World Library  
Flag as Inappropriate
Email this Article

Neurobiological effects of physical exercise

A woman engaging in aerobic exercise

Physical exercise, particularly continuous aerobic exercises such as running, cycling and swimming, has many cognitive benefits and effects on the brain. Influences on the brain include increases in neurotransmitter levels, improved oxygen and nutrient delivery, and increased neurogenesis in the hippocampus. The effects of exercise on memory have important implications for improving children's academic performance, maintaining mental abilities in old age, and the prevention and potential cure of neurological diseases.

Exercise has many physiological benefits, including advantageous effects on learning and memory. Gene expression associated with brain plasticity increases with exercise, which enhances neurogenesis, blood flow, and neuronal resistance to injury, specifically in the hippocampus.[1] The hippocampus is crucial for learning and memory storage. Neuroimaging techniques also show changes in brain structure and function with regular exercise in human studies. Increases in cerebral blood volume in the dentate gyrus of the hippocampus are associated with verbal learning and memory improvements, with cerebral blood volume possibly indicating neurogenesis.[2] Animal research has shown that exercise increases neuronal growth, cognitive function, and positively impacts neural systems associated with learning and memory.[2]

Physical activity benefits cognition as a whole. Specifically, however, executive control processes (such as working memory, multitasking or planning) are more positively affected in comparison to other regions of the brain. This demonstrates the direct link between the improvement in memory processes and aerobic exercise. The prefrontal cortex is primarily responsible for supporting executive control processes, and studies suggest exercise may be used as an intervention to prevent age-related decline in executive control and memory.[2]

The type of exercise is also related to the neurological improvements seen. Aerobic exercise (also known as "cardio") is physical exercise of low to high intensity.[3] People who regularly participate in aerobic exercise have greater scores on neuropsychological function and performance tests compared to people that participate in strength and flexibility training.[4] Examples of aerobic exercise that produce these changes are running, jogging, and brisk walking, swimming, and cycling.


  • Long Term Effects 1
    • Neuroplasticity and neurogenesis 1.1
      • BDNF 1.1.1
      • IGF-1 1.1.2
      • ΔFosB 1.1.3
    • Structural growth 1.2
  • Short term effects 2
    • Reduced stress 2.1
    • Cortisol 2.2
    • Changes in Neurotransmitter Levels 2.3
      • Dopamine 2.3.1
      • Serotonin 2.3.2
      • Norepinephrine 2.3.3
      • Glutamate 2.3.4
  • Types of Memory Impacted by Exercise 3
    • Spatial Memory 3.1
    • Learning and Consolidation 3.2
      • Classical Conditioning 3.2.1
    • Retrieval 3.3
      • State-dependent Learning 3.3.1
  • Physical Activity and Children 4
    • Education and Learning Implications 4.1
  • Physical Activity and the Elderly 5
    • Implications in Neurodegenerative Disorders 5.1
      • Alzheimer's Disease 5.1.1
      • Huntington's Disease 5.1.2
      • Parkinson's Disease 5.1.3
  • See also 6
  • References 7

Long Term Effects

Neuroplasticity and neurogenesis

Neuroplasticity is essentially the ability of neurons in the brain to adapt over time, and most often occurs in response to repeated stimuli exposure;[5] whereas neurogenesis is the postnatal (after-birth) growth of new neurons, a beneficial form of neuroplasticity.[5] Exercise increases neurotrophic factors (compounds which promote the growth or survival of neurons) such as brain-derived neurotrophic factor (BDNF) and Insulin-like growth factor 1 (IGF-1).[6][7] Evidence supports that voluntary exercise leads to increased axon regeneration and neurite outgrowth compared to sedentary animals.[8] The growth directly correlated with the amount of exercise the animal participated in, specifically the total distance the animal had run. The animals in the exercise condition showed an increased level of axonal regrowth after neural injury, due to higher neurotrophin levels such as BDNF. This shows how behaviours such as voluntary exercise can impact neurotrophin levels and neurogenesis, inducing activity-dependent neuroplasticity. Exercise increases the expression of genes that are required for this rapid neural growth in the brain.[8] Neurogenesis in the hypothalamus is linked to improvements in learning as well as in memory.[1] For example, one study demonstrated exercise-induced neurogenesis in the hippocampus improved spatial memory.[9]


One of the most significant effects of exercise on the brain is the increased expression of BNDF and one of its tyrosine kinase receptors, tropomyosin receptor kinase B (TrkB). BDNF is a secreted protein encoded by the BDNF gene, with highest levels of expression found within the cerebral cortex, hippocampus, thalamus, hypothalamus and cerebellum.[10] 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, stimulates greater expression of BDNF and TrkB receptor. Animal studies have shown that mice forced to run on a treadmill show greater concentration of serum BNDF and enhanced performance on the Morris Water Maze (MWM) than sedentary mice. Exercising mice that are given a specific protein to prevent the binding of BDNF to the TrkB receptor show no difference in spatial memory performance on the MWM when compared to the sedentary control group.[11] Exercise has also been shown to have a protective effect on BDNF, preventing a decrease in hippocampal BDNF proteins typically brought on by acute immobilization stress.[12] Exercise negates the effects of stress on BDNF proteins, which in turn benefits the hippocampus by maintaining levels of neurotrophins in the brain.


IGF-1 is a single chain protein consisting of 70 amino acids with a similar chemical structure to insulin. It is produced primarily by the liver and functions to control body growth and tissue remodeling.[13] Studies have shown that IGF-1 also plays a role in brain neurogenesis, angiogenesis and neural plasticity. Mice with low serum IGF-1 levels due to disruption of the IGF-1 gene within the liver showed impaired performance on spatial recognition tasks requiring the hippocampus. These deficits were removed by synaptic administration of IGF-1.[14]

Physical activity is associated with increased IGF-1 activity within the brain, as well as enhanced cognitive abilities. The process of release of IGF-1 is proportional to the strenuousness of the exercise and humans can adapt to the strenuousness and release less IGF-1 over time.[15] Rats forced to run on treadmills over a two-week period showed higher levels of circulating IGF-1 accompanied by an increase in cell proliferation in the dentate gyrus and dendritic spine density of CA1 pyramidal cells. IGF-1 knockout mice who completed the same exercise program did not show these effects.[16] The decline in neurogenesis typically associated with old age was slowed by exercise combined with IGF-1 treatment in rats.[17]


Aerobic exercise induces a gene transcription factor known as ΔFosB (Delta FBJ murine osteosarcoma viral oncogene homolog B) in the nucleus accumbens like other natural reinforcers and drugs of abuse;[18] however, its effects on addiction-related behavioral plasticity are entirely opposite to that of psychostimulants like amphetamine.[18] Aerobic exercise decreases psychostimulant self-administration, attenuates sensitization to the rewarding effects of psychostimulants, lowers the incidence of drug-seeking behavior, and induces opposite effects on striatal dopamine receptor D2 signaling.[18] These findings and the limited available clinical evidence in humans suggest that endurance exercise (e.g., marathon running) has the capacity to reduce addiction liability to psychostimulants and serve as an adjunct treatment for psychostimulant addiction.[18]

Summary of addiction-related plasticity
Form of neural or behavioral plasticity Type of reinforcer Sources
Opiates Psychostimulants High fat or sugar food Sexual reward Exercise Environmental enrichment
ΔFosB expression
in the nucleus accumbens
Behavioral Plasticity
Escalation of intake Yes Yes Yes [18]
Yes Not applicable Yes Yes Attenuated Attenuated [18]
conditioned place preference
Reinstatement of drug-seeking behavior [18]
Neurochemical Plasticity
CREB phosphorylation
in the nucleus accumbens
Sensitized dopamine response
in the nucleus accumbens
No Yes No Yes [18]
Altered striatal dopamine signaling DRD2, ↑DRD3 DRD1, ↓DRD2, ↑DRD3 DRD1, ↓DRD2, ↑DRD3 DRD2 DRD2 [18]
Altered striatal opioid signaling μ-opioid receptors μ-opioid receptors
κ-opioid receptors
μ-opioid receptors μ-opioid receptors No change No change [18]
Changes in striatal opioid peptides dynorphin dynorphin enkephalin dynorphin dynorphin [18]
Mesocorticolimbic Synaptic Plasticity
Number of dendrites in the nucleus accumbens [18]
Dendritic spine density in
the nucleus accumbens
No change [18]

Structural growth

Neuroimaging studies have revealed that physical activity is correlated with an increase in gray matter volume in several cortical regions associated with memory and encoding processes. Research on healthy adults engaging in medium intensity exercise has shown that the greatest changes in gray matter takes place within the cingulate cortex, prefrontal cortex, sections of the dorsal anterior cingulate cortex, supplementary motor area, and middle frontal gyrus.[19] Areas implicated in memory and cognition that show increased gray matter volume in response to exercise include:

  • Dorsolateral Prefrontal Cortex: promotes long-term memory formation.[20]
  • Anterior Prefrontal Cortex: involved in monitoring and verification of memory searches.[19]
  • Anterior Cingulate Cortex: involved in early learning and problem solving[19]
    • Ventral Anterior Cingulate Cortex: processes emotional content[19]
    • Dorsal Anterior Cingulate Cortex: processes cognitive information.[19]
  • Posterior Cingulate Cortex: shows activation in episodic recognition of previously encountered information.[19]

Slight increases in gray matter volume following exercise has also been seen in the parietal cortex, specifically in the precuneus, that plays a role in episodic memory retrieval.

The brain structure most highly affected by physical activity is the hippocampus.[9] Regular exercise has been shown to counter the shrinking of the hippocampus that naturally occurs in late adulthood.[9] 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.[9] Adults who only engaged in low intensity stretching exercises showed a 1.40% and 1.43% decline in the left and right hippocampus respectively.[9] Neuroimaging also revealed that exercise increases the volume of the anterior hippocampus but not the posterior hippocampus.[9] Regions in the anterior hippocampus such as the dentate gyrus have been shown to be most involved in cell proliferation and spatial memory acquisition.[9] Subjects in the study who underwent the greatest improvement in aerobic fitness level over the one year period as determined by VO2 max showed greater increases in hippocampal volume.[9] 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.[9]

Short term effects

Reduced stress

Stress has many physiological effects and pathological impacts on the body. Significant stress-related decreases in the volume of the hippocampus can be seen in rats, and longer depression duration is also linked to hippocampal atrophy.[21] When exposed to a psychosocial laboratory stress, subjects with high stress-induced cortisol levels showed poorer memory performance, specifically in declarative memory.[22] If a patient is administered cortisol, independent of the psychological stress, they show impaired performance in declarative memory as well as spatial tasks.[22] The negative impact of stress can also be seen at the genetic level. Physiologically, stress exposure induces a decrease in BDNF mRNA levels which can lead to depression.[23] Exercise can treat or prevent the stress-induced decrease in BDNF expression associated with acute stress exposure.To combat these detrimental effects on the body, exercise is a natural way of relieving everyday stress.

There are a number of ways in which exercise may serve to reduce stress and consequently free up one's attentional resources and improve memory:[24]

  • Exercise relaxes muscles: Being stressed causes the muscles in the body to become tense and stiff. Physical activity improves oxygen delivery to the muscles, removing tension and muscle soreness.
  • Exercise produces feeling of happiness: Through the production of endorphins, exercise removes stress by creating a peaceful feeling of euphoria.
  • Exercise reduces feelings of frustration: A good way to relieve yourself of stressful thoughts is to go for a walk or jog. Performing physical activity forces the brain to concentrate on your body and its surroundings, giving the mind a break from focusing solely on frustrations.
  • Exercise improves stress resiliency: People who exercise are more likely to have less of a stress reaction to adverse situations.


Cortisol is a glucocorticoid that is released from the adrenal gland in response to stressful situations. Studies have shown that excessive cortisol interferes with the function of neurotransmitters and impairs the ability to retrieve long term memories. Rats stressed by an electrical shock thirty minutes before navigating through a familiar maze show significantly lowered performance. This same result occurs in rats injected with cortisol directly, confirming its role in memory impairment. A study at the University of Zurich also demonstrated the detrimental effects of cortisol on memory. Healthy adults were asked to memorize a series of unrelated nouns presented on a screen for four seconds each, and were then required to recall the words immediately after the learning trial, and one day after. Subjects who took a tablet of cortisone (a precursor of cortisol) one hour before the recall test administered the day after showed impaired memory performance. Memory was not affected when subjects took the cortisone one hour before the initial word presentation, or immediately after the word presentation. This suggests that cortisol impairs the ability to retrieve older memories (long term memory), but not the ability to encode or retrieve short term memories.[25]

The primary effect of cortisol on memory function is its negative influence on the hippocampus. The natural stress response is mediated by the hypothalamic-pituitary-adrenal axis. When a stressor is present, the hypothalamus releases corticotropin-releasing hormone (CRF), which stimulates the anterior pituitary gland to release adrenocorticotropic hormone (ACTH). This hormone travels to the adrenal glands, which are signalled to release cortisol. This cortisol is released into the body and travels to the hippocampus, which acts as a negative feedback mechanism. When cortisol reaches the hippocampus, it signals the hypothalamus to shut off CRF release, thereby shutting off the release of cortisol as well. Cortisol has been found to accelerate the degeneration of the hippocampus. Since aging naturally results in hippocampal atrophy, this presents an even larger problem. As the hippocampus shrinks over time, it loses its ability to provide proper feedback to the hypothalamus during the stress response, causing cortisol release to occur for longer periods of time. This, in turn, leads to further hippocampal decay due to the greater amounts of cortisol[25]

Moderate-intense exercise produces stress on the body, and therefore releases cortisol. However exercise training increases the threshold for cortisol release, making the body more resilient to the effects of stress. The more physical activity you do, the more efficient the body becomes at dealing with both physical and mental stressors. Engaging in regular exercise therefore serves a protective function, warding off hippocampal atrophy by cortisol. This has serious implications for the prevention of neurological diseases such as Alzheimer's, since individuals with smaller hippocampi have been found to be at increased risk.[26]

Changes in Neurotransmitter Levels


central nervous system (CNS). In the CNS, it acts through four major pathways: the mesolimbic (reward or pleasure), mesocortical (cognitive control, motivation, emotion), nigrostriatal (motor control), and tuberoinfundibular (prolactin regulation) pathways. Low levels of dopamine are associated with depression, whereas high levels of dopamine are experienced when participating in pleasurable activities such as eating, exercise or sex. Dopamine is a precursor to norepinephrine and epinephrine, and levels of dopamine are responsive to levels in serotonin.[27] All four neurotransmitters are involved in the effects of exercise on memory and cognitive processes.

Exercise increases dopamine levels in the brain through a calcium-dependent process.[28] Regular aerobic exercise has a protective effect on D2 dopamine receptor levels, also preventing any modifications in dopamine metabolism due to the aging process.[29] The release of dopamine by neurons is necessary for sustaining neural activity and working memory.[30]

One experiment showed the impact of administration of a dopamine receptor D1 and D5 antagonist, which bound to these receptors in the hippocampus.[31] The reduction in dopamine receptor activity caused impaired memory for encoding of new memories in an episodic-like memory task, but did not affect previous memories that had already been encoded.[31]


Serotonin (5-hydroxytryptamine: 5-HT) is a monoamine neurotransmitter derived from the amino acid tryptophan. It is found mainly within the gastrointestinal tract, but can also be found in the brain. Brain serotonin levels are elevated following physical activity through two mechanisms:

  1. Motor activity increases both the release and synthesis of serotonin
  2. Exercise increases levels of tryptophan in the brain, which can be used to manufacture serotonin[32]

Exercise has been found to increase brain serotonin levels in rodents.[32] As such, physical activity has been proposed as a non-pharmacological intervention for depression.[32]

Serotonin plays an important role in learning and memory, particularly in the acquisition and retrieval of short term memories. All serotonin receptor classes except for the 5-HT5 receotir. Agonists at the 5-HT2A, 5-HT2C and 5-HT4 receptor have produced improvements in memory.[33] There is also evidence to suggest that serotonin may have a reciprocal relationship with BDNF, the neurotrophic factor strongly implicated in hippocampal neurogenesis and long term potentiation (LTP). BDNF elevates serotonin production and serotonergic signalling stimulates BDNF expression. Since exercise is known to substantially increase BDNF expression, this may be another mechanism through which physical activity increases brain levels of serotonin.

Serotonin is known to play a role in depression. Depressed individuals sometimes have lower levels of serotonin than nondepressed individuals, and most antidepressant medications act to potentiate serotonergic activity.


Norepinephrine has several roles as a hormone and as a neurotransmitter. Synthesized from dopamine, it acts in the central and sympathetic nervous systems by binding to adrenergic receptors. Packaged into vesicles, it is released into the synaptic cleft, transmitting signals by acting on adrenergic receptors. Norepinephrine is later degraded or taken up by other cells. The effect of norepinephrine depends on the expression of the receptors on the different cell types. It impacts the environment surrounding neurons, glial cells, neocortex, and hippocampus through its anti-inflammatory properties. Stressful events result in physiological changes that lead to the release of norepinephrine. It is released from the locus ceruleus, which is associated with most norepinephrine pathways in the central nervous system. Norepinephrine, as well as epinephrine, are responsible for the “fight or flight” response, increasing heart rate, glucose levels and blood flow which enhances alertness and arousal. Tyrosine is a precursor to dopamine, which is a precursor to norepinephrine and epinephrine. It is an amino acid found in meat, cheese, nuts and eggs. Norepinephrine has therapeutic uses. If not present in sufficient amounts it negatively impacts physiological and cognitive processes. Deficiencies in norepinephrine can lead to:[34]

  • lack of motivation
  • lack of energy
  • depression

Attention and focus are largely influenced by norepinephrine and dopamine concentrations. Norepinephrine has a stimulating effect that promotes long-term memory.[34] It also prolongs the euphoric effect stimulated by endorphins by protecting them from being degraded prematurely.[34] Psycho-stimulating drugs are prescribed in order to increase levels of norepinephrine and dopamine in patients with ADHD (Attention Deficit Hyperactivity Disorder). In Alzheimer’s Disease most norepinephrine projecting cells are lost. Norepinephrine is prescribed to people with severe hypertension, or to patients as an anti-depressant in serotonin-norepinephrine reuptake inhibitors.[34] Levels of norepinephrine increase through exercise and through increased consumption of foods high in tyrosine in the diet.[35] Exercise improves depression by increasing galinin, which is a neurotransmitter that controls norepinephrine production.[35]

Emotional memory consolidation has been shown to be amplified by norepinephrine concentrations.[36] The higher the noradrenergic activation is when presented emotion-evoking material, the greater the memory consolidation.[36] Exercise directly post-learning increased norepinephrine levels that improved retrograde memory.[36] The study independently separated the effects of norepinephrine on men and women, and found norepinephrine increased emotional memory consolidation regardless of age.[36] An animal model demonstrating high levels of running activity was used in another study contrasting levels of norepinephrine in these active rats versus control rats.[37] Results showed norepinephrine transmission in the hippocampus of active rats was higher than controls even when sedentary.[37] Hippocampal norepinephrine levels play a role in memory and are elevated with regular exercise.


Glutamate, the most common neurotransmitter in the brain, is an excitatory neurotransmitter involved in many aspects of brain function, including learning and memory.[38] Animal studies have shown that treadmill running significantly increases glutamate levels during and for a short while following exercise in rats.[39] The major role of glutamate in memory is through cotransmission with dopamine and its activation of NMDA receptors within the hippocampus.[38] The NMDA receptor is a type of glutamate receptor that plays a key role in spatial memory function and long term potentiation (LTP).[38] Studies have suggested that the NMDA receptor system may be important in the formation of new memories, but not in memory maintenance. This has been demonstrated by the fact that blocking the NMDA receptor after learning a task has no effect on memory performance in humans, whereas blocking these receptors before learning results in memory impairment.[40]

Types of Memory Impacted by Exercise

Spatial Memory

A rat completing the MWM spatial learning task

Spatial memory is the part of memory responsible for regulating and encoding information about the surroundings and orientation in space. This type of memory is primarily controlled by the hippocampus. Since exercise has such a large impact on hippocampal growth and neurogenesis, it is not much of a surprise that spatial memory is one of the main types of memory affected by physical activity. Neuroimaging has provided evidence for larger hippocampi in physically fit adults. These people also show better performance on various spatial memory tasks than adults low in physical fitness. Animal studies have provided substantial evidence for the role of exercise in spatial memory. Healthy adolescent rats submitted to daily sessions of treadmill running show increased hippocampal mossy fiber density in adulthood, and improved performance in the Morris Water Maze (MWM) (when placed in a large pool of water, the time it took for rats to swim to a submerged platform on successive trials decreased at a greater rate than rats who had not run on the treadmills).[41] Rats given lesions to the hippocampus show impaired spatial memory in the MWM compared to healthy controls. A recent study subjected lesioned rats to treadmill running at 17 meters per minute for 1 hour per day, 7 days a week for 60 days in total. Results showed that, compared to the lesioned rats who had not participated in exercise, the treadmill running lesioned rats demonstrated improved MWM performance.[42] This has implications for neurological diseases such as Alzheimer's, since it is clear that physical activity can improve spatial memory even in the presence of hippocampal damage.

Learning and Consolidation

Most of the research done concerning the impact of physical activity on learning has been conducted through classical conditioning animal studies using rats and mice. However there is also evidence for exercise improving memory consolidation and learning performance in humans. One study assessed the ability of 27 healthy adult subjects to learn a novel vocabulary either directly after high intensity anaerobic sprints, low intensity aerobic running, or a period of rest. Results revealed that vocabulary learning was 20% faster when it took place after the high intensity exercise compared to the low intensity and sedentary conditions. Learning was slowest during the rest condition, confirming the hypothesis that any level of exercise may have an impact on memory compared to remaining sedentary. Levels of BDNF and catecholamines (dopamine, epinephrine and norepinephrine) were also assessed prior to and after the interventions and after learning took place. High intensity exercise led to the strongest increases in both BDNF and catecholamine levels. This suggests that the mechanism through which physical activity improves memory may in fact be through these chemical mediators.[43] These findings concerning the ability for physical activity to facilitate learning has implications for helping students of all ages to improve their efficiency and capacity to absorb information when studying.

Classical Conditioning

Animal studies in conditioned fear conditioning have provided evidence that physical activity is involved in learning, particularly learning consolidation. Mice given 2 weeks of access to a running wheel prior to experiencing paired tone and foot shock conditioned faster (as indicated by the startle response) than mice who underwent conditioning with no prior exercise. Subsequent experiments gave the mice access to wheel running either immediately before fear conditioning (acquisition), immediately after conditioning (consolidation), or 2 weeks after conditioning had taken place, prior to a test (retrieval). Results revealed that fear conditioning was enhanced in the mice that exercised immediately prior and after conditioning, but showed no difference compared to sedentary mice when the exercise had taken place 2 weeks after the initial learning. This suggests that exercise improves learning acquisition and consolidation, but may not have an impact on memory retrieval.[44] Studies seem to suggest that aerobic exercise has the greatest impact on improving learning and memory consolidation. Rats who exercised on a running wheel for 17 days prior to eye-blink conditioning learned the association between a tone and an air puff faster, and showed a larger reflexive eye-blink response than rats who did not exercise. Rats who participated in 17 days of acrobatic training (navigating through an elevated obstacle course) showed no difference in eye-blink conditioning compared to sedentary rats.[45]


Enhanced physical activity is associated with improved cognitive function in both rodent and human models.[46] While the MWM is used to test spatial memory in rats, it has been used to test memory retrieval as well. Van Praag and colleagues (1999) performed a study where mice had one month of voluntary running before performing the MWM, compared to control mice who were sedentary during that time. The authors found that the exercise mice group mastered the MWM faster than the control group that did not have any physical activity.[47] They attributed this difference to an increase in hippocampus size and [46] An increase in freezing behaviour meant that once rats experienced the fear conditioning task once, they were more capable of retrieving the memory of the first unpleasant event, and better able to prepare when they recognize the same situation.

State-dependent Learning

  1. ^ a b Cotman, C., Berchtold, N. (2002) Exercise: a behavioural intervention to enhance brain health and plasticity. Trends in Neuroscience. 295–301.
  2. ^ a b c Hillman, C.H., Erickson, K.I., Kramer, A.F. (2008) Be smart, exercise your heart: exercise effects on brain and cognition. ‘’Neuroscience: Nature Reviews’’ 59–65.
  3. ^ Sharon A. Plowman; Denise L. Smith (1 June 2007). Exercise Physiology for Health, Fitness, and Performance. Lippincott Williams & Wilkins. p. 61.  
  4. ^ Dustman, R.E., Ruhling, R.O., Russell E.M., Shearer, D.E., Bonekat, W., Shigeoka, J.W., Wood, J.S., Bradford, D.C. (1983) Aerobic Exercise Training and Improved Neuropsychological Function of Older Individuals. ‘’Neurobiology of Aging’’. 35–42.
  5. ^ a b Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 4: Basic Principles of Neuropharmacology". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. p. 4.  
  6. ^ Szuhany KL, Bugatti M, Otto MW (October 2014). "A meta-analytic review of the effects of exercise on brain-derived neurotrophic factor". J Psychiatr Res 60C: 56–64.  
  7. ^ Eliakim A, Nemet D (2012). "Interval training and the GH-IGF-I axis - a new look into an old training regimen". J. Pediatr. Endocrinol. Metab. 25 (9-10): 815–821.  
  8. ^ a b Molteni, Raffaella; Zheng, Jun-Qi; Ying, Zhe; Gómez-Pinilla, Fernando; Twiss, Jeffery L. (2004). "Voluntary exercise increases axonal regeneration from sensory neurons". Proceedings of the National Academy of Sciences ( 101 (22): 8473–8.  
  9. ^ a b c d e f g h i Erickson KI, Voss MW, Prakash RS, Basak C, Szabo A, Chaddock L, Kim JS, Heo S, Alves H, White SM, Wojcicki TR, Mailey E, Vieira VJ, Martin SA, Pence BD, Woods JA, McAuley E, Kramer AF (February 2011). "Exercise training increases size of hippocampus and improves memory". Proc. Natl. Acad. Sci. U.S.A. 108 (7): 3017–22.  
  10. ^ Klintsova, A., Dickson, E., Yoshida, R., William, G. (2004). Altered expression of BDNF and its high-affinity receptor TrkB in response to complex motor learning and moderate exercise. Brain Research,1028,92–104
  11. ^ Vaynman, S., Ying, Z., Gomez-Pinilla, F. (2004). Hippocampal BDNF mediates the efficacy of exercise on synaptic plasticity and cognition. European Journal of Neurosciance,20(10),2580–2590
  12. ^ Adlard P.A., Cotman, C.W. (2004) Voluntary Exercise protects against stress-induced decreases in brain-derived neurotrophic factor protein expression. ‘’Neuroscience’’ 985–992.
  13. ^ Tornes-Aleman, I.(2010). Toward a comprehensive neurobiology of IGF-1. Developmental Neurobiology,70(5), 384–396
  14. ^ Trejo, J.I., Piriz, J., Llorens-Martin, M.V., Fernandez, A.M., Bolos, M.(2007).Central actions of liver-derived insulin-like growth factor 1 underlying its procognitive effects.Molecular Psychiatry,12, 1118–1128
  15. ^ Gatti, R., De Palo, E. F., Antonelli, G. & Spinella, P. IGF-I/IGFBP system: metabolism outline and physical exercise. Journal of endocrinological investigation 35, 699–707, doi:10.3275/8456 (2012).
  16. ^ Glasper, E.R., Llorens-Martin, M.V., Leuner, B., Gould, E., Trejo, J.L.(2010). Blockade of insulin-like growth factor-1 has complex effects structural plasticity in the hippocampus. Hippocampus,20(6), 706–712
  17. ^ Koltai, E., Zhao, Z., Lacza, Z., Cselenyak, A., Vacz, G., Nyakas, C., Boldogh, I., Ichinoseki-Sekine, N., Radak, Z. (2011) Combined exercise and insulin-like growth factor-1 supplementation induces neurogenesis in old rats, but do not attenuate age-associated DNA damage. ‘’Rejuvenation Research.” 585–596.
  18. ^ a b c d e f g h i j k l m n o p q Olsen CM (December 2011). "Natural rewards, neuroplasticity, and non-drug addictions". Neuropharmacology 61 (7): 1109–1122.  
  19. ^ a b c d e f Ruscheweyh R, Willemer C, Krüger K, Duning T, Warnecke T, Sommer J, Völker K, Ho HV, Mooren F, Knecht S, Flöel A (July 2011). "Physical activity and memory functions: an interventional study". Neurobiol. Aging 32 (7): 1304–19.  
  20. ^ Blumenfeld RS, Ranganath C (January 2006). "Dorsolateral prefrontal cortex promotes long-term memory formation through its role in working memory organization". J. Neurosci. 26 (3): 916–25.  
  21. ^ Sapolsky, R.M. (1996) Why stress is bad for your brain ‘’Science’’ Vol. 273 no. 5276 pp. 749–750
  22. ^ a b Kirschbaum, C., Wolf, O.T., May, M., Wippich, W., Hellhammer, D.H. (1996) Stress- and Treatment-Induced Elevations of Cortisol Levels Associated with Impaired Declarative Memory in healthy Adults. ‘’Life Sciences’’ vol.58, 1475–1483.
  23. ^ Cotman, C., Engesser-Cesar, C. (2002) Exercise Enhances and Protects Brain Function. Exercise and Sports Sciences Reviews. 75–79.
  24. ^ "How Exercise Reduces Stress". Retrieved 16 September 2013. 
  25. ^ a b "The Human Brain – Stress". 27 September 2007. Retrieved 16 September 2013. 
  26. ^ Sara Mahoney. "Exercise & Cortisol Levels". Livestrong.Com. Retrieved 16 September 2013. 
  27. ^ "Dopamine: Natural Ways to Increase Dopamine Levels". Retrieved 16 September 2013. 
  28. ^ Sutoo, D., Akiyama, K. (2003) Regulation of brain function by exercise. ‘’Neurobiology of Disease’’ 1–14.
  29. ^ Uysal, N., Tugyan, K., Kayatekin, B.M., Acikgoz, O., Bagriyanik, H.A., Gonenca, S., Ozdemir, D., Aksua, I., Topcu, A., Semin, I. (2005) The effects of regular aerobic exercise in adolescent period on hippocampal neuron density, apoptosis and spatial memory. ‘’Neuroscience Letters’’ 241–245.
  30. ^ Surmeier, D.J. (2007) Dopamine and working memory mechanisms in prefrontal cortex. ‘’Journal of Physiology.’’ 885.
  31. ^ a b Ingrid Bethus, Dorothy Tse, and Richard G. M. Morris (3 February 2010). "Dopamine and Memory: Modulation of the Persistence of Memory for Novel Hippocampal NMDA Receptor-Dependent Paired Associates". Retrieved 16 September 2013. 
  32. ^ a b c Young, SN (November 2007). "How to increase serotonin in the human brain without drugs.". Journal of psychiatry & neuroscience : JPN 32 (6): 394–9.  
  33. ^ Harvey,J.A. (2003). Role of Serotonin 5-HT2A Receptor in Learning. Learning and Memory,10, 355–362
  34. ^ a b c d "Norepinephrine". Neurogenesis. Retrieved 16 September 2013. 
  35. ^ a b Kristin Dorman. "Natural Ways To Raise Norepinephrine". Livestrong.Com. Retrieved 16 September 2013. 
  36. ^ a b c d Segal, S., Cahill, L.F., Cotman, C. (2010) Influences and interactions between norepinephrine and glucocorticoids on emotional memory consolidation for men and women. University of California, Irvine.
  37. ^ a b Morishima, M., Harada, N., Hara, S., Sano, A., Seno, H., Takahashi, A., Morita, Y., Nakaya, Y. (2006) Monoamine Oxidase A activity and norepinephrine level in hippocampus determine hyperwheel running in SPORTS rats. ‘’Neuropsychopharmacology.’’ 2627–2638.
  38. ^ a b c "Glutamate". 13 March 2006. Retrieved 16 September 2013. 
  39. ^ Leung, L., Tong, K, Zhang, S., Zeng, X., Zhang, K., Zheng, X.(2006). Neurochemical effects of exercise and neuromuscular electrical stimulation on brain after stroke: A microdialysis study using rat model. Neuroscience Letters,397(1–2),135–139
  40. ^ "Involvement of the NMDA System in Learning and Memory – Animal Models of Cognitive Impairment – NCBI Bookshelf". 25 March 2013. Retrieved 16 September 2013. 
  41. ^ Gomes da Silva, S., Unsain, N., Masco, D.H., Toscano-Silva, M., De Ammonim, H.A., et al. (2012). Early exercise promotes hippocampal plasticity and improves spatial memory in the adult life of rats. Hippocampus,22(2), 347–358.
  42. ^ Hoveida, R., Alaei, H., Oryan, S., Parivar, K., Reisi, R. (2011). Treadmill running improves spatial memory in an animal model of alzheimer's disease. Behavioural Brain Research,216(1), 270–274.
  43. ^ Winter,B., Breitenstein, C., Mooren, F.C., Voelker, K., Fobkes, M., et al. (2007). High impact running improves learning. Neurobiology of Learning and Memory,87(4), 597–609
  44. ^ Falls, W.A., Fox, J.H., MacAulay, C.M. (2010). Voluntary exercise improves both learning and consolidation of cued conditioned fear in C57 mice.Behavioural Brain Research,207(2), 321–331
  45. ^ Green, J.T., Chess, A.C., Burns, M., Schachinger, K. M., Thanellou, A. (2011). The effects of two forms of physical activity on eyeblink classical conditioning.Behavioural Brain Research,219(1), 165–174
  46. ^ a b Van der Borght, K., Havekes, R., Bos, T., Eggen, B. J. L. and Van der Zee, E. A. 2007. Exercise Improves Memory Acquisition and Retrieval in the Y-Maze Task: Relationship With Hippocampal Neurogenesis. Behavioral Neuroscience. 121(2):324–334.
  47. ^ Van Praag, H., Christie, B. R., Sejnowski, T. J. and Gage, F. H. 1999. Running enhances neurogenesis, learning, and long-term potentiation in mice. Proceedings of the National Academy of Sciences, USA. 96:13427-13431.
  48. ^ Miles, C., Hordman, E. (1998). State-dependent memory produced by aerobic exercise. Ergonomics,41(1), 20–28
  49. ^ a b c d Hillman, C.H., Erickson, K.I., and Kramer, A.F. 2008. Be smart, exercise your heart: exercise effects on brain and cognition. Nature Reviews Neuroscience. 9:58–65.
  50. ^ a b c Sibley, B. A. and Etnier, J. L. 2003. The Relationship Between Physical Activity and Cognition in Children: A Meta-Analysis. Pediatric Exercise Science. 15(3):243–256.
  51. ^ a b Chaddock, L., Hillman, C. H., Buck, S. M. and Cohen, N. J. 2011. Aerobic Fitness and Executive Control of Relational Memory in Preadolescent Children. Medicine & Science in Sports & Exercise. 43(2):344–349.
  52. ^ a b c Chaddock, I., Erickson, K. I., Prakash, R. S., Kim, J. S., Voss, M. A., VanPatter, M. et al.. 2010. A neuroimaging investigation of the association between aerobic fitness, hippocampal volume, and memory performance in preadolescent children. Brain Research. 1358:172–183.
  53. ^ a b c Best, J. R. 2010. Effects of physical activity on children’s executive function: Contributions of experimental research on aerobic exercise. Developmental Review. 30(4):331–351. doi: 10.1016/j.brainres.2010.08.049
  54. ^ Dik, M. G., Deeg, D. J. H., Visser, M. and Jonker, C. 2003. Early Life Physical Activity and Cognition at Old Age. Journal of Clinical and Experimental Neuropsychology. 25(5):643–653.
  55. ^ Swardfager W, Herrmann N, Marzolini S, Saleem M, Kiss A, Shammi P, Oh PI and Lanctôt KL, 2010. Cardiopulmonary fitness is associated with cognitive performance in patients with coronary artery disease. J. Amer. Geriatrics. Soc. 58(8):1519–25.
  56. ^ a b c Adlard, P. A., V. M. Perreau, V. Pop, and C. W. Cotman. 2005. Voluntary Exercise Decreases Amyloid Load in a Transgenic Model of Alzheimer's Disease. The Journal of Neuroscience. 25(17): 4217–4221.
  57. ^ McKhann, G., Drachman, D., Folstein, M., Katzman, R., Price, D. and Stadlan, E. M. 1984. Clinical diagnosis of Alzheimer's disease: Report of the NINCDS-ADRDA Work Group* under the auspices of Department of Health and Human Services Task Force on Alzheimer's Disease. American Academy of Neurology. 34:939–944.
  58. ^ Yang, Y., Mufson, E. J. and Herrup, K. 2003. Neuronal Cell Death Is Preceded by Cell Cycle Events at All Stages of Alzheimer's Disease. The Journal of Neuroscience. 23(7):2557–2563.
  59. ^ a b Förstl, H. and Kurz, A. 1999. Clinical features of Alzheimer's disease. Eur Arch Psychiatry Clin Neurosci. 249:288–290.
  60. ^ a b Friedland, R. P., Fritsch, T., Smyth, K.A., Koss, E., Lerner, A. J., Chen, C. H. et al.. 2001. Patients with Alzheimer's disease have reduced activities in midlife compared with healthy control-group members. The National Academy of Sciences. 98(6): 3440–3445.
  61. ^ Elwood P, Galante J, Pickering J, et al. Healthy Lifestyles Reduce the Incidence of Chronic Diseases and Dementia: Evidence from the Caerphilly Cohort Study. PLOS ONE 2013;8(12)e81877.
  62. ^ a b Rolland, Y., Abellan van Kan, G. and Vellas, B. 2008. Physical Activity and Alzheimer's Disease: From Prevention to Therapeutic Perspectives. J Am Med Dir Assoc. 9:390–405.
  63. ^ Kivipelto, M., T. Ngandu, L. Fratiglioni, M. Viitanen, I. Kareholt, B. Winblad et al.. 2005. Obesity and Vascular Risk Factors at Midlife and the Risk of Dementia and Alzheimer Disease. Archives of Neurology. 62(10):1556–1560.
  64. ^ a b c d Kohl, Z., Kandasamy, M., Winner, B., Aigner, R., Gross, C., Couillard-Despres et al.. 2007. Physical activity fails to rescue hippocampal neurogenesis deficits in the R6/2 mouse model of Huntington's disease. Trends in Cognitive Sciences. 11(8):342–348.
  65. ^ a b c d e Pang, T.Y.C., Stam, N. C., Nithianantharajah, J., Howard, M. L., and Hannan, A. J. 2006. Differential effects of voluntary physical exercise on behavioral and brain-derived neurotrophic factor expression deficits in Huntington's disease transgenic mice. Neuroscience. 141:569–584.
  66. ^ a b Zakzanis, K. K. 2010. The Subcortical Dementia of Huntington's Disease. Journal of Clinical and Experimental Neuropsychology. 20(4):565–578.
  67. ^ Baatile, J., Langbein, W.E., Weaver, F., Maloney, C., and Jost, M.B. 2000. Effect of exercise on perceived quality of life of individuals with Parkinson's Disease. Journal of Rehabilitation Research and Development. 37(5):529–534.
  68. ^ a b Tillerson, J. L., Caudle, W. M., Reverón and Miller, G.W. 2003. Exercise induces behavioural recovery and attenuates neurochemical deficits in rodent models of Parkinson’s disease. Neuroscience. 119(3):899–911.
  69. ^ Cruise, K. E., Bucks, R. S., Loftus, A. M., Newton, R. U., Pegoraro, R. and Thomas, M. G. 2011. Exercise and Parkinson's: benefits for cognition and quality of life. Acta Neurologica Scandinavica. 123:13–19.
  70. ^ a b c d e Nocera, J. R., Altman, L. J. P., Sapienza, C., Okun, M. S. and Hass, C. J. 2010. Can exercise improve language and cognition in Parkinson's disease? A case report. Neurocase: The Neural Basis of Cognition. 16(4):301–306.
  71. ^ a b c Kramer, A. F., Erickson, K. I. And Colcombe, S. J. 2006. Exercise, cognition, and the aging brain. Journal of Applied Physiology. 101(4):1237–1242.
  72. ^ Lawrence, A. D., Evans, A. H. and Lees, A. J. 2003. Compulsive use of dopamine replacement therapy in Parkinson's disease: reward systems gone awry?. The Lancet: Neurology. 2(10):595–604.
  73. ^ Kramer, A. F., Hahn, S., Cohen, N. J., Banich, M. T., McAuley, Harrison, C. R. et al. 1999. Ageing, fitness and neurocognitive function. Nature. 400:418–419.


See also

A review by Kramer and colleagues (2006) found that some neurotransmitter systems are affected by exercise in a positive way.[71] A few studies reported seeing an improvement in brain health and cognitive function due to exercise.[71] 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.[73] 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.[70] 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,[70] providing evidence that such exercise regimens may be beneficial to patients with PD.

While PD is classified as a disorder that leads to a deterioration of motor skill, progression of the disease will eventually result in cognitive and behavioural deficits. Psychosocial well-being is thought to be a contributing factor to the quality of life of PD patients,[69] and has become a key focus of research in recent years. Cognitive dysfunction will impair normal everyday activities of life. These disturbances mainly disrupt executive functions, such as multitasking, driving, and situations that require planning.[70] Certain methods to improve motor functions of PD patients do not generally impact the cognitive deficits.[71] For instance, dopamine replacement therapy, which releases the dopamine precursor L-DOPA within the brain and allows it to cross the blood-brain barrier,[72] will improve motor ability but has no association with cognitive function.[70] Deep brain stimulation that may result in improved motor function, may in turn have negative effects on cognitive function.[70]

Parkinson's disease (PD) is a neurodegenerative disorder. It is generally recognized as a movement disorder that produces symptoms such as bradykinesia, rigidity, shaking, and impaired gait.[67] It affects about 1 million people in the United States.[68] Motor symptoms of PD are caused by the death of dopamine-containing neurons in the substantia nigra pars compacta, which is located in the mesencephalon (midbrain),[68] and the accumulation of Lewy bodies and neurites.

Parkinson's Disease

Physical therapy can be sought to help improve the motor impairments of the disease. The conclusions about the effects of exercise on cognitive function in HD patients have varied across the literature. Pang and colleagues (2006) studied R6/1 transgenic mice models of HD, with results that showed exercise delayed the onset of symptoms and slowed cognitive decline.[65] On the other hand, another study by Kohl and colleagues (2007) used the R6/2 transgenic mouse model of HDstrain to see if physical activity could stimulate hippocampal neurogenesis from neural stem cells.[64] Their study found that physical exercise did stimulate cell proliferation and survival in normal healthy mice, but did not enhance hippocampal neurogenesis in the transgenic mice.[64] They speculated that this result may be due to an effect the mutated Huntingtin gene, and by extension the mutated Huntingtin protein, has on the mechanisms needed for successful hippocampal neurogenesis in HD patients.[64] Further research needs to be done before a solid conclusion can be reached about the effects of exercise on HD cognitive function, specifically in human models.

Huntington's Disease (HD) is an autosomal dominant neurodegenerative disorder where protein aggregates in neurons, destroying them,[64] leading to a decline in motor skills, chorea, subcortical dementia, and other psychiatric symptoms.[65] These symptoms include mood change,[66] impaired memory formation, information-processing deficits and a disruption in spatial working memory.[65] Neurological alterations occur in the caudate nucleus, hippocampus, and in the putamen and globus pallidus to a lesser degree.[66] The onset of the disease is related to the CAG trinucleotide expansion in the Huntingtin gene that codes for the amino acid glutamine. The normal range is 10–35 repeats, while diseased individuals will generally have 36 or more repeats, although the excessive repeats do not necessarily mean symptoms will develop.[65] Environmental factors also have an impact on disease onset and progression.[65] Each generation, the number of repeats increases, thus the age of onset decreases every generation. As with AD, there is no cure for HD, only treatment to improve the various conditions associated with it. Patients generally die within 10–20 years of disease onset.

Huntington's Disease

Current literature focuses on how physical activity can reduce the chance of onset of AD, and what it can do to slow down symptom progression when the patient is already diagnosed. A study by Friedland and colleagues (2001) surveyed 193 AD patients and 358 healthy participants 20–60 years of age. They collected data based on 26 activities in passive, intellectual, and physical categories in early adulthood (20–39 years) and middle adulthood (40–59 years). It was observed that people who developed AD were those who participated in less intellectual, passive, and physically activities in their midlife.[60] The Caerphilly Heart Disease Study followed 2,375 male subjects over 30 years and examined the association between healthy lifestyles and dementia. The study identified that men who undertook regular physical exercise had a 59% reduction in dementia when compared to the men who didn't exercise regularly.[61] A literature review by Rolland and colleagues (2008) found that AD individuals who incorporated physical activity in their daily lives would reduce cognitive decline and improve psychological and/or physical performance, as well as mobility, balance, and strength.[62] Reasons physical activity leads to a reduced risk of AD include lowering body weight, as obesity is a risk factor for AD,[63] a healthier diet, and improved blood pressure & cardiovascular health.[60] Depression, malnutrition and behaviour disturbances, which can lead to faster cognitive decline, are also held off with exercise.[62]

[56] Many studies have been done to see if exercise preserves cognitive function, though results have varied. Exercise has been shown to play a role in decreasing the risk of developing AD, and may be protective against the development of cognitive impairment.[56]. There is no cure for AD, only means of slowing down the progression and improving the condition of symptoms, but no treatment targets the underlying mechanism of disease.septicaemia and myocardial infarction Death in AD is most frequently caused by pneumonia that leads to [59], a reduction in language, and overall cognitive function is severely impaired.biographical memories Late stage AD can be characterized by a loss of [59]

Alzheimer's Disease

Implications in Neurodegenerative Disorders

Signs of cognitive decline become more evident with age. Cross-sectional studies have shown a positive link between exercise and general cognitive function in older individuals.[54] Fitness is associated with better cognitive performance in individuals with cardiovascular disease,[55] which is associated with an increased rate of cognitive decline during aging. The protective effects of fitness may be relevant to the prevention of cognitive decline due to neurodegenerative disorders. Summarized below are the effects that physical activity are though to have on three neurodegenerative conditions that usually manifest in mid to late adulthood causing cognitive symptoms (Alzheimer's disease, Huntington's disease and Parkinson's disease).

Physical Activity and the Elderly

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.[49] Neuroimaging of the human brain has yielded similar results, where exercise leads to changes in brain structure and function.[49] 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.[51]

Physical activity has contributed to reducing childhood obesity and the incidences of cardiovascular disease, colon & breast cancer, and depression & anxiety across the adult lifespan.[49] The connection between physical activity and cognitive performance has been investigated in a number of studies, many of which observed a positive correlation between the two. Sibley and Etnier (2003) performed a meta-analysis that looked at the relationship 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.[50] The correlation was strongest for the age ranges of 4–7 and 11–13 years.[50] 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.[51] 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.[52] They concluded that hippocampal volume was positively associated with performance on relational memory tasks.[52] Their findings are the first to indicate that aerobic fitness may relate to the structure and function of the preadolescent human brain.[52] 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.[53] The second is acute exercise, which examines the immediate changes in cognitive functioning after each session.[53] The results of both suggest that aerobic exercise may briefly aid children’s executive function and also influence more lasting improvements to executive function.[53] Other studies have suggested that exercise is unrelated to academic performance, perhaps due to the parameters used to determine exactly what academic achievement is.[49] 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.[50]

Education and Learning Implications

Physical Activity and Children

This has implications for students who like to study while working out at the gym. Although the increased oxygenation caused by exercise will certainly help students sustain attention while learning the material, state-dependent learning suggests that recall during the actual exam may not be the best (assuming that the exam is given in the conventional, classroom setting with students seated at their desks). It may therefore be better for students to study at a desk after having exercised so that they will reap the benefits of brain circulation, but not be in the state of exercising (increased heart rate, physical exertion) that later may influence retrieval. [48]

This article was sourced from Creative Commons Attribution-ShareAlike License; additional terms may apply. World Heritage Encyclopedia content is assembled from numerous content providers, Open Access Publishing, and in compliance with The Fair Access to Science and Technology Research Act (FASTR), Wikimedia Foundation, Inc., Public Library of Science, The Encyclopedia of Life, Open Book Publishers (OBP), PubMed, U.S. National Library of Medicine, National Center for Biotechnology Information, U.S. National Library of Medicine, National Institutes of Health (NIH), U.S. Department of Health & Human Services, and, which sources content from all federal, state, local, tribal, and territorial government publication portals (.gov, .mil, .edu). Funding for and content contributors is made possible from the U.S. Congress, E-Government Act of 2002.
Crowd sourced content that is contributed to World Heritage Encyclopedia is peer reviewed and edited by our editorial staff to ensure quality scholarly research articles.
By using this site, you agree to the Terms of Use and Privacy Policy. World Heritage Encyclopedia™ is a registered trademark of the World Public Library Association, a non-profit organization.

Copyright © World Library Foundation. All rights reserved. eBooks from Project Gutenberg are sponsored by the World Library Foundation,
a 501c(4) Member's Support Non-Profit Organization, and is NOT affiliated with any governmental agency or department.