as increased BDNF-levels, neurogenesis, and improved cognitive
functioning in tests.
A study using FNDC5 knock-out mice as well as artificial elevation of circulating irisin
levels showed that irisin confers beneficial cognitive effects of
physical exercise and that it can serve an exercise mimetic in mice in
which it could "improve both the cognitive deficit and neuropathology in
Alzheimer's disease
mouse models". The mediator and its regulatory system is therefore
being investigated for potential interventions to improve – or further
improve – cognitive function or alleviate Alzheimer's disease in humans.Experiments indicate irisin may be linked to regulation of BDNF and neurogenesis in mice.
In addition to the persistent effects on cognition that result from
several months of daily exercise, acute exercise (i.e., a single bout of
exercise) has been shown to transiently improve a number of cognitive
functions.
Reviews and meta-analyses of research on the effects of acute exercise
on cognition in healthy young and middle-aged adults have concluded that
information processing speed and a number of executive functions –
including attention, working memory, problem solving, cognitive
flexibility, verbal fluency, decision making, and inhibitory control –
all improve for a period of up to 2 hours post-exercise.
A systematic review of studies conducted on children also suggested
that some of the exercise-induced improvements in executive function are
apparent after single bouts of exercise, while other aspects (e.g.,
attentional control) only improve following consistent exercise on a
regular basis.
Other research has suggested immediate performative enhancements during
exercise, such as exercise-concurrent improvements in processing speed
during visual working memory tasks.
β-Phenylethylamine, commonly referred to as phenethylamine, is a human trace amine and potent catecholaminergic and glutamatergicneuromodulator that has similar psychostimulant and euphoriant effects and a similar chemical structure to amphetamine. Thirty minutes of moderate to high intensity physical exercise has been shown to induce an enormous increase in urinary β-phenylacetic acid, the primary metabolite of phenethylamine. Two reviews noted a study where the average 24 hour urinary β-phenylacetic acid
concentration among participants following just 30 minutes of intense
exercise increased by 77% relative to baseline concentrations in resting
control subjects;
the reviews suggest that phenethylamine synthesis sharply increases
while an individual is exercising, during which time it is rapidly
metabolized due to its short half-life of roughly 30 seconds. In a resting state, phenethylamine is synthesized in catecholamine neurons from L-phenylalanine by aromatic amino acid decarboxylase (AADC) at approximately the same rate at which dopamine is produced.
In light of this observation, the original paper and both reviews
suggest that phenethylamine plays a prominent role in mediating the
mood-enhancing euphoric effects of a runner's high, as both phenethylamine and amphetamine are potent euphoriants.
β-Endorphin
β-Endorphin (contracted from "endogenous morphine") is an endogenous opioidneuropeptide that binds to μ-opioid receptors, in turn producing euphoria and pain relief. A meta-analytic review found that exercise significantly increases the secretion of β-endorphin and that this secretion is correlated with improved mood states. Moderate intensity exercise produces the greatest increase in β-endorphin synthesis, while higher and lower intensity forms of exercise are associated with smaller increases in β-endorphin synthesis. A review on β-endorphin
and exercise noted that an individual's mood improves for the remainder
of the day following physical exercise and that one's mood is
positively correlated with overall daily physical activity level.
However, data from rodents and humans have shown that pharmacological
blockade of endogenous endorphins does not prevent the development of a
runner's high, while blockade of endocannabinoids does.
Anandamide
Anandamide is an endogenous cannabinoid and retrograde neurotransmitter that binds to cannabinoid receptors (primarily CB1), in turn producing euphoria.
It has been shown that aerobic exercise causes an increase in plasma
anandamide levels, where the magnitude of this increase is highest at
moderate exercise intensity (i.e., exercising at ~70–80% maximum
heart rate). Increases in plasma anandamide levels are associated with psychoactive effects because anandamide is able to cross the blood–brain barrier and act within the central nervous system.
Thus, because anandamide is a euphoriant and aerobic exercise is
associated with euphoric effects, it has been proposed that anandamide
partly mediates the short-term mood-lifting effects of exercise (e.g.,
the euphoria of a runner's high) via exercise-induced increases in its
synthesis.
In mice it was demonstrated that certain features of a runner's
high depend on cannabinoid receptors. Pharmacological or genetic
disruption of cannabinoid signaling via cannabinoid receptors prevents
the analgesic and anxiety-reducing effects of running.
The "stress hormone", cortisol, is a glucocorticoid that binds to glucocorticoid receptors. Psychological stress induces the release of cortisol from the adrenal gland by activating the hypothalamic–pituitary–adrenal axis (HPA axis).
Short-term increases in cortisol levels are associated with adaptive
cognitive improvements, such as enhanced inhibitory control;
however, excessively high exposure or prolonged exposure to high levels
of cortisol causes impairments in cognitive control and has neurotoxic effects in the human brain. For example, chronic psychological stress decreases BDNF expression, which has detrimental effects on hippocampal volume and can lead to depression.
As a physical stressor, aerobic exercise stimulates cortisol secretion in an intensity-dependent manner;
however, it does not result in long-term increases in cortisol
production since this exercise-induced effect on cortisol is a response
to transient negative energy balance. Individuals who have recently exercised exhibit improvements in stress coping behaviors. Aerobic exercise increases physical fitness and lowers neuroendocrine (i.e., HPA axis)
reactivity and therefore reduces the biological response to
psychological stress in humans (e.g., reduced cortisol release and
attenuated heart rate response). Exercise also reverses stress-induced decreases in BDNF expression and signaling in the brain, thereby acting as a buffer against stress-related diseases like depression.
Glutamate and GABA
Glutamate, one of the most common neurochemicals in the brain, is an excitatory neurotransmitter involved in many aspects of brain function, including learning and memory. Based upon animal models, exercise appears to normalize the excessive levels of glutamate neurotransmission into the nucleus accumbens that occurs in drug addiction.
A review of the effects of exercise on neurocardiac function in
preclinical models noted that exercise-induced neuroplasticity of the rostral ventrolateral medulla (RVLM) has an inhibitory effect on glutamatergic neurotransmission in this region, in turn reducing sympathetic activity;
the review hypothesized that this neuroplasticity in the RVLM is a
mechanism by which regular exercise prevents inactivity-related cardiovascular disease.
Exerkines are "signalling moieties released in response to acute and/or chronic exercise, which exert their effects through endocrine, paracrine and/or autocrine
pathways" and are "increasingly recognized as critical mediators of
exercise-related changes and health benefits". They have "a multitude of
purported effects on the nervous system".
A study found that Lac-Phe was the most significantly induced circulating metabolite
in two animal models of exercise, with increases also being observed in
humans, which – including via chronic administration – reduces food
intake or appetite in the obese and suppresses obesity.
Sibley and Etnier (2003) performed a meta-analysis that looked at the
relationship between physical activity and cognitive performance in
children.
They reported a beneficial relationship in the categories of perceptual
skills, intelligence quotient, achievement, verbal tests, mathematic
tests, developmental level/academic readiness and other, with the
exception of memory, that was found to be unrelated to physical
activity. The correlation was strongest for the age ranges of 4–7 and 11–13 years.
On the other hand, Chaddock and colleagues (2011) found results that
contrasted Sibley and Etnier's meta-analysis. In their study, the
hypothesis was that lower-fit children would perform poorly in executive
control of memory and have smaller hippocampal volumes compared to
higher-fit children.
Instead of physical activity being unrelated to memory in children
between 4 and 18 years of age, it may be that preadolescents of higher
fitness have larger hippocampal volumes, than preadolescents of lower
fitness. According to a previous study done by Chaddock and colleagues
(Chaddock et al. 2010), a larger hippocampal volume would result in better executive control of memory. They concluded that hippocampal volume was positively associated with performance on relational memory tasks.
Their findings are the first to indicate that aerobic fitness may
relate to the structure and function of the preadolescent human brain.
In Best's (2010) meta-analysis of the effect of activity on children's
executive function, there are two distinct experimental designs used to
assess aerobic exercise on cognition. The first is chronic exercise, in
which children are randomly assigned to a schedule of aerobic exercise
over several weeks and later assessed at the end. The second is acute exercise, which examines the immediate changes in cognitive functioning after each session.
The results of both suggest that aerobic exercise may briefly aid
children's executive function and also influence more lasting
improvements to executive function.
Other studies have suggested that exercise is unrelated to academic
performance, perhaps due to the parameters used to determine exactly
what academic achievement is.
This area of study has been a focus for education boards that make
decisions on whether physical education should be implemented in the
school curriculum, how much time should be dedicated to physical
education, and its impact on other academic subjects.
Another study found that sixth-graders who participated in
vigorous physical activity at least three times a week had the highest
scores compared to those who participated in moderate or no physical
activity at all. The kids who participated in vigorous physical activity
scored three points higher, on average, on their academic test, which
consisted of math, science, English, and world studies.
Animal studies have also shown that exercise can impact brain
development early on in life. Mice that had access to running wheels and
other such exercise equipment had better neuronal growth in the neural
systems involved in learning and memory. Neuroimaging of the human brain has yielded similar results, where exercise leads to changes in brain structure and function.
Some investigations have linked low levels of aerobic fitness in
children with impaired executive function in older adults, but there is
mounting evidence it may also be associated with a lack of selective
attention, response inhibition, and interference control.
Exercise as prevention and treatment of drug addictions
Clinical and preclinical evidence indicate that consistent aerobic exercise, especially endurance exercise (e.g., marathon running), actually prevents the development of certain drug addictions and is an effective adjunct treatment for drug addiction, and psychostimulant addiction in particular.
Consistent aerobic exercise magnitude-dependently (i.e., by duration
and intensity) reduces drug addiction risk, which appears to occur
through the reversal of drug-induced, addiction-related neuroplasticity.One review noted that exercise may prevent the development of drug addiction by altering ΔFosB or c-Fosimmunoreactivity in the striatum or other parts of the reward system. Moreover, aerobic exercise decreases psychostimulant self-administration, reduces the reinstatement (i.e., relapse) of drug-seeking, and induces opposite effects on striataldopamine receptor D2 (DRD2) signaling (increased DRD2 density) to those induced by pathological stimulant use (decreased DRD2 density). Consequently, consistent aerobic exercise may lead to better treatment
outcomes when used as an adjunct treatment for drug addiction. As of 2016,
more clinical research is still needed to understand the mechanisms and
confirm the efficacy of exercise in drug addiction treatment and
prevention.
Regular physical exercise, particularly aerobic exercise, is an effective add-on treatment for ADHD in children and adults, particularly when combined with stimulant medication (i.e., amphetamine or methylphenidate), although the best intensity and type of aerobic exercise for improving symptoms are not currently known.
In particular, the long-term effects of regular aerobic exercise in
ADHD individuals include better behavior and motor abilities, improved executive functions (including attention, inhibitory control, and planning, among other cognitive domains), faster information processing speed, and better memory.
Parent-teacher ratings of behavioral and socio-emotional outcomes in
response to regular aerobic exercise include: better overall function,
reduced ADHD symptoms, better self-esteem, reduced levels of anxiety and
depression, fewer somatic complaints, better academic and classroom
behavior, and improved social behavior. Exercising while on stimulant medication augments the effect of stimulant medication on executive function. It is believed that these short-term effects of exercise are mediated by an increased abundance of synaptic dopamine and norepinephrine in the brain.
Major depressive disorder
A number of medical reviews have indicated that exercise has a marked and persistent antidepressant effect in humans, an effect believed to be mediated through enhanced BDNF signaling in the brain. Several systematic reviews have analyzed the potential for physical exercise in the treatment of depressive disorders. The 2013 Cochrane Collaboration review on physical exercise
for depression noted that, based upon limited evidence, it is more
effective than a control intervention and comparable to psychological or
antidepressant drug therapies.
Three subsequent 2014 systematic reviews that included the Cochrane
review in their analysis concluded with similar findings: one indicated
that physical exercise is effective as an adjunct treatment (i.e., treatments that are used together) with antidepressant medication;
the other two indicated that physical exercise has marked
antidepressant effects and recommended the inclusion of physical
activity as an adjunct treatment for mild–moderate depression and mental
illness in general. One systematic review noted that yoga may be effective in alleviating symptoms of prenatal depression. Another review asserted that evidence from clinical trials supports the efficacy of physical exercise as a treatment for depression over a 2–4 month period. These benefits have also been noted in old age,
with a review conducted in 2019 finding that exercise is an effective
treatment for clinically diagnosed depression in older adults.
A meta-analysis
from July 2016 concluded that physical exercise improves overall
quality of life in individuals with depression relative to controls.
Cerebrovascular disease
Physical exercise plays a significant role in the prevention and management of stroke. It is well established that physical activity decrease the risk of ischemic stroke and intracerebral haemorrhage.
Engaging in physical activity before experiencing a stroke has been
found to have a positive impact on the severity and outcomes of stroke.
Physical activity can increase the ischemic tolerance of the brain via
several mechanisms. Performing exercise decreases the expression and
activation of inflammatory cytokines, such as tumor necrosis factor alpha (TNFα), interleukins (ILs), and nuclear factor kappa B (NF-κB) following a stroke which mitigate post-stroke inflammation. Exercise has the potential to increase the expression of VEGF, caveolin, and angiopoietin in the brain. These changes may promote angiogenesis and neovascularization that contribute to improved blood supply to the stroke affected areas of the brain. Preconditioning physical activity reduce the post-stroke expression and activation of matrix metalloproteases (MMPs) while increasing the expression of integrin proteins.
These effects help reduce the disruption of the blood-brain barrier,
which normally occurs after a stroke and may lead to improved
preservation of brain tissue. Exercise can enhance the activation of endothelial nitric oxide synthase (eNOS) and subsequent production of nitric oxide (NO).
The increase in NO production may lead to improved post-stroke cerebral
blood flow, ensuring a sufficient oxygen and nutrient supply to the
brain. Physical activity has been associated with increased expression
and activation of hypoxia-inducible factor 1 alpha (HIF-1α), heat shock proteins, and brain-derived neurotrophic factor (BDNF).
These factors play crucial roles in promoting cellular survival,
neuroprotection, and repair processes in the brain following a stroke.
Exercise also inhibit glutamate and caspase activities, which are involved in neuronal death pathways. Additionally, it may promote neurogenesis
in the brain. These effects collectively contribute to the reduction of
brain infarction and edema, leading to potential improvements in
neurological and functional outcomes. The neuroprotective properties of
physical activity in relation to haemorrhagic strokes are less studied.
Pre-stroke physical activity has been associated with improved outcomes
after intracerebral haemorrhages. Furthermore, physical activity may reduce the volume of intracerebral haemorrhages. Being physically active after stroke also enhance the functional recovery.
Mild cognitive impairment
The American Academy of Neurology's January 2018 update of their clinical practice guideline for mild cognitive impairment
states that clinicians should recommend regular exercise (two times per
week) to individuals who have been diagnosed with this condition.
This guidance is based upon a moderate amount of high-quality evidence
which supports the efficacy of regular physical exercise (twice weekly
over a 6-month period) for improving cognitive symptoms in individuals
with mild cognitive impairment.
Neurodegenerative disorders
Alzheimer's disease
Alzheimer's disease is a cortical neurodegenerative disorder and the most prevalent form of dementia,
representing approximately 65% of all cases of dementia; it is
characterized by impaired cognitive function, behavioral abnormalities,
and a reduced capacity to perform basic activities of daily life. Two meta-analytic systematic reviews of randomized controlled trials
with durations of 3–12 months have examined the effects of physical
exercise on the aforementioned characteristics of Alzheimer's disease.
The reviews found beneficial effects of physical exercise on cognitive
function, the rate of cognitive decline, and the ability to perform
activities of daily living in individuals with Alzheimer's disease.
One review suggested that, based upon transgenic mouse models, the
cognitive effects of exercise on Alzheimer's disease may result from a
reduction in the quantity of amyloid plaque.
The Caerphilly Prospective study
followed 2,375 male subjects over 30 years and examined the association
between healthy lifestyles and dementia, among other factors.
Analyses of the Caerphilly study data have found that exercise is
associated with a lower incidence of dementia and a reduction in
cognitive impairment. A subsequent systematic review of longitudinal studies also found higher levels of physical activity to be associated with a reduction in the risk of dementia and cognitive decline; this review further asserted that increased physical activity appears to be causally related with these reduced risks.
Parkinson's disease
Research also suggests that physical exercise is beneficial for those with Parkinson's disease, a neurodegenerative condition characterised by a loss of dopaminergic neurons in an area of the brain known as the substantia nigra.
A growing body of evidence suggests that physical exercise may be
protective against Parkinson's, reducing the risk by around 29%.
These findings are supported by animal studies, which indicate that
physical exercise may protect against the loss of dopaminergic neurons
by increasing the number of neurotrophic factors in the brain, proteins known to protect against degeneration.
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