Neurobiological Effects of Physical Exercise

Neurobiological effects of physical exercise
From Wikipedia, the free encyclopedia
The neurobiological effects of physical exercise are numerous

and involve a wide range of interrelated effects on brain structure, Neurobiological effects of
brain function, and cognition.[1][2][3][4] A large body of research in physical exer cise
humans has demonstrated that consistent aerobic exercise (e.g., Exercise therapy medical intervention
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.[1][2][3][4][5][6][7][8][9][10] 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 A woman engaging in aerobic exercise
or treating certain neurological disorders, and improving overall ICD-9-CM 93.19
quality of life.[1][11][12]
MeSH D005081
In healthy adults, aerobic exercise has been shown to induce LOINC 73986-2
transient effects on cognition after a single exercise session and
eMedicine 324583
persistent effects on cognition following regular exercise over the
course of several months.[1][10][13] People who regularly perform
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.[1][5][7][9][10][13] 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.[13]
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.[13] Over the short-
term, aerobic exercise functions as both an antidepressant and euphoriant,[14][15][16][17] whereas consistent exercise
produces general improvements in mood and self-esteem.[18][19]
Regular aerobic exercise improves symptoms associated with a variety of central nervous system disorders and may
be used as an adjunct therapy for these disorders. There is clear evidence of exercise treatment efficacy for major
depressive disorder and attention deficit hyperactivity disorder.[11][16][20][21][22][23] A large body of preclinical
evidence and emerging clinical evidence supports the use of exercise therapy for treating and preventing the
development of drug addictions.[24][25][26][27][28] Reviews of clinical evidence also support the use of exercise as an
adjunct therapy for certain neurodegenerative disorders, particularly Alzheimers disease and Parkinson's
disease.[29][30][31][32][33][34] Regular exercise is also associated with a lower risk of developing neurodegenerative
disorders.[32][35] Regular exercise has also been proposed as an adjunct therapy for brain cancers.[36]
Contents
1 Long-term effects
1.1 Neuroplasticity
1.1.1 BDNF signaling
1.1.2 IGF-1 signaling
1.1.3 VEGF signaling
1.2 Structural growth
1.3 Long-term effects on cognition
2 Short-term effects
2.1 Short-term effects on cognition
2.2 Psychological stress and cortisol
2.3 Euphoria
2.4 Effects on neurochemicals
2.4.1 -Phenylethylamine
2.4.2 -Endorphin
2.4.3 Anandamide
2.4.4 Monoamine neurotransmitters
2.4.5 Glutamate and GABA
2.4.6 Acetylcholine
3 Effects in children
4 Effects on central nervous system disorders
4.1 Addiction
4.2 Attention deficit hyperactivity disorder
4.3 Major depressive disorder
4.4 Brain cancers
4.5 Neurodegenerative disorders
4.5.1 Alzheimer's disease
4.5.2 Parkinson's disease
5 See also
6 Notes
7 References
Long-term effects
Neuroplasticity
Neuroplasticity is the process by which neurons adapt to a disturbance over time, and most often occurs in response
to repeated exposure to stimuli.[37] Aerobic exercise increases the production of neurotrophic factors[note 1] (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,[note 2] and other forms of
neuroplasticity.[2][5][18][39][40] Consistent aerobic exercise over a period of several months induces clinically
significant improvements in executive functions and increased gray matter volume in multiple brain regions,
particularly those which give rise to executive functions.[1][5][6][7][9] 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;[1][5][6][8] less significant increases in gray matter volume occur in the anterior cingulate cortex, parietal
cortex, cerebellum, and nucleus accumbens.[5][6][8] 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.[6][41] Exercise-induced neurogenesis (i.e., the increases in gray matter volume) in the hippocampus
is associated with measurable improvements in spatial memory.[6][8][19][42] 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.[1][6] 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).[4][43]
BDNF signaling
One of the most significant effects of exercise on the brain is the increased synthesis and expression of BDNF, a
neuropeptide hormone, in the brain and periphery, resulting in increased signaling through its tyrosine kinase
receptor, tropomyosin receptor kinase B (TrkB).[4][44][45] Since BDNF is capable of crossing the bloodbrain barrier,
higher peripheral BDNF synthesis also increases BDNF signaling in the brain.[39] Exercise-induced increases in brain
BDNF signaling are associated with beneficial epigenetic changes, improved cognitive function, improved mood, and
improved memory.[4][8][18][44] Furthermore, research has provided a great deal of support for the role of BDNF in
hippocampal neurogenesis, synaptic plasticity, and neural repair.[5][44] 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 brain BDNF levels;[4][44][45] exercise intensity is positively
correlated with the magnitude of increased BDNF biosynthesis and expression.[4][44][45] A meta-analysis of studies
involving the effect of exercise on BDNF levels found that consistent exercise modestly increases resting BDNF
levels as well.[18]
IGF-1 signaling
IGF-1 is a peptide and neurotrophic factor that mediates some of the effects of growth hormone;[46] IGF-1 elicits its
physiological effects by binding to a specific tyrosine kinase receptor, the IGF-1 receptor, to control tissue growth
and remodeling.[46] In the brain, IGF-1 functions as a neurotrophic factor that, like BDNF, plays a significant role in
cognition, neurogenesis, and neuronal survival.[44][47][48] 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 bloodcerebrospinal fluid barrier;[5][44][46][47] 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".[46][47] The amount of IGF-1 released into blood plasma during exercise is positively
correlated with exercise intensity and duration.[49]
VEGF signaling
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.[48]
Hypoxia, or inadequate cellular oxygen supply, strongly upregulates VEGF expression and VEGF exerts a
neuroprotective effect in hypoxic neurons.[48] Like BDNF and IGF-1, aerobic exercise has been shown to increase
VEGF biosynthesis in peripheral tissue which subsequently crosses the bloodbrain barrier and promotes
neurogenesis and blood vessel formation in the central nervous system.[39][40][50] Exercise-induced increases in
VEGF signaling have been shown to improve cerebral blood volume and contribute to exercise-induced neurogenesis
in the hippocampus.[5][40][50]
Structural growth
Reviews of neuroimaging studies indicate that consistent aerobic exercise increases gray matter volume in brain
regions associated with memory processing, cognitive control, motor function, and reward;[1][5][6][8] 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.[1][6][8][9] 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.[1][7] 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.[1][6][51] 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.[5][6][8][52]
Regular exercise has been shown to counter the shrinking of the hippocampus and memory impairment that naturally
occurs in late adulthood.[5][6][8] Sedentary adults over age 55 show a 12% decline in hippocampal volume
annually.[8][53] 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.[8][53] 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.[53]
In general, individuals that exercise more over a given period have greater hippocampal volumes and better memory
function.[5][8] Aerobic exercise has also been shown to induce growth in the white matter tracts in the anterior corpus
callosum, which normally shrink with age.[5][51]
The various functions of the brain structures that show exercise-induced increases in gray matter volume include:
Prefrontal and anterior cingulate cortices required for the cognitive control of behavior, particularly: working
memory, attentional control, decision-making, cognitive flexibility, social cognition, and inhibitory control of
behavior;[54][55] implicated in attention deficit hyperactivity disorder (ADHD) and addiction[54]
Nucleus accumbens responsible for incentive salience ("wanting" or desire, the form of motivation associated
with reward) and positive reinforcement; implicated in addiction[56]
Hippocampus responsible for storage and consolidation of declarative memory and spatial memory;[6][57]
implicated in depression[8]
Cerebellum responsible for motor coordination and motor learning[58]
Caudate nucleus responsible for stimulus-response learning and inhibitory control; implicated in Parkinson's
disease, Huntington's disease and ADHD[54][57]
Parietal cortex responsible for sensory perception, working memory, and attention[54][59]
Long-term effects on cognition
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.[5][7][9][60][61] In particular, consistent aerobic exercise has been shown to improve
attentional control,[note 3] information processing speed, cognitive flexibility (e.g., task switching), inhibitory
control,[note 4] working memory updating and capacity,[note 5] declarative memory,[note 6] and spatial
memory.[5][6][7][9][10][60][61] 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.[1][10] Individuals who have a sedentary lifestyle tend to have impaired executive functions relative
to other more physically active non-exercisers.[9][60] 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.[9]
Short-term effects
Short-term effects on cognition
In addition to the persistent effects of regular exercise over the course of several months on cognitive functions, acute
exercise (i.e., a single bout of exercise) has been shown to transiently improve a number of cognitive
functions.[13][63][64] Reviews and meta-analyses of research on the effects of acute exercise in healthy young and
middle-aged adults on cognition 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.[13][63][64] 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.[61]
Psychological stress and cortisol

The "stress hormone", cortisol, is a glucocorticoid that binds
to glucocorticoid receptors.[65][66][67] Psychological stress
induces the release of cortisol from the adrenal gland by
activating the hypothalamicpituitaryadrenal axis (HPA
axis).[65][66][67] Short-term increases in cortisol levels are
associated with adaptive cognitive improvements, such as
enhanced inhibitory control;[40][66][67] 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.[40][60][67] For example, chronic
psychological stress decreases BDNF expression which has
detrimental effects on hippocampal volume and can lead to
depression.[40][65]
As a physical stressor, aerobic exercise stimulates cortisol

Diagram of the hypothalamicpituitaryadrenal axis
secretion in an intensity-dependent manner;[66] 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.[note 7][66] Individuals
who have recently exercised exhibit improvements in stress coping behaviors.[4][40][43] 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).[13][40][68] 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.[40][65][68]
Euphoria
Continuous exercise can produce short-term euphoria, an affective state associated with feelings of profound
contentment, elation, and well-being, which is colloquially known as a "runner's high" in distance running or a
"rower's high" in rowing.[14][15][69][70] Current medical reviews indicate that several endogenous euphoriants are
responsible for producing exercise-related euphoria, specifically phenethylamine (a stimulant), -endorphin (an
opioid), and anandamide (an endocannabinoid).[71][72][73][74][75]
Effects on neurochemicals
-Phenylethylamine
-Phenylethylamine, commonly referred to as phenethylamine, is a potent human trace amine and neuromodulator
which functions as endogenous amphetamine.[note 8][76][77] Thirty minutes of moderate to high intensity physical
exercise has been shown to induce an enormous increase in urinary -phenylacetic acid, the primary metabolite of
phenethylamine.[71][72][73] Two reviews noted a study where the mean 24 hour urinary -phenylacetic acid
concentration following just 30 minutes of intense exercise rose 77% above its base level;[71][72][73] the reviews
suggest that phenethylamine synthesis sharply increases during physical exercise during which it is rapidly
metabolized due to its short half-life of roughly 30 seconds.[71][72][73][78] In a resting state, phenethylamine is
synthesized in catecholamine neurons from L-phenylalanine by aromatic amino acid decarboxylase at approximately
the same rate at which dopamine is produced.[78]
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.[71][72][73]
-Endorphin
-Endorphins (contracted from "endogenous morphine") are endogenous opioid neuropeptides that bind to -opioid
receptors, in turn producing euphoria and pain relief.[74] A meta-analytic review found that exercise significantly
increases the secretion of -endorphins and that this secretion is correlated with improved mood states.[74] -
endorphins have also been found to improve sleep.[79] Moderate intensity exercise produces the greatest increase in
-endorphin synthesis, while higher and lower intensity forms of exercise are associated with smaller increases in -
endorphin synthesis.[74]
A review on -endorphins 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.[74]
Exercise-induced improvements in mood occur in sedentary individuals, recreational exercisers, and marathon
runners, but recreational athletes and marathon runners experience more pronounced mood-lifting effects from
exercising.[74]
Anandamide
Anandamide is an endogenous cannabinoid neurotransmitter that binds to cannabinoid receptors.[75] 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 ~7080% maximum heart rate).[75] Increases in plasma
anandamide levels are associated with psychoactive effects because anandamide is able to cross the bloodbrain
barrier and act within the central nervous system.[75] 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.[69][75]
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.[80]
Monoamine neurotransmitters
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.[81] Exercise normalizes the cotransmission of glutamate
and dopamine in the nucleus accumbens.[25] 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 turn reducing sympathetic activity;[82] the review
hypothesized that this neuroplasticity in the RVLM is a mechanism by which regular exercise prevents inactivity-
related cardiovascular disease.[82]
Acetylcholine
Effects in children
Sibley and Etnier (2003) performed a meta-analysis that looked at the relationship between physical activity and
cognitive performance in children.[83] 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.[83] The correlation was strongest
for the age ranges of 47 and 1113 years.[83] 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.[84]
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.[85] They concluded that hippocampal volume was positively associated
with performance on relational memory tasks.[85] Their findings are the first to indicate that aerobic fitness may relate
to the structure and function of the preadolescent human brain.[85] In Bests (2010) meta-analysis of the effect of
activity on childrens 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.[86] The second is acute exercise, which examines the immediate
changes in cognitive functioning after each session.[86] The results of both suggest that aerobic exercise may briefly
aid childrens executive function and also influence more lasting improvements to executive function.[86] Other
studies have suggested that exercise is unrelated to academic performance, perhaps due to the parameters used to
determine exactly what academic achievement is.[87] 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.[83]
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.[87] Neuroimaging of the human brain has yielded similar results, where exercise leads to
changes in brain structure and function.[87] 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.[84]
Effects on central nervous system disorders

Addiction
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, psychostimulant addiction in particular.[24][25][26][27][28] 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.[25][26] One review noted that exercise may prevent the
development of drug addiction by altering FosB or c-Fos immunoreactivity in the striatum or other parts of the
reward system.[28] Moreover, aerobic exercise decreases psychostimulant self-administration, reduces the
reinstatement (i.e., relapse) of drug-seeking, and induces opposite effects on striatal dopamine receptor D2 (DRD2)
signaling (increased DRD2 density) to those induced by pathological stimulant use (decreased DRD2 density).[25][26]
Consequently, consistent aerobic exercise may lead to better treatment outcomes when used as an adjunct treatment
for drug addiction.[25][27] 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.[24][28]
Summary of addiction-related plasticity
Form of Type of reinforcer
neuroplasticity Physical
or behavioral High fat or Sexual Environmental Sources
Opiates Psychostimulants exercise
plasticity sugar food intercourse enrichment
(aerobic)
FosB expression
in [26]

nucleus accumbens
D1-type MSNs
Behavioral plasticity
Escalation of [26]
Yes Yes Yes
intake
Psychostimulant [26]
Yes Not applicable Yes Yes Attenuated Attenuated
cross-sensitization
Psychostimulant [26]

self-administration
Psychostimulant
conditioned place [26]
preference
Reinstatement of
drug-seeking [26]
behavior
Neurochemical plasticity
CREB
phosphorylation [26]

in the
nucleus accumbens
Sensitized
dopamine response [26]
No Yes No Yes
in the
nucleus accumbens
Altered striatal DRD1,
DRD2, DRD1, DRD2, [26]
dopamine DRD2, DRD2 DRD2
DRD3 DRD3
signaling DRD3
No change -opioid
Altered striatal or receptors -opioid -opioid [26]
No change No change
opioid signaling -opioid -opioid receptors receptors
receptors receptors
dynorphin
Changes in striatal [26]
No change: dynorphin enkephalin dynorphin dynorphin
opioid peptides
enkephalin
Mesocorticolimbic synaptic plasticity
Number of
dendrites in the [26]
nucleus accumbens
Dendritic spine
density in [26]

the
nucleus accumbens
Attention deficit hyperactivity disorder

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.[22][23][88] 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.[22][23][88] 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.[22] Exercising while on stimulant medication augments the
effect of stimulant medication on executive function.[22] It is believed that these short-term effects of exercise are
mediated by an increased abundance of synaptic dopamine and norepinephrine in the brain.[22]
Major depressive disorder
A number of medical reviews have indicated that exercise has a marked and persistent antidepressant effect in
humans,[5][16][17][20][89][90] an effect believed to be mediated through enhanced BDNF signaling in the brain.[8][20]
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.[89] 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;[20] the other two indicated that physical exercise
has marked antidepressant effects and recommended the inclusion of physical activity as an adjunct treatment for
mildmoderate depression and mental illness in general.[16][17] One systematic review noted that yoga may be
effective in alleviating symptoms of prenatal depression.[91] Another review asserted that evidence from clinical trials
supports the efficacy of physical exercise as a treatment for depression over a 24 month period.[5]
A 2015 review of clinical evidence and medical guideline for the treatment of depression with exercise noted that the
available evidence on the effectiveness of exercise therapy for depression suffers from some limitations;[21]
nonetheless, it stated that there is clear evidence of efficacy for reducing symptoms of depression.[21] The review also
noted that patient characteristics, the type of depressive disorder, and the nature of the exercise program all affect the
antidepressant properties of exercise therapy.[21] A July 2016 meta-analysis concluded that physical exercise
improves overall quality of life in individuals with depression relative to controls.[11]
Brain cancers
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.[29][30] Two meta-analytic systematic
reviews of randomized controlled trials with durations of 312 months have examined the effects of physical exercise
on the aforementioned characteristics of Alzheimer's disease.[29][30] 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.[29][30] 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.[29][92]
The Caerphilly Prospective study followed 2,375 male subjects over 30 years and examined the association between
healthy lifestyles and dementia, among other factors.[93] Analyses of the Caerphilly study data have found that
exercise is associated with a lower incidence of dementia and a reduction in cognitive impairment.[93][94] 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;[35] this review further asserted that increased physical
activity appears to be causally related with these reduced risks.[35]
Parkinson's disease
Parkinson's disease (PD) is a movement disorder that produces symptoms such as bradykinesia, rigidity, shaking, and
impaired gait.[95]
A review by Kramer and colleagues (2006) found that some neurotransmitter systems are affected by exercise in a
positive way.[96] A few studies reported seeing an improvement in brain health and cognitive function due to
exercise.[96] One particular study by Kramer and colleagues (1999) found that aerobic training improved executive
control processes supported by frontal and prefrontal regions of the brain.[97] These regions are responsible for the
cognitive deficits in PD patients, however there was speculation that the difference in the neurochemical environment
in the frontal lobes of PD patients may inhibit the benefit of aerobic exercise.[98] Nocera and colleagues (2010)
performed a case study based on this literature where they gave participants with early-to mid-staged PD, and the
control group cognitive/language assessments with exercise regimens. Individuals performed 20 minutes of aerobic
exercise three times a week for 8 weeks on a stationary exercise cycle. It was found that aerobic exercise improved
several measures of cognitive function,[98] providing evidence that such exercise regimens may be beneficial to
patients with PD.
See also
Brain fitness
Memory improvement
Nootropic
Exercise therapy
Exercise is Medicine
Exercise prescription
Notes
1. Neurotrophic factors arepeptides or other small proteins that promote the growth, survival, anddifferentiation of neurons by
binding to and activating their associatedtyrosine kinases.[38]
2. Adult neurogenesis is the postnatal (after-birth) growth of new neurons, a beneficial form of neuroplasticity .[37]
3. Attentional control allows an individual to focus their attention on a specific source and ignore other stimuli that compete for
one's attention,[41] such as in the cocktail party effect.
4. Inhibitory control is the process of altering one's learned behavioral responses, sometimes called "prepotent responses", in a
way that makes it easier to complete a particular goal. [54][62] Inhibitory control allows individuals to control their impulses and
habits when necessary or desired, [54][60][62] e.g., to overcome procrastination.

5. Working memory is the form of memory usedby an individual at any given moment for active information processing, [41] such
as when reading or writing an encyclopedia article. W orking memory has a limited capacity and functions as an information
buffer, analogous to a computer'sdata buffer, that permits the manipulation of information for comprehension, decision-
making, and guidance of behavior.[54]
6. Declarative memory, also known as explicit memory, is the form of memory that pertains to facts and events. [57]
7. In healthy individuals, this energy deficit resolves simply from eating and drinking a suf ficient amount of food and beverage
after exercising.
8. In other words, phenethylamine and amphetamine have roughly identical fects ef on the central nervous system.
References
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6. Erickson KI, Leckie RL, Weinstein AM (September 2014). "Physical activity, fitness, and gray matter volume"(http://www.ne
urobiologyofaging.org/article/S0197-4580(14)00349-2/fulltext).Neurobiol. Aging. 35 Suppl 2: S20528.PMC 4094356 (http
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8. Erickson KI, Miller DL, Roecklein KA (2012)."The aging hippocampus: interactions between exercise, depression, and
BDNF" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3575139) . Neuroscientist. 18 (1): 8297. PMC 3575139 (https://ww
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10. Cox EP, O'Dwyer N, Cook R, Vetter M, Cheng HL, Rooney K, O'Connor H (August 2016). "Relationship between physical
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i.org/10.1016%2Fj.jsams.2015.09.003).
11. Schuch FB, Vancampfort D, Rosenbaum S, Richards J, W ard PB, Stubbs B (July 2016). "Exercise improves physical and
psychological quality of life in people with depression: A meta-analysis including the evaluation of control group response".
Psychiatry Res. 241: 4754. PMID 27155287 (https://www.ncbi.nlm.nih.gov/pubmed/27155287).
doi:10.1016/j.psychres.2016.04.054(https://doi.org/10.1016%2Fj.psychres.2016.04.054). "Exercise has established efficacy as
an antidepressant in people with depression. ... Exercise significantly improved physical and psychological domains and overall
QoL. ... The lack of improvement among control groups reinforces the role of exercise as a treatment for depression with
benefits to QoL."
12. Pratali L, Mastorci F, Vitiello N, Sironi A, Gastaldelli A, Gemignani A (November 2014)."Motor Activity in Aging: An
Integrated Approach for Better Quality of Life"(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4897547) . Int. Sch. Res.
Notices. 2014: 257248. PMC 4897547 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4897547) . PMID 27351018 (https://
www.ncbi.nlm.nih.gov/pubmed/27351018). doi:10.1155/2014/257248 (https://doi.org/10.1155%2F2014%2F257248).
13. Basso JC, Suzuki WA (March 2017). "The Effects of Acute Exercise on Mood, Cognition, Neurophysiology , and
Neurochemical Pathways: A Review"(http://content.iospress.com/articles/brain-plasticity/bpl160040) . Brain Plasticity. 2 (2):
127152. doi:10.3233/BPL-160040(https://doi.org/10.3233%2FBPL-160040) . Lay summary (http://neurosciencenews.com/
brain-exercise-6892/) Can A Single Exercise Session Benefit Your Brain? (12 June 2012). "A large collection of research in
humans has shown that a single bout of exercise alters behavior at the level of fective
af state and cognitive functioning in
several key ways. In terms of affective state, acute exercise decreases negative af fect, increases positive affect, and decreases
the psychological and physiological response to acute stress [28]. These fectsef have been reported to persist for up to 24 hours
after exercise cessation [28, 29, 53]. In terms of cognitive functioning, acute exercise primarily enhances executive functions
dependent on the prefrontal cortex including attention, working memory , problem solving, cognitive flexibility, verbal fluency,
decision making, and inhibitory control [9]. These positive changes have been demonstrated to occur with very low to very
high exercise intensities [9], with effects lasting for up to two hours after the end of the exer
cise bout (Fig. 1A) [27]."
14. Cunha GS, Ribeiro JL, Oliveira AR (June 2008). "[Levels of beta-endorphin in response to exercise and overtraining]". Arq
Bras Endocrinol Metabol(in Portuguese). 52 (4): 589598. PMID 18604371 (https://www.ncbi.nlm.nih.gov/pubmed/1860437
1). "Interestingly, some symptoms of OT are related to beta-endorphin (beta-end(1-31)) fects. ef Some of its effects, such as
analgesia, increasing lactate tolerance, and exercise-induced euphoria, are important for training. "
15. Boecker H, Sprenger T, Spilker ME, Henriksen G, Koppenhoefer M, W agner KJ, Valet M, Berthele A, Tolle TR (2008). "The
runner's high: opioidergic mechanisms in the human brain".Cereb. Cortex. 18 (11): 25232531. PMID 18296435 (https://www.
ncbi.nlm.nih.gov/pubmed/18296435). doi:10.1093/cercor/bhn013(https://doi.org/10.1093%2Fcercor%2Fbhn013). "The
runner's high describes a euphoric state resulting from long-distance running. "
16. Josefsson T, Lindwall M, Archer T (2014). "Physical exercise intervention in depressive dis orders: meta-analysis and
systematic review".Scand J Med Sci Sports. 24 (2): 259272. PMID 23362828 (https://www.ncbi.nlm.nih.gov/pubmed/233628
28). doi:10.1111/sms.12050 (https://doi.org/10.1111%2Fsms.12050).
17. Rosenbaum S, Tiedemann A, Sherrington C, Curtis J, W ard PB (2014). "Physical activity interventions for people with mental
illness: a systematic review and meta-analysis".J Clin Psychiatry. 75 (9): 964974. PMID 24813261 (https://www.ncbi.nlm.ni
h.gov/pubmed/24813261). doi:10.4088/JCP.13r08765 (https://doi.org/10.4088%2FJCP.13r08765).
18. Szuhany KL, Bugatti M, Otto MW (October 2014)."A meta-analytic review of the effects of exercise on brain-derived
neurotrophic factor"(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4314337) . J Psychiatr Res. 60C: 5664. PMC 4314337
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4314337) . PMID 25455510 (https://www.ncbi.nlm.nih.gov/pubmed/254555
10). doi:10.1016/j.jpsychires.2014.10.003(https://doi.org/10.1016%2Fj.jpsychires.2014.10.003).
19. Lees C, Hopkins J (2013)."Effect of aerobic exercise on cognition, academic achievement, and psychosocial function in
children: a systematic review of randomized control trials"(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3809922) . Prev
Chronic Dis. 10: E174. PMC 3809922 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3809922) . PMID 24157077 (https://
www.ncbi.nlm.nih.gov/pubmed/24157077). doi:10.5888/pcd10.130010(https://doi.org/10.5888%2Fpcd10.130010).
20. Mura G, Moro MF, Patten SB, Carta MG (2014). "Exercise as an add-on strategy for the treatment of major depressive
disorder: a systematic review".CNS Spectr. 19 (6): 496508. PMID 24589012 (https://www.ncbi.nlm.nih.gov/pubmed/245890
12). doi:10.1017/S1092852913000953(https://doi.org/10.1017%2FS1092852913000953).
21. Ranjbar E, Memari AH, Hafizi S, Shayestehfar M, Mirfazeli FS, Eshghi MA (June 2015). "Depression and Exercise: A
Clinical Review and Management Guideline"(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4592762) . Asian J. Sports Med.
6 (2): e24055. PMC 4592762 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4592762) . PMID 26448838 (https://www.ncb
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5).
Box 1: Patients with Depression Who May Particularly Benefit From Exercise Programs (http://www.ncbi.nlm.nih.gov/pmc/art
icles/PMC4592762/table/tbl26409/)
Box 2: Depressive Disorders Other Than Major Depression That May Benefit From Exercise Programs (http://www.ncbi.nlm.n
ih.gov/pmc/articles/PMC4592762/table/tbl26410/)
Box 3: The Characteristics of an Exercise Program that will Maximize the Anti-depressive Properties (http://www.ncbi.nlm.ni
h.gov/pmc/articles/PMC4592762/table/tbl2641 1/)
22. Den Heijer AE, Groen Y, Tucha L, Fuermaier AB, Koerts J, Lange KW, Thome J, Tucha O (July 2016)."Sweat it out? The
effects of physical exercise on cognition and behavior in children and adults with ADHD:systematic
a literature review"(htt
p://link.springer.com/article/10.1007%2Fs00702-016-1593-7) . J. Neural. Transm. (Vienna). PMID 27400928 (https://www.ncb
i.nlm.nih.gov/pubmed/27400928). doi:10.1007/s00702-016-1593-7(https://doi.org/10.1007%2Fs00702-016-1593-7).
23. Kamp CF, Sperlich B, Holmberg HC (July 2014). "Exercise reduces the symptoms of attention-deficit/hyperactivity disorder
and improves social behaviour, motor skills, strength and neuropsychological parameters"(http://onlinelibrary.wiley.com/doi/1
0.1111/apa.12628/epdf). Acta Paediatr. 103 (7): 70914. PMID 24612421 (https://www.ncbi.nlm.nih.gov/pubmed/24612421).
doi:10.1111/apa.12628 (https://doi.org/10.1111%2Fapa.12628). "The present review summarises the impact of exercise
interventions (110 weeks in duration with at least two sessions each week) on parameters related to ADHD in 7-to 13-year -old
children. We may conclude that all different types of exercise (here yoga, active games with and without the involvement of
balls, walking and athletic training) attenuate the characteristic symptoms of ADHD and improve social behaviour , motor
skills, strength and neuropsychological parameters without any undesirable side fects.ef Available reports do not reveal which
type, intensity, duration and frequency of exercise is most ef
fective in this respect and future research focusing on this question
with randomised and controlled long-term interventions is warranted. "
24. Carroll ME, Smethells JR (February 2016)."Sex Differences in Behavioral Dyscontrol: Role in Drug Addiction and Novel
Treatments" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC47451 13). Front. Psychiatry. 6: 175. PMC 4745113 (https://ww
w.ncbi.nlm.nih.gov/pmc/articles/PMC47451 13) . PMID 26903885 (https://www.ncbi.nlm.nih.gov/pubmed/26903885).
doi:10.3389/fpsyt.2015.00175(https://doi.org/10.3389%2Ffpsyt.2015.00175).
25. Lynch WJ, Peterson AB, Sanchez V , Abel J, Smith MA (September 2013)."Exercise as a novel treatment for drug addiction: a
neurobiological and stage-dependent hypothesis"(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3788047) . Neurosci
Biobehav Rev. 37 (8): 16221644. PMC 3788047 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3788047) .
PMID 23806439 (https://www.ncbi.nlm.nih.gov/pubmed/23806439). doi:10.1016/j.neubiorev.2013.06.011 (https://doi.org/10.1
016%2Fj.neubiorev.2013.06.011).
26. Olsen CM (December 2011). "Natural rewards, neuroplasticity, and non-drug addictions"(https://www.ncbi.nlm.nih.gov/pmc/a
rticles/PMC3139704). Neuropharmacology. 61 (7): 11091122. PMC 3139704 (https://www.ncbi.nlm.nih.gov/pmc/articles/PM
C3139704) . PMID 21459101 (https://www.ncbi.nlm.nih.gov/pubmed/21459101). doi:10.1016/j.neuropharm.2011.03.010 (htt
ps://doi.org/10.1016%2Fj.neuropharm.2011.03.010).
27. Linke SE, Ussher M (2015)."Exercise-based treatments for substance use disorders: evidence, theory , and practicality" (https://
www.ncbi.nlm.nih.gov/pmc/articles/PMC4831948) . Am J Drug Alcohol Abuse. 41 (1): 715. PMC 4831948 (https://www.ncbi.
nlm.nih.gov/pmc/articles/PMC4831948) . PMID 25397661 (https://www.ncbi.nlm.nih.gov/pubmed/25397661).
doi:10.3109/00952990.2014.976708(https://doi.org/10.3109%2F00952990.2014.976708). "The limited research conducted
suggests that exercise may be an effective adjunctive treatment for SUDs. In contrast to thescarce intervention trials to date, a
relative abundance of literature on the theoretical and practical reasons supporting the investigation of this topic has been
published. ... numerous theoretical and practical reasons support exercise-based treatments for SUDs, including psychological,
behavioral, neurobiological, nearly universal safety profile, and overall positive healthfects."
ef
28. Zhou Y, Zhao M, Zhou C, Li R (July 2015). "Sex differences in drug addiction and responseto exercise intervention: From
human to animal studies".Front. Neuroendocrinol. 40: 2441. PMID 26182835 (https://www.ncbi.nlm.nih.gov/pubmed/26182
835). doi:10.1016/j.yfrne.2015.07.001(https://doi.org/10.1016%2Fj.yfrne.2015.07.001). "Collectively, these findings
demonstrate that exercise may serve as a substitute or competition for drug abuse by changing FosB or cFos
immunoreactivity in the reward system to protect against later or previous drug use. ... As briefly reviewed above, age lar
number of human and rodent studies clearly show that there are sex dif ferences in drug addiction and exercise. The sex
differences are also found in the effectiveness of exercise on drug addiction prevention and treatment, as well as underlying
neurobiological mechanisms. The postulate that exercise serves as an ideal intervention for drug addiction has been widely
recognized and used in human and animal rehabilitation. ... In particular , more studies on the neurobiological mechanism of
exercise and its roles in preventing and treating drug addiction are needed. "
29. Farina N, Rusted J, Tabet N (January 2014). "The effect of exercise interventions on cognitive outcome in Alzheimer's disease:
a systematic review".Int Psychogeriatr. 26 (1): 918. PMID 23962667 (https://www.ncbi.nlm.nih.gov/pubmed/23962667).
doi:10.1017/S1041610213001385(https://doi.org/10.1017%2FS1041610213001385).
30. Rao AK, Chou A, Bursley B, Smulofsky J, Jezequel J (January 2014). "Systematic review of thefects ef of exercise on
activities of daily living in people with Alzheimer's disease".Am J Occup Ther. 68 (1): 5056. PMID 24367955 (https://www.n
cbi.nlm.nih.gov/pubmed/24367955). doi:10.5014/ajot.2014.009035(https://doi.org/10.5014%2Fajot.2014.009035).
31. Mattson MP (2014). "Interventions that improve body and brain bioener getics for Parkinson's disease risk reduction and
therapy". J Parkinsons Dis. 4 (1): 113. PMID 24473219 (https://www.ncbi.nlm.nih.gov/pubmed/24473219).
doi:10.3233/JPD-130335(https://doi.org/10.3233%2FJPD-130335).
32. Grazina R, Massano J (2013). "Physical exercise and Parkinson's disease: influence on symptoms, disease course and
prevention". Rev Neurosci. 24 (2): 139152. PMID 23492553 (https://www.ncbi.nlm.nih.gov/pubmed/23492553).
doi:10.1515/revneuro-2012-0087(https://doi.org/10.1515%2Frevneuro-2012-0087).
33. van der Kolk NM, King LA (September 2013). "Ef fects of exercise on mobility in people with Parkinson's disease".Mov.
Disord. 28 (11): 15871596. PMID 24132847 (https://www.ncbi.nlm.nih.gov/pubmed/24132847). doi:10.1002/mds.25658(htt
ps://doi.org/10.1002%2Fmds.25658).
34. Tomlinson CL, Patel S, Meek C, Herd CP , Clarke CE, Stowe R, et al. (September 2013). "Physiotherapy versus placebo or no
intervention in Parkinson's disease".Cochrane Database Syst Rev. 9: CD002817. PMID 24018704 (https://www.ncbi.nlm.nih.g
ov/pubmed/24018704). doi:10.1002/14651858.CD002817.pub4(https://doi.org/10.1002%2F14651858.CD002817.pub4).
35. Blondell SJ, Hammersley-Mather R, V eerman JL (May 2014)."Does physical activity prevent cognitive decline and
dementia?: A systematic review and meta-analysis of longitudinal studies" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC40
64273). BMC Public Health. 14: 510. PMC 4064273 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4064273) .
PMID 24885250 (https://www.ncbi.nlm.nih.gov/pubmed/24885250). doi:10.1186/1471-2458-14-510(https://doi.org/10.1186%
2F1471-2458-14-510). "Longitudinal observational studies show an association between higher levels of physical activity and
a reduced risk of cognitive decline and dementia. A case can be made for a causal interpretation. Future research should use
objective measures of physical activity,adjust for the full range of confounders and have ad equate follow-up length. Ideally,
randomised controlled trials will be conducted. ... On the whole the results do, however , lend support to the notion of a causal
relationship between physical activity,cognitive decline and dementia, according to the esta blished criteria for causal
inference."
36. Cormie P, Nowak AK, Chambers SK, Galvo DA, Newton RU (April 2015). "The potential role of exercise in neuro-
oncology" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4389372) . Front. Oncol. 5: 85. PMC 4389372 (https://www.ncbi.nl
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doi:10.3389/fonc.2015.00085(https://doi.org/10.3389%2Ffonc.2015.00085).
37. Malenka RC, Nestler EJ, Hyman SE (2009). Sydor A, Brown Y R, eds. Molecular Neuropharmacology: A Foundationfor
Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 5, 351.ISBN 9780071481274. "The clinical actions of
fluoxetine, like those of many neuropharmacologic agents, reflect drug-induced neural plasticity , which is the process by which
neurons adapt over time in response to chronic disturbance. ... For example, evidence indicates that prolonged increases in
cortisol may be damaging to hippocampal neurons and can suppress hippocampal neurogenesis (the generation of new neurons
postnatally)."
38. Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 8:Atypical Neurotransmitters". In Sydor A, BrownY.RMolecular
Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 199, 215.
ISBN 9780071481274. "Neurotrophic factors are polypeptides or small proteins that support the growth, dif ferentiation, and
survival of neurons. They produce their effects by activation of tyrosine kinases."
39. Tarumi T, Zhang R (January 2014)."Cerebral hemodynamics of the aging brain: risk of Alzheimer disease and benefit of
aerobic exercise" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3896879) . Front Physiol. 5: 6. PMC 3896879 (https://www.
ncbi.nlm.nih.gov/pmc/articles/PMC3896879) . PMID 24478719 (https://www.ncbi.nlm.nih.gov/pubmed/24478719).
doi:10.3389/fphys.2014.00006(https://doi.org/10.3389%2Ffphys.2014.00006). "Exercise-related improvements in brain
function and structure may be conferred by the concurrent adaptations in vascular function and structure. Aerobic exercise
increases the peripheral levels of growth factors (e.g., BDNF , IFG-1, and VEGF) which cross the blood-brain barrier (BBB)
and stimulate neurogenesis and angiogenesis (T rejo et al., 2001; Lee et al., 2002; Fabel et al., 2003; Lopez-Lopez et al., 2004)."
40. Silverman MN, Deuster PA (October 2014). "Biological mechanisms underlying the role of physical fitness in health and
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42. Carvalho A, Rea IM, Parimon T, Cusack BJ (2014)."Physical activity and cognitive function in individuals over 60 years of
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"Alterations in epigenetic modification patterns have been demonstrated to be dependent on exercise and growth hormone
(GH), insulin-like growth factor 1 (IGF-1), and steroid administration. ... the authors observed improved stress coping in
exercised subjects. Investigating the dentate gyrus, a brain region which is involved in learning and coping with stressful and
traumatic events, they could show that this effect is mediated by increased phosphorylationof serine 10 combined with H3K14
acetylation, which is associated with local opening of condensed chromatin. Consequently , they found increased immediate
early gene expression as shown for c-FOS (FBJ murine osteosarcoma viral oncogene homologue). "
44. Phillips C, Baktir MA, Srivatsan M, Salehi A (2014)."Neuroprotective effects of physical activity on the brain: a closer look at
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45. Heinonen I, Kalliokoski KK, Hannukainen JC, Duncker DJ, Nuutila, PKnuuti J (November2014). "Organ-Specific
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49. Gatti R, De Palo EF, Antonelli G, Spinella P (July 2012). "IGF-I/IGFBP system: metabolism outline and physical exercise". J.
Endocrinol. Invest. 35 (7): 699707. PMID 22714057 (https://www.ncbi.nlm.nih.gov/pubmed/22714057). doi:10.3275/8456 (h
ttps://doi.org/10.3275%2F8456). "Copeland et al. (90) studied the effect of a moderate-intensity exercise and a high-intensity
equal duration intervalled exercise in healthy males. IGF-I and IGFBP-3 increased during both exercise trials, but only the
IGFBP-3 area under curve was significantly greater during high-intensity exercise than resting control session. ... Decreased
IGF-I and increased IGFBP-1 levels, observed by Rarick et al. (100) after mild aerobic training, might be an adaptive
physiological response to prevent hypoglycemia following insulin-sensitizing training. In fact the decrease of circulating IGF-I
during short-term training seems to be reflective of favorable neuromuscular anabolic adaptation and is a normal adaptive
response to increased physical activity.The potential for exercise-induced increases in circu lating IGF-I seems to require
longer training duration (100)."
50. Bouchard J, Villeda SA (2015). "Aging and brain rejuvenation as systemic events"(https://www.ncbi.nlm.nih.gov/pmc/articles/
PMC4301186). J. Neurochem. 132 (1): 519. PMC 4301186 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4301186) .
PMID 25327899 (https://www.ncbi.nlm.nih.gov/pubmed/25327899). doi:10.1111/jnc.12969 (https://doi.org/10.1111%2Fjnc.12
969).
51. Valkanova V, Eguia Rodriguez R, Ebmeier KP(June 2014). "Mind over matterwhat do we know about neuroplasticity in
adults?". Int Psychogeriatr. 26 (6): 891909. PMID 24382194 (https://www.ncbi.nlm.nih.gov/pubmed/24382194).
doi:10.1017/S1041610213002482(https://doi.org/10.1017%2FS1041610213002482). "Control group: Active
Intervention: Aerobic exercise
[Increased GMV in:] Lobes (dorsal anterior cingulate cortex, supplementary motor area, middle frontal gyrus bilaterally); R
inferior frontal gyrus, middle frontal gyrus and L superior temporal lobe; increase in the volume of anterior white matter
tracts ... GMV anterior hippocampus"
52. Ruscheweyh R, Willemer C, Krger K, Duning T, Warnecke T, Sommer J, Vlker K, Ho HV, Mooren F, Knecht S, Flel A
(July 2011). "Physical activity and memory functions: an interventional study".Neurobiol. Aging. 32 (7): 130419.
PMID 19716631 (https://www.ncbi.nlm.nih.gov/pubmed/19716631). doi:10.1016/j.neurobiolaging.2009.08.001(https://doi.or
g/10.1016%2Fj.neurobiolaging.2009.08.001) .
53. Erickson KI, Voss MW, Prakash RS, Basak C,Szabo A, Chaddock L, Kim JS, Heo S, Alves H, White SM, W ojcicki TR,
Mailey E, Vieira VJ, Martin SA, Pence BD, Woods JA, McAuley E, Kramer AF (February 201 1). "Exercise training increases
size of hippocampus and improves memory"(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3041121). Proc. Natl. Acad. Sci.
U.S.A. 108 (7): 30173022. PMC 3041121 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3041121) . PMID 21282661 (http
s://www.ncbi.nlm.nih.gov/pubmed/21282661). doi:10.1073/pnas.1015950108(https://doi.org/10.1073%2Fpnas.1015950108).
54. Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 13: Higher Cognitive Function and Behavioral Control". In Sydor A,
Brown RY. Molecular Neuropharmacology: A Foundationfor Clinical Neuroscience (2nd ed.). New York: McGraw-Hill
Medical. pp. 313321.ISBN 9780071481274.
55. Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 13: Higher Cognitive Function and Behavioral Control". In Sydor A,
Brown RY. Molecular Neuropharmacology: A Foundationfor Clinical Neuroscience (2nd ed.). New York: McGraw-Hill
Medical. p. 315. ISBN 9780071481274. "The anterior cingulate cortexis involved in processes that require correct decision-
making, as seen in conflict resolution (eg, the Stroop test, see in Chapter 16), or cortical inhibition (eg, stopping one task and
switching to another). Themedial prefrontal cortex is involved in supervisory attentional functions (eg, action-outcome rules)
and behavioral flexibility (the ability to switch strategies). Thedorsolateral prefrontal cortex, the last brain area to undergo
myelination during development in late adolescence, is implicated in matching sensory inputs with planned motor responses.
The ventromedial prefrontal cortex seems to regulate social cognition, including empathy . The orbitofrontal cortex is involved
in social decision making and in representing the valuations assigned to dif ferent experiences."
Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 147, 266, 376.ISBN 9780071481274.
Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 148, 324328, 438.ISBN 9780071481274.
58. Grimaldi G, Argyropoulos GP, Bastian A, Cortes M, Davis NJ, Edwards DJ, Ferrucci R, Fregni,FGalea JM, Hamada M,
Manto M, Miall RC, Morales-Quezada L, Pope A P , Priori A, Rothwell J, Tomlinson SP, Celnik P (2014). "Cerebellar
Transcranial Direct Current Stimulation (ctDCS): A Novel Approach to Understanding Cere bellar Function in Health and
Disease" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4712385) . Neuroscientist. 22: 8397. PMC 4712385 (https://www.n
cbi.nlm.nih.gov/pmc/articles/PMC4712385) . PMID 25406224 (https://www.ncbi.nlm.nih.gov/pubmed/25406224).
doi:10.1177/1073858414559409(https://doi.org/10.1177%2F1073858414559409).
59. Sereno MI, Huang RS (2014)."Multisensory maps in parietal cortex"(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC396929
4). Curr. Opin. Neurobiol. 24 (1): 3946. PMC 3969294 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3969294) .
PMID 24492077 (https://www.ncbi.nlm.nih.gov/pubmed/24492077). doi:10.1016/j.conb.2013.08.014(https://doi.org/10.101
6%2Fj.conb.2013.08.014).
60. Diamond A (2013)."Executive functions"(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4084861) . Annu Rev Psychol. 64:
135168. PMC 4084861 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4084861) . PMID 23020641 (https://www.ncbi.nl
m.nih.gov/pubmed/23020641). doi:10.1146/annurev-psych-113011-143750 (https://doi.org/10.1146%2Fannurev-psych-113011
-143750).
61. Janssen M, Toussaint HM, van Mechelen W, Verhagen EA (2014)."Effects of acute bouts of physical activity on children's
attention: a systematic review of the literature"(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4132441) . Springerplus. 3:
410. PMC 4132441 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4132441) . PMID 25133092 (https://www.ncbi.nlm.nih.
gov/pubmed/25133092). doi:10.1186/2193-1801-3-410(https://doi.org/10.1186%2F2193-1801-3-410). "There is weak
evidence for the effect of acute bouts of physical activity on attention. ... Fortunately
, the literature-base on the acute effect of
PA on the underlying cognitive processes of academic performance is growing. Hillman etl. a(2011) found in their review a
positive effect of acute PA on brain health and cognition in children, but concluded it was complicated to compare the dif ferent
studies due to the different outcome measures (e.g. memory,response time and accuracy, attention, and comprehension).
Therefore, this review focuses on the sole outcome measure attention as a mediator for cognition and achievement. "
62. Ilieva IP, Hook CJ, Farah MJ (2015). "Prescription Stimulants' Ef fects on Healthy Inhibitory Control, W orking Memory, and
Episodic Memory: A Meta-analysis".J Cogn Neurosci. 27: 121. PMID 25591060 (https://www.ncbi.nlm.nih.gov/pubmed/255
91060). doi:10.1162/jocn_a_00776 (https://doi.org/10.1162%2Fjocn_a_00776).
63. Basso JC, Shang A, Elman M, Karmouta R, Suzuki W A (November 2015). "Acute ExerciseImproves Prefrontal Cortex but not
Hippocampal Function in Healthy Adults".Journal of the International Neuropsychological Society : JINS. 21 (10): 791801.
PMID 26581791 (https://www.ncbi.nlm.nih.gov/pubmed/26581791). doi:10.1017/S135561771500106X(https://doi.org/10.101
7%2FS135561771500106X).
64. McMorris T, Hale BJ (December 2012). "Differential effects of differing intensities of acute exercise on speed and accuracy of
cognition: a meta-analytical investigation".Brain and Cognition. 80 (3): 338351. PMID 23064033 (https://www.ncbi.nlm.nih.
gov/pubmed/23064033). doi:10.1016/j.bandc.2012.09.001(https://doi.org/10.1016%2Fj.bandc.2012.09.001).
65. Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 14: Mood and Emotion". In Sydor A, BrownY.RMolecular
Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 350359.
ISBN 9780071481274. "The excessive release of stress hormones, such as cortisol, which occurs in many individuals with
mood disorders, may result from hyperfunctioning of the PVN of the hypothalamus, hyperfunctioning of the amygdala (which
activates the PVN), or hypofunctioning of the hippocampus (which exerts a potent inhibitory influence on the PVN). ...
Chronic stress decreases the expression of brain-derived neurotrophic factor (BDNF) in the hippocampus, which in turn may
contribute to the atrophy of CA3 neurons and their increased vulnerability to a variety of neuronal insults. Chronic elevation of
glucocorticoid levels is also known to decrease the survival of these neurons. Such activity may increase the dendritic
arborizations and survival of the neurons, or help repair or protect the neurons from further damage. ... Stress and
glucocorticoids inhibit, and a wide variety of antidepressant drugs, exercise, and enriched environments activate hippocampal
neurogenesis."
66. Fuqua JS, Rogol AD (July 2013). "Neuroendocrine alterations in the exercising human: implications for ener gy homeostasis".
Metab. Clin. Exp. 62 (7): 911921. PMID 23415825 (https://www.ncbi.nlm.nih.gov/pubmed/23415825).
doi:10.1016/j.metabol.2013.01.016(https://doi.org/10.1016%2Fj.metabol.2013.01.016).
67. Ebner NC, Kamin H, Diaz V, Cohen RA, MacDonald K (January 2015)."Hormones as "difference makers" in cognitive and
socioemotional aging processes"(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4302708) . Front Psychol. 5: 1595.
ubmed/25657633). doi:10.3389/fpsyg.2014.01595(https://doi.org/10.3389%2Ffpsyg.2014.01595).
68. Zschucke E, Gaudlitz K, Strhle A (January 2013)."Exercise and physical activity in mental disorders: clinical and
experimental evidence"(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3567313) . J Prev Med Public Health. 46 Suppl 1:
S12521. PMC 3567313 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3567313) . PMID 23412549 (https://www.ncbi.nl
m.nih.gov/pubmed/23412549). doi:10.3961/jpmph.2013.46.S.S12(https://doi.org/10.3961%2Fjpmph.2013.46.S.S12). "In
psychiatric patients, different mechanisms of action for PA and EX have been discussed: On a neurochemical and physiological
level, a number of acute changes occur during and following bouts of EX, and several long-term adaptations are related to
regular EX training. For instance, EX has been found to normalize reduced levels of brain-derived neurotrophic factor (BDNF)
and therefore has neuroprotective or even neurotrophic ef fects [79]. Animal studies foundEX-induced changes in different
neurotransmitters such as serotonin and endorphins [10,1 1], which relate to mood, and positive effects of EX on stress
reactivity (e.g., the hypothalamus-pituitary-adrenal axis [12,13]). Finally, anxiolytic effects of EX mediated by atrial natriuretic
peptide have been reported [14]. Potential psychological mechanisms of action include learning and extinction, changes in
body scheme and health attitudes/behaviors, social reinforcement, experience of mastery , shift of external to more internal
locus of control, improved coping strategies, or simple distraction [15,16]. "
69. Raichlen DA, Foster AD, Gerdeman GL, Seillier A, Giuf frida A (2012). "Wired to run: exercise-induced endocannabinoid
signaling in humans and cursorial mammals with implications for the 'runner's high ' ". J. Exp. Biol. 215 (Pt 8): 13311336.
PMID 22442371 (https://www.ncbi.nlm.nih.gov/pubmed/22442371). doi:10.1242/jeb.063677(https://doi.org/10.1242%2Fjeb.0
63677). "Humans report a wide range of neurobiological rewards following moderate and intense aerobic activity , popularly
referred to as the 'runner's high', which may function to encourage habitual aerobic exercise. ... Thus, a neurobiological reward
for endurance exercise may explain why humans and other cursorial mammals habitually engage in aerobic exercise despite the
higher associated energy costs and injury risks"
70. Cohen EE, Ejsmond-Frey R, Knight N, Dunbar RI (2010)."Rowers' high: behavioural synchrony is correlated with elevated
pain thresholds" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2817271) . Biol. Lett. 6 (1): 106108. PMC 2817271 (https://
www.ncbi.nlm.nih.gov/pmc/articles/PMC2817271) . PMID 19755532 (https://www.ncbi.nlm.nih.gov/pubmed/19755532).
doi:10.1098/rsbl.2009.0670(https://doi.org/10.1098%2Frsbl.2009.0670).
71. Szabo A, Billett E, Turner J (2001). "Phenylethylamine, a possible link to the antidepressant ef fects of exercise?" (https://www.
ncbi.nlm.nih.gov/pmc/articles/PMC1724404) . Br J Sports Med. 35 (5): 342343. PMC 1724404 (https://www.ncbi.nlm.nih.go
v/pmc/articles/PMC1724404) . PMID 11579070 (https://www.ncbi.nlm.nih.gov/pubmed/11579070).
doi:10.1136/bjsm.35.5.342 (https://doi.org/10.1136%2Fbjsm.35.5.342). "The 24 hour mean urinary concentration of
phenylacetic acid was increased by 77% after exercise. ... As phenylacetic acid reflects phenylethylamine levels 3, and the latter
has antidepressant effects, the antidepressant effects of exercise appear to be linked to increased phenylethylamine
concentrations. Furthermore, considering the structural and pharmacological analogy between amphetamines and
phenylethylamine, it is conceivable that phenylethylamine plays a role in the commonly reported "runners high" thought to be
linked to cerebral -endorphin activity.The substantial increase in phenylacetic acid excreti on in this study implies that
phenylethylamine levels are affected by exercise. ... A 30 minute bout of moderate to highntensity i aerobic exercise increases
phenylacetic acid levels in healthy regularly exercising men. "
72. Lindemann L, Hoener MC (2005). "A renaissance in trace amines inspired by a novel GPCR family". Trends Pharmacol. Sci.
26 (5): 274281. PMID 15860375 (https://www.ncbi.nlm.nih.gov/pubmed/15860375). doi:10.1016/j.tips.2005.03.007(https://d
oi.org/10.1016%2Fj.tips.2005.03.007). "The pharmacology of TAs might also contribute to a molecular understanding of the
well-recognized antidepressant effect of physical exercise [51]. In addition to the various be neficial effects for brain function
mainly attributed to an upregulation of peptide growth factors [52,53], exercise induces a rapidly enhanced excretion of the
main -PEA metabolite -phenylacetic acid (b-P AA) by on average 77%, compared with resting control subjects [54], which
mirrors increased -PEA synthesis in view of its limited endogenous pool half-life of ~30 s [18,55]. "
73. Berry MD (2007). "The potential of trace amines and their receptors for treating neurological and psychiatric diseases". Rev
Recent Clin Trials. 2 (1): 319. PMID 18473983 (https://www.ncbi.nlm.nih.gov/pubmed/18473983).
doi:10.2174/157488707779318107(https://doi.org/10.2174%2F157488707779318107). "It has also been suggested that the
antidepressant effects of exercise are due to an exercise-induced elevation of PE [151]. "
74. Dinas PC, Koutedakis Y, Flouris AD (2011). "Effects of exercise and physical activity on depression". Ir J Med Sci. 180 (2):
319325. PMID 21076975 (https://www.ncbi.nlm.nih.gov/pubmed/21076975). doi:10.1007/s11845-010-0633-9 (https://doi.or
g/10.1007%2Fs11845-010-0633-9).
75. Tantimonaco M, Ceci R, Sabatini S, Catani MV , Rossi A, Gasperi V, Maccarrone M (2014). "Physical activity and the
endocannabinoid system: an overview".Cell. Mol. Life Sci. 71 (14): 26812698. PMID 24526057 (https://www.ncbi.nlm.nih.g
ov/pubmed/24526057). doi:10.1007/s00018-014-1575-6(https://doi.org/10.1007%2Fs00018-014-1575-6).
76. "-phenylethylamine: Biological activity"(http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?tab=biology&
ligandId=2144). Guide to Pharmacology. The International Union of Basic and Clinical Pharmacology . Retrieved 10 February
2015.
77. "Dexamfetamine: Biological activity"(http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?tab=biology&liga
ndId=2147). Guide to Pharmacology. The International Union of Basic and Clinical Pharmacology . Retrieved 10 February
2015.
78. Broadley KJ (March 2010). "The vascular ef fects of trace amines and amphetamines".Pharmacol. Ther. 125 (3): 363375.
PMID 19948186 (https://www.ncbi.nlm.nih.gov/pubmed/19948186). doi:10.1016/j.pharmthera.2009.11.005 (https://doi.org/10.
1016%2Fj.pharmthera.2009.11.005). "Trace amines are metabolized in the mammalian body via monoamine oxidase (MAO;
EC 1.4.3.4) (Berry, 2004) (Fig. 2) ... It deaminates primary and secondary amines that are ee fr in the neuronal cytoplasm but
not those bound in storage vesicles of the sympathetic neurone ... Similarly , -PEA would not be deaminated in the gut as it is a
selective substrate for MAO-B which is not found in the gut ...
Brain levels of endogenous trace amines are several hundred-fold below those for the classical neurotransmitters noradrenaline,
dopamine and serotonin but their rates of synthesis are equivalent to those of noradrenaline and dopamine and they have a very
rapid turnover rate (Berry, 2004). Endogenous extracellular tissue levels of trace amines me asured in the brain are in the low
nanomolar range. These low concentrations arise because of their very short half-life"...
79. "Physical Activity Reduces Stress | Anxiety and Depression Association of America, ADAA" (http://www.adaa.org/understand
ing-anxiety/related-illnesses/other-related-conditions/stress/physical-activity-reduces-st).www.adaa.org. Retrieved 2016-04-19.
80. Fuss J, Steinle J, Bindila L, Auer MK, Kirchherr H, Lutz B, and Gass P (2015). "A runners high depends on cannabinoid
receptors in mice" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4620874) . PNAS. 112 (42): 1310513108.PMC 4620874
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4620874) . PMID 26438875 (https://www.ncbi.nlm.nih.gov/pubmed/264388
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81. Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 5: Excitatory and Inhibitory Amino Acids". In Sydor A, BrownY.R
Molecular Neuropharmacology: A Foundationfor Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical.
pp. 117130. ISBN 9780071481274. " The major excitatory neurotransmitter in the brain is glutamate; the major inhibitory
neurotransmitter is GABA. ...
The most extensively studied form of synaptic plasticity is long-term potentiation TP) (L in the hippocampus, which is
triggered by strong activation of NMDA receptors and the consequent lar ge rise in postsynaptic calcium concentration.
Long-term depression (LTD), a long-lasting decrease in synaptic strength, also occurs at mo st excitatory and some inhibitory
synapses in the brain. ... The bidirectional control of synaptic strength byTP L and LTD is believed to underlie some forms of
learning and memory in the mammalian brain. "
82. Mischel NA, Subramanian M, Dombrowski MD, Llewellyn-Smith IJ, Mueller PJ (May 2015). "(In)activity-related
neuroplasticity in brainstem control of sympathetic outflow: unraveling underlying molecular , cellular, and anatomical
mechanisms" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4504968) . Am. J. Physiol. Heart Circ. Physiol. 309 (2): H235
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84. Chaddock L, Hillman CH, Buck SM, Cohen NJ (201 1). "Aerobic Fitness and Executive Control of Relational Memory in
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85. Chaddock I, Erickson KI, Prakash RS, Kim JS, V oss MA, VanPatter M, et al. (2010)."A neuroimaging investigation of the
association between aerobic fitness, hippocampal volume, and memory performance in preadolescent children" (https://www.n
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86. Best JR (2010). "Effects of physical activity on children's executive function: Contributions of experimental research on
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08.001).
87. Hillman CH, Erickson KI, Kramer AF (2008). "Be smart, exercise your heart: exercisefects ef on brain and cognition".Nature
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88. Rommel AS, Halperin JM, Mill J, Asherson ,PKuntsi J (September 2013)."Protection from genetic diathesis in attention-
deficit/hyperactivity disorder: possible complementary roles of exercise" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC425
7065). J. Am. Acad. Child Adolesc. Psychiatry. 52 (9): 900910. PMC 4257065 (https://www.ncbi.nlm.nih.gov/pmc/articles/P
MC4257065) . PMID 23972692 (https://www.ncbi.nlm.nih.gov/pubmed/23972692). doi:10.1016/j.jaac.2013.05.018(https://d
oi.org/10.1016%2Fj.jaac.2013.05.018). "As exercise has been found to enhance neural growth and development, and improve
cognitive and behavioural functioning in [healthy] individuals and animal studies, we reviewed the literature on thefects ef of
exercise in children and adolescents with ADHD and animal models of ADHD behaviours.
A limited number of undersized non-randomized, retrospective and cross-sectional studies have investigated the impact of
exercise on ADHD and the emotional, behavioural and neuropsychological problems associated with the disorder . The findings
from these studies provide some support for the notion that exercise has the potential to act as a protective factor for ADHD. ...
Although it remains unclear which role, if any , BDNF plays in the pathophysiology of ADH D, enhanced neural functioning has
been suggested to be associated with the reduction of remission of ADHD symptoms. 49,50,72 As exercise can elicit gene
expression changes mediated by alterations in DNA methylation 38 , the possibility emerges that some of the positive effects of
exercise could be caused by epigenetic mechanisms, which may set of f a cascade of processes instigated by altered gene
expression that could ultimately link to a change in brain function.
"
89. Cooney GM, Dwan K, Greig CA, Lawlor DA, Rimer J, W augh FR, McMurdo M, Mead GE (September 2013). "Exercise for
depression". Cochrane Database Syst. Rev. 9 (9): CD004366. PMID 24026850 (https://www.ncbi.nlm.nih.gov/pubmed/240268
50). doi:10.1002/14651858.CD004366.pub6(https://doi.org/10.1002%2F14651858.CD004366.pub6)."Exercise is moderately
more effective than a control intervention for reducing symptoms of depression, but analysi s of methodologically robust trials
only shows a smaller effect in favour of exercise. When compared to psychological or pharm acological therapies, exercise
appears to be no more effective, though this conclusion is based on a few small trials. "
90. Bren S, Bjrnebekk A, Aberg E, Math AA, Olson L, Werme M (2007). "Running is rewarding and antidepressive"(https://w
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91. Gong H, Ni C, Shen X, Wu T, Jiang C (February 2015)."Yoga for prenatal depression: a systematic review and meta-analysis"
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h.gov/pmc/articles/PMC4323231) . PMID 25652267 (https://www.ncbi.nlm.nih.gov/pubmed/25652267). doi:10.1186/s12888-
015-0393-1 (https://doi.org/10.1186%2Fs12888-015-0393-1).
92. Adlard PA, Perreau VM, Pop V, Cotman CW (2005). "Voluntary exercise decreases amyloid load in a transgenic model of
Alzheimer's disease".J. Neurosci. 25 (17): 421721. PMID 15858047 (https://www.ncbi.nlm.nih.gov/pubmed/15858047).
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93. Elwood P, Galante J, Pickering J, Palmer S, Bayer A, Ben-Shlomo ,YLongley M, Gallacher J (December 2013)."Healthy
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nlm.nih.gov/pmc/articles/PMC3857242). PLoS ONE. 8 (12): e81877. PMC 3857242 (https://www.ncbi.nlm.nih.gov/pmc/articl
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Neurobiological Effects of Physical Exercise

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Neurobiological Effects of Physical Exercise

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Neurobiological effects of physical exercise

From Wikipedia, the free encyclopedia

The neurobiological effects of physical exercise are numerous

Long-term effects on cognition

Psychological stress and cortisol

As a physical stressor, aerobic exercise stimulates cortisol

Glutamate and GABA

Effects on central nervous system disorders

Attention deficit hyperactivity disorder

Major depressive disorder

habits when necessary or desired, [54][60][62] e.g., to overcome procrastination.

Retrieved from "https://en.wikipedia.org/w/index.php?

Categories: Aerobic exercise Antidepressants Attention Cognition Cognitive neuroscience Epigenetics

This page was last edited on 25 June 2017, at 07:32.

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