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Effects of Physical Exercise on Cognitive Functioning and Wellbeing: Biological and Psychological Benefits

Laura Mandolesi, Arianna Polverino, Simone Montuori and 4 more

Frontiers in Psychology · 2018 · Review

doi:10.3389/fpsyg.2018.00509

Abstract

Much evidence shows that physical exercise (PE) is a strong gene modulator that induces structural and functional changes in the brain, determining enormous benefit on both cognitive functioning and wellbeing. PE is also a protective factor for neurodegeneration. However, it is unclear if such protection is granted through modifications to the biological mechanisms underlying neurodegeneration or through better compensation against attacks. This concise review addresses the biological and psychological positive effects of PE describing the results obtained on brain plasticity and epigenetic mechanisms in animal and human studies, in order to clarify how to maximize the positive effects of PE while avoiding negative consequences, as in the case of exercise addiction.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 16, 2026. Paragraph numbers are ours, so an answer can point at one.

Introduction

Many evidences demonstrated that physical exercise (PE) affects brain plasticity, influencing cognition and wellbeing (Weinberg and Gould,; for review see Fernandes et al., ). In fact, experimental and clinical studies have reported that PE induces structural and functional changes in the brain, determining enormous biological, and psychological benefits.

In general, when reported PE effects, it is customary to separate the biological aspects from the psychological ones. In fact, most of the studies documented either the effects of PE on the brain (and then on the cognitive functioning) or on the wellbeing (in terms of physical and mental health). In this review, we merge both these aspects as they influence each other. In fact, behaviorally appropriate choices depend upon efficient cognitive functioning. Furthermore, emotional states influence cognitive functions through specific cerebral circuitry involving prefrontal areas and limbic structures (Barbas, ).

Before analyzing the benefits of PE, it is necessary to define PE precisely. Indeed, PE is a term often incorrectly used interchangeably with physical activity (PA) that is “any bodily movement produced by skeletal muscles that requires energy expenditure” (World Health Organization, ). Then, PA includes any motor behavior such as daily and leisure activities and it is considered a determinant lifestyle for general health status (Burkhalter and Hillman, ). Instead, PE is “a sub classification of PA that is planned, structured, repetitive, and has as a final or an intermediate objective the improvement or maintenance of one or more components of physical fitness” (World Health Organization, ). Examples of PE are aerobic and anaerobic activity, characterized by a precise frequency, duration and intensity.

In this review, we illustrate the biological and psychological benefits of PE on cognition and wellbeing both in health and diseases, reporting data from both animal and human studies. The biological basis at both molecular and supramolecular level have been largely studied. The other aim of present work is to report the actual evidence on the epigenetic mechanisms that determine or modulate the biological effects of PE on the brain. In fact, while the biologic mechanisms are sufficiently studied both at the molecular and supramolecular levels (see Lista and Sorrentino, ), little is known about the epigenetic ones. Finally, the modality with which PE should be practiced to gain such advantages while avoiding negative consequences will be discussed. In Table 1 are reported the inclusion and exclusion criteria for studies discussed in this review.

Physical exercise, brain, and cognition

Among the biological effects of PE, those linked to “neuroplasticity” are quite important.

Neuroplasticity is an important feature of the nervous system, which can modify itself in response to experience (Bavelier and Neville, ). For this reason, PE may be considered as an enhancer environmental factor promoting neuroplasticity.

In animal studies, the structural changes analyzed concern the cellular (neurogenesis, gliogenesis, synaptogenesis, angiogenesis) and molecular (alteration in neurotransmission systems and increasing in some neurotrophic factors) level (Gelfo et al., ), while the functional activity has been measured using the levels of performance in behavioral tasks, such as spatial tasks that allow to analyze the different facets of spatial cognitive functions (Mandolesi et al., ). In humans, indicators of structural changes correspond for example to brain volumes, measures of white matter integrity or modulation in neurotrophins levels (by correlation with trophic factors plasma levels). Such metrics can be correlated to cognitive performances, defining the functional neural efficiency (Serra et al., ). To this regard, it should be emphasized that any morphological change results in a modification of the functional properties of a neural circuit and vice versa any change in neuronal efficiency and functionality is based on morphological modifications (Mandolesi et al., ).

Experimental and clinical studies have shown that PE induces important structural and functional changes in brain functioning. In Table 2 are reported the more evident effects induced by PE.

Animal studies

In animals, motor activity or motor exercise are terms often used instead of PE. The effects of motor exercise are mainly studied in rodents by means of specific training on wheels or by locomotor activity analyses.

Studies on healthy animals have demonstrated that intense motor activity increases neurons and glia cells proliferation rates in the hippocampus and the neocortex (van Praag et al.,,; Brown et al.,; Ehninger and Kempermann,; Steiner et al.,; Hirase and Shinohara, ) and induces angiogenesis in the neocortex, hippocampus, and cerebellum (Black et al.,; Isaacs et al.,; Kleim et al.,; Swain et al.,; Ekstrand et al.,; Gelfo et al., ). At the molecular level, motor activity causes changes in neurotrasmitters such as serotonin, noradrenalin, and acetylcholine (Lista and Sorrentino,; for a review, see Lin and Kuo, ) and induces the release of the brain-derived neurotrophic factor (BDNF Vaynman et al.,; Lafenetre et al., ) and the insulin-like growth factor-1 (IGF-1; for a review, van Praag, ).

Animals performing motor exercise showed improvements in spatial abilities (van Praag et al.,; Snigdha et al., ) and in other cognitive domains such as executive functions (Langdon and Corbett, ), evidencing thus that motor exercise improve cognitive functions.

Similar structural and functional changes were evident even in older animals (Kronenberg et al., ) and in animal models of neurodegenerative diseases (Nithianantharajah and Hannan, ), suggesting that motor exercise is a potent neuroprotective factor against physiological and pathological aging (Gelfo et al., ). In this context, one can use transgenic models to determine exactly when a structural alteration occurs, and then to study when the animals should undergo motor training in order to maximize its effects. To this regard, converging evidence is showing that motor activity should be performed before the development of neurodegeneration in order to exert its protective role (Richter et al.,; Lin et al., ) such as before the formation of beta amyloid plaques in Alzheimer's disease (Adlard et al., ). However, there are some experimental evidences showing that motor exercise performed after neurodegenerative lesions permits to improve spatial abilities, hence being also a potent therapeutic agent (Sim,; Ji et al., ).

Interestingly, PE induces modifications that can be passed on to the offspring. In fact, positive maternal experiences can influence the offspring at both behavioral and biochemical levels (see Cutuli et al.,, ). Preclinical studies also indicated that the effects of maternal exercise during pregnancy can be passed on to offspring (Robinson et al., ). However, it is not clear if the possibilities of inheritance are limited to motor exercise alone. To this regard, it has been seen that pregnant rats exposed to motor exercise on wheel-running and treadmill running have offspring with improved spatial memory, and increased hippocampal BDNF level (Akhavan et al.,; Aksu et al., ). However, further studies are necessary since it remains unclear whether these beneficial effects result from physiological changes to the in utero environment and/or from epigenetic modifications to the developing embryo (Short et al., ). On the other hand, few studies, conflicting and hard to replicate, do not yet allow to explore the transgenerational effects of paternal motor exercise (Short et al., ).

Human studies

Neuroplasticity phenomena following PE have been evidenced even in humans. A great number of studies demonstrated that in adults, PE determines structural changes such as increased gray matter volume in frontal and hippocampal regions (Colcombe et al.,; Erickson et al., ) and reduced damage in the gray matter (Chaddock-Heyman et al., ).

Moreover, PE facilitates the release of neurotrophic factors such as peripheral BDNF (Hötting et al., ), increases blood flow, improves cerebrovascular health and determines benefits on glucose and lipid metabolism carrying “food” to the brain (Mandolesi et al., ).

These effects are reflected on cognitive functioning (for a review see Hötting and Röder, ). In fact, the results of cross-sectional and epidemiological studies showed that PE enhances cognitive functions in young and older adults (Lista and Sorrentino,; Fernandes et al., ), improving memory abilities, efficiency of attentional processes and executive-control processes (Kramer et al.,; Colcombe and Kramer,; Grego et al.,; Pereira et al.,; Winter et al.,; Chieffi et al., ). Furthermore, structural changes following PE have been related to academic achievement in comparison to sedentary individuals (Lees and Hopkins,; Donnelly et al., ). In this line, it has been also showed that children who practice regular aerobic activity performed better on verbal, perceptual and arithmetic test in comparison to sedentary ones of same age (Sibley and Etnier,; Voss et al., ).

Numerous studies have demonstrated that PE prevents cognitive decline linked to aging (Yaffe et al.,; Hötting and Röder,; Niemann et al., ), reduces the risk of developing dementia (Colberg et al.,; Mandolesi et al., ), the level of deterioration in executive functions (Hollamby et al., ) and improves the quality of life (Pedrinolla et al., ). Furthermore, positron emission tomography based studies evidenced that PE determines changes in metabolic networks that are related to cognition (Huang et al., ).

Recently, studies on magnetoencephalography based (MEG) functional connectivity evidenced that PE influences network topology (Foster, ). It is important to underlie that MEG is a much more direct measure of neural activity in comparison to fRMI, with the advantage of combining good spatial and high temporal resolution. In healthy individuals, PE was related to better intermodular integration (Douw et al., ) and to improvements in cognitive functions (Huang et al., ). Benefits of PE are evidenced even in individuals at risk for AD (Deeny et al., ), thus once again suggesting a protective role of PE.

A possible explanation for these ameliorative structural and functional effects could be that PE stimulates blood circulation in the neural circuits involved in cognitive functioning (Erickson et al., ). Another interpretation could be found in the concept of “cerebral reserves” (Stern,, ) a mechanisms that might explain why, in the face of neurodegenerative changes that are similar in nature and extent, individuals vary considerably in the severity of cognitive aging and clinical dementia (Petrosini et al., ). Two types of reserves are recognized: brain reserve and cognitive reserve. The former is based on the protective potential of anatomical features such as brain size, neuronal density and synaptic connectivity, the latter is based on the efficient connectivity among neural circuits (Stern,; Mandolesi et al., ).

According to the reserves hypothesis and taking into account the numerous evidences described above, we could advance that PE is an environmental factor that permits to gain reserves.

However, one must underline that if on the one hand PE improves the cognitive functioning, providing reserves to be spent in the case of a brain lesion, on the other hand the modifications of the clinical expression of neurodegeneration delays the diagnosis. It has been seen that patients with higher cognitive reserve take longer to manifest the symptoms of memory loss (Zanetti et al., ). It has been hypothesized a neural compensation mechanism that permits to perform complex activities (Stern, ). Obviously, these conclusions open important reflections more for the diagnosis of neurodegenerative disease than for the practice of PE.

The effects of PE on cognitive functioning have been shown across the lifespan from childhood to the old age (Hötting and Röder, ). In particular, it has been evidenced that cognitive functions that are influenced the most by brain maturation, such as attention or cognitive flexibility, and the cognitive functions that depend the most upon experiences, such as memory, are the most sensitive ones to PE (Hötting and Röder, ). Overall, these studies, together with those analyzing the effects of combined environmental factors, suggest that for a positive effect on cognitive function, it is necessary to maintain an “enriched lifestyle” up to middle life. In fact, the exposure to PE together to other many experiences provides a “reserve”-like advantage which supports an enduring preservation of cognitive function in old age (Chang et al.,; Loprinzi et al., ).

Physical exercise and wellbeing

There are consistent evidences that PE has many benefits for people of any age, improving psychological wellbeing (Zubala et al., ) and quality of life (Penedo and Dahn,; Windle et al.,; Table 3).

In children, PE is correlated with high levels of self-efficacy, tasks goal orientation, and perceived competence (Biddle et al., ). In youth and adulthood, most studies evidenced that PE is associated with better health outcomes, such as better mood and self-concept (Berger and Motl,; Landers and Arent,; Penedo and Dahn, ). In the aging population, PE helps maintaining independence (Stessman et al., ), favoring social relations and mental health.

It was now well-accepted that is the interaction between biological and psychological mechanisms linked to PE enhances the wellbeing (Penedo and Dahn, ). Biological mechanisms of beneficial effects of PE are mainly related to increasing in cerebral blood flow and in maximal oxygen consumption, to delivery of oxygen to cerebral tissue, to reduction in muscle tension and to increased serum concentrations of endocannabinoid receptors (Thomas et al.,; Dietrich and McDaniel,; Querido and Sheel,; Gomes da Silva et al.,; Ferreira-Vieira et al., ). Moreover, neuroplasticity phenomena such as changes in neurotransmitters are recognized to affect wellbeing. For example, PE increases the levels of serotonin (Young,; Korb et al., ) and the levels of beta-endorphins, such as anandamide (Fuss et al., ).

Among the psychological hypothesis proposed to explain how PE enhances wellbeing, it has been underlined feeling of control (Weinberg and Gould, ), competency and self-efficacy (Craft,; Rodgers et al., ), improved self-concept and self-esteem (Marsh and Sonstroem,; Fox,; Zamani Sani et al., ), positive social interactions and opportunities for fun and enjoyment (Raedeke,; Bartlett et al., ).

Psychological research evidenced that PE can even modulate the personality and the development of Self (Weinberg and Gould, ). Moreover, PE has been correlated with hardiness, a personality style that enables a person to withstand or cope with stressful situations (Weinberg and Gould, ).

In the following sections, we will focus on correlations among PE and the most common mental illnesses.

Depression and anxiety

Depression is the most common type of mental illness and will be the second leading cause of disease by 2020 (Farioli-Vecchioli et al., ). Similar entity concerns anxiety disorders that are among the most prevalent mental disorders in the world population (Weinberg and Gould, ).

Epidemiological studies have consistently reported benefits of PE on reductions in depression (Mammen and Faulkner, ) and anxiety (DeBoer et al., ). For example, it has been seen that individuals that practice PE regularly are less depressed or anxious than those who do not (De Moor et al., ), suggesting the use of exercise as a treatment for these illnesses (Carek et al., ).

Most of the research on the relationship between PE and positive changes in mood state has evidenced positive effects, especially as a consequence of aerobic exercise, regardless of the specific type of activity (Knapen et al., ), even if the correct intensity of aerobic PE to control and reduce symptoms is debated (de Souza Moura et al., ). For example, it has been revealed that after about 16 weeks of an aerobic exercise program, individuals with major depressive disorder (MDD), significantly reduced their depressive symptoms (Craft and Perna, ). However, there are evidenced that documented that even anaerobic activity has positive effects on treatment of clinical depression (Martinsen, ). For anxiety disorders, it has been evidenced that the positive effects of PE are visible even with short bursts of exercise, independently from the nature of the exercise (Scully et al., ).

A physiologic mechanism correlated to the improvement in depressed mood post-exercise PE was identified in modulation of peripheral levels of BDNF (Coelho et al., ). In this line, it was suggested recently that the intensity of exercise to improve mood should be prescribed on individual basis and not on the patient's preferred intensity (Meyer et al.,,). Conversely, physical inactivity correlated to worse depressive symptoms and, then, to lower peripheral levels of BDNF (Brunoni et al., ). Post-PE mood improvement might also be due to lower oxidative stress (Thomson et al., ). In this contest, it was evidenced that there is an abnormal oxidative stress in individuals with MDD or bipolar disorder (Cataldo et al.,; Andreazza et al., ) and that PE, particularly in higher intensity, decreases oxidative stress with consequent mood improvement (Urso and Clarkson, ).

Addictive and unhealthy behaviors

PE has been widely evidenced to be an effective tool for treating several addictive and unhealthy behaviors. PE tends to reduce and prevent behaviors such as smoking, alcohol, and gambling, and to regulate the impulse for hunger and satiety (Vatansever-Ozen et al.,; Tiryaki-Sonmez et al., ). In this context, several studies evidenced substance abusers benefit from regular PE, that also helps increasing healthy behaviors (Giesen et al., ). It has been evidenced that regular PE reduces tobacco cravings and cigarette use (Haasova et al., ). Although PE has positive effects on psychological wellbeing, in this context it is right underline that in some cases PE could reveal unhealthy behaviors with negative consequence on health (Schwellnus et al., ). It is the case of exercise addiction, a dependence on a regular regimen of exercise that is characterized by withdrawal symptoms, after 24–36 h without exercise (Sachs, ), such as anxiety, irritability, guilt, muscle twitching, a bloated feeling, and nervousness (Weinberg and Gould, ). There is a strong correlation between exercise addiction and eating disorders (Scully et al., ) suggesting thus a comorbidity of these disorders and a common biological substrate. In particular, recent studies have shown that these unhealthy behaviors are associated to lower prefrontal cortex volume, activity and oxygenation, with consequent impairment in cognitive functions, such as the inhibitory control with the consequent compulsive behaviors (Asensio et al.,; Wang et al.,; Pahng et al., ). Also, it has been seen that a few days of PE increase oxygenation of prefrontal cortex, improving mental health (Cabral et al., ).

Epigenetic mechanisms

Biological and psychological effects of PE could be partly explained through epigenetic mechanisms. The term “epigenetics,” coined by Waddington, is based on a conceptual model designed to account for how genes might interact with their environment to produce the phenotype (Waddington,; Fernandes et al., ).

In particular, epigenetics is referred to all those mechanisms, including functional modifications of the genome such as DNA methylation, post-translational histone modifications (i.e., acetylation and methylation) and microRNA expression (Deibel et al.,; Grazioli et al., ), which tend to regulate gene expression, modeling the chromatin structure but maintaining the nucleotide sequence of DNA unchanged.

The current literature clearly demonstrates that these mechanisms are strongly influenced by different biological and environmental factors, such as PE (Grazioli et al., ), which determine the nature and the mode of epigenetic mechanisms activation.

Epigenetics plays an essential role in neural reorganization, including those that govern the brain plasticity (Deibel et al., ). For example, a growing body of evidence indicates that regulates neuroplasticity and memory processes (Ieraci et al., ).

Several animal studies reveal how motor activity is able to improve cognitive performances acting on epigenetic mechanisms and influencing the expression of those genes involved in neuroplasticity (Fernandes et al., ). The main molecular processes that underlie the epigenetic mechanisms are the following: through DNA methylation, histone modifications and microRNA expression (Fernandes et al., ).

DNA methylation is a chemical covalent modification on the cytosine of the double stranded DNA molecule. It has been recognized that DNA methylation plays a key role in long-term memory (Deibel et al.,; Kim and Kaang, ). In particular, mechanisms related to DNA methylation relieve the repressive effects of memory-suppressor genes to favor the expression of plasticity-promoting and memory consolidation genes. Several evidences showed that PE is able to coordinate the action of the genes involved in synaptic plasticity that regulate memory consolidation (Molteni et al.,; Ding et al., ).

Histone modifications are post-translational chemical changes in histone proteins. They include histone methylation/demethylation, acetylation/deacetylation, and phosphorylation, all due to the activity of specific enzymes, which modify the chromatin structure, thereby regulating gene expression. It has been demonstrated that histone acetylation is a requisite for long-term memory (LTM) (Barrett and Wood,; Fernandes et al., ). In animals, motor activity increases these genetic mechanisms in the hippocampus and the frontal cortex, improving memory performances in behavioral tasks (Cechinel et al., ). Recently, following 4 weeks of motor exercise, it has been evidenced an increasing of the activity of enzymes involved in histone acetylation/deacetylation, the epigenetic mechanisms that determine an enhancing in the expression of BDNF (Maejima et al., ).

MicroRNAs (miRNAs) are small, single stranded RNA molecules able to inhibit the expression of target genes. They are widely expressed in the brain, participating in epigenetic mechanisms and acting as regulators of numerous biological processes in the brain, ranging from cell proliferation, differentiation, apoptosis, synaptic plasticity, and memory consolidation (Saab and Mansuy, ). Recent evidences demonstrate that PE can mitigate the harmful effects of traumatic brain injury and aging on cognitive function by regulating the hippocampal expression of miR21 (Hu et al., ) and miR-34a (Kou et al., ). Furthermore, PE contributes to attenuate the effects of stress-related increase in miR-124, involved in neurogenesis and memory formation (Pan-Vazquez et al., ).

What kind of physical exercise?

Sport psychology has suggested that the success or failure of PE programs depends on several factors such as the intensity, frequency, duration of the exercise, and whether the PE is done in group or alone (Weinberg and Gould, ). These aspects are important in terms of maintenance of PE practice and in order to gain benefits for brain and behavior, and they are affected by individual characteristics. Although such aspects have to be taken into account when training is proposed, scientific reports have evidenced different effects on cognitive functioning and wellbeing if PE is performed in aerobic or anaerobic modality.

Aerobic exercise allows the resynthesis of adenosine—triphosphate (ATP) by aerobic mechanisms, adjusting intensity (from low to high intensity), duration (usually long), and oxygen availability. The intensity depends on the cardiorespiratory effort with respect to the maximum heart rate (HRmax) or the maximum oxygen consumption (Vo2max), which determines an increase in oxygen consumption with respect to the rest condition. Examples of aerobic PE are jogging, running, cycling, and swimming.

On the contrary, anaerobic exercise has high intensity, short duration and unavailability of oxygen, determining the depletion of the muscles' ATP and/or phosphocreatine (PCr) reserves, shifting the production of ATP, to anaerobic energy mechanisms, lactacid or alactacid. Examples of anaerobic exercises are weight lifting or sprint in 100 m.

Robust literature demonstrated that chronic aerobic exercise is associated with potent structural and functional neuroplastic changes, with an improvement in cognitive functions (Colcombe et al.,; Hillman et al.,; Erickson et al.,; Mandolesi et al., ) and increased feeling of general wellbeing (Berger and Tobar,; Biddle et al., ) (Table 4).

Recently, growing evidence showed that acute aerobic exercise, defined as a single bout of exercise, relates to improved cognitive functions, especially prefrontal cortex-dependent cognition (Tomporowski,; Lambourne and Tomporowski,; Chang et al.,; Ludyga et al.,; Basso and Suzuki, ). However, the effects of a single session of exercise on cognitive functioning are generally small (Chang et al., ). In this line, it was evidenced that even a single bout of moderate-intensity aerobic exercise enhances, mood and emotional states and improves the wellbeing in MDD individuals (Bartholomew et al.,; Basso and Suzuki, ) (Table 4).

Beside frequency and duration over time, even the intensity is a parameter to be considered when evaluating the PE effects. It has been showed that moderate intensity exercise is related to increased performance in working memory and cognitive flexibility, whereas high-intensity exercise improves the speed of information processing (Chang and Etnier, ). In this context, it has been reported that peripheral BDNF was significantly increased after high intensity exercise, but not after low-intensity exercise (Hötting et al., ). In fact, it is evidenced that high-intensity exercise provides greater benefit to cognitive functions than low-intensity exercise in the elderly (Brown et al., ).

With regard to the psychological beneficial effects related to PE, research has evidenced that major benefits in reduction of anxiety and depression are determined by longer training program (several months), as compared to shorter ones (some days) for training session lasting over 30 min. Moreover, anxiety and depression reduction after aerobic exercise may be achieved with exercise intensity between 30 and 70% of maximal heart rate (Weinberg and Gould, ). To achieve positive mood changes, an important role is played even by anaerobic activity, such as yoga, or in all PEs in which there is rhythmic abdominal breathing, enjoyment, rhythmic, and repetitive movements and relative absence of interpersonal competition (Berger and Motl, ).

Conclusion

PE determines positive biological and psychological effects that affect the brain and the cognitive functioning and promote a condition of wellbeing. PE plays an important role in counteract normal and pathological aging. Recent evidences have shown that PE triggers potent neuroplastic phenomena, partly mediated by epigenetic mechanisms. In fact, PE cause profound alterations in gene expression and its protein products in the form of epigenomic manifestations (Fernandes et al., ).

A growing body of literature indicates that both chronic and aerobic PE can achieve similar benefits.

These results should lead to reflect on beneficial effects of PE and to promote its use as a modifiable factor for prevention, to improve cognitive abilities and to enhance mood.

Despite all these positive effects, it must be underlined that PE should be tailored to the individual. In fact, even PE, when excessive, can have a dark side, when PE becomes compulsive and facilitates addictive behaviors.

Author contributions

LM, AP, SM, FF, GF, PS, and GS: designed the review; LM and GS: wrote the paper. All authors read, revised, and approved the final manuscript.

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

References 149

  1. 1.

    Adlard P. A. Perreau V. M. Pop V. Cotman C. W. (2005 ). Voluntary exercise decreases amyloid load in a transgenic model of Alzheimer's disease. J. Neurosci. 25, 4217–4221.

    Not in our library10.1523/jneurosci.0496-05.2005

  2. 2.

    Akhavan M. M. Emami-Abarghoie M. Safari M. Sadighi-Moghaddam B. Vafaei A. A. Bandegi A. R.. (2008 ). Serotonergic and noradrenergic lesions suppress the enhancing effect of maternal exercise during pregnancy on learning and memory in rat pups. Neuroscience 151, 1173–1183.

    Not in our library10.1016/j.neuroscience.2007.10.051

  3. 3.

    Aksu I. Baykara B. Ozbal S. Cetin F. Sisman A. R. Dayi A.. (2012 ). Maternal treadmill exercise during pregnancy decreases anxiety and increases prefrontal cortex VEGF and BDNF levels of rat pups in early and late periods of life. Neurosci. Lett. 516, 221–225.

    Not in our library10.1016/j.neulet.2012.03.091

  4. 4.

    Andreazza A. C. Wang J. F. Salmasi F. Shao L. Young L. T. (2013 ). Specific subcellular changes in oxidative stress in prefrontal cortex from patients with bipolar disorder. J. Neurochem. 127, 552–561.

    Not in our library10.1111/jnc.12316

  5. 5.

    Asensio S. Morales J. L. Senabre I. Romero M. J. Beltran M. A. Flores-Bellver M.. (2016 ). Magnetic resonance imaging structural alterations in brain of alcohol abusers and its association with impulsivity. Addict. Biol. 21, 962–971.

    Not in our library10.1111/adb.12257

  6. 6.

    Barbas H. (2000 ). Connections underlying the synthesis of cognition, memory, and emotion in primate prefrontal cortices. Brain Res. Bull. 52, 319–330.

    Not in our library10.1016/s0361-9230(99)00245-2

  7. 7.

    Barrett R. M. Wood M. A. (2008 ). Beyond transcription factors: the role of chromatin modifying enzymes in regulating transcription required for memory. Learn. Mem. 15, 460–467.

    Not in our library10.1101/lm.917508

  8. 8.

    Bartholomew J. B. Morrison D. Ciccolo J. T. (2005 ). Effects of acute exercise on mood and well-being in patients with major depressive disorder. Med. Sci. Sport. Exerc. 37, 2032–2037.

    Not in our library10.1249/01.mss.0000178101.78322.dd

  9. 9.

    Bartlett J. D. Close G. L. MacLaren D. P. M. Gregson W. Drust B. Morton J. P. (2011 ). High-intensity interval running is perceived to be more enjoyable than moderate-intensity continuous exercise: implications for exercise adherence. J. Sports Sci. 29, 547–553.

    Not in our library10.1080/02640414.2010.545427

  10. 10.

    Basso J. C. Suzuki W. A. (2017 ). The effects of acute exercise on mood, cognition, neurophysiology and neurochemical pathways: a review. Brain Plast. 2, 127–152.

    Not in our library10.3233/bpl-160040

  11. 11.

    Bavelier D. Neville H. J. (2002 ). Cross-modal plasticity: where and how? Nat. Rev. Neurosci. 3, 443–452.

    Not in our library10.1038/nrn848

  12. 12.

    Berger B. Motl R. (2001 ). Physical activity and quality of life, in Handbook of Sport Psychology, eds Singer R. N. Hausenblas H. A. Janelle C. (New York, NY: Wiley), 636–670.

    Not in our library

  13. 13.

    Berger B. Tobar D. (2011 ). Exercise and quality of life, in The NEW Sport and Exercise Psychology Companion, eds Morris T. Terry P. (Morgantown, WV: Fitness Information Technology), 483–505.

    Not in our library

  14. 14.

    Biddle S. J. H. Atkin A. J. Cavill N. Foster C. (2011 ). Correlates of physical activity in youth: a review of quantitative systematic reviews. Int. Rev. Sport Exerc. Psychol. 4, 25–49.

    Not in our library10.1080/1750984x.2010.548528

  15. 15.

    Black J. E. Isaacs K. R. Anderson B. J. Alcantara A. A. Greenough W. T. (1990 ). Learning causes synaptogenesis, whereas motor activity causes angiogenesis, in cerebellar cortex of adult rats. Proc. Natl. Acad. Sci. U.S.A. 87, 5568–5572.

    Not in our library10.1073/pnas.87.14.5568

  16. 16.

    Brown B. M. Peiffer J. J. Sohrabi H. R. Mondal A. Gupta V. B. Rainey-Smith S. R.. (2012 ). Intense physical activity is associated with cognitive performance in the elderly. Transl. Psychiatry 2:e191.

    Not in our library10.1038/tp.2012.118

  17. 17.

    Brown J. Cooper-Kuhn C. M. Kempermann G. Van Praag H. Winkler J. Gage F. H. (2003 ). Enriched environment and physical activity stimulate hippocampal but not olfactory bulb neurogenesis. Eur. J. Neurosci. 17, 2042–2046.

    Not in our library10.1046/j.1460-9568.2003.02647.x

  18. 18.

    Brunoni A. R. Lopes M. Fregni F. (2008 ). A systematic review and meta-analysis of clinical studies on major depression and BDNF levels: implications for the role of neuroplasticity in depression. Int. J. Neuropsychopharmacol. 11, 1169–1180.

    Not in our library10.1017/s1461145708009309

  19. 19.

    Burkhalter T. M. Hillman C. H. (2011 ). A narrative review of physical activity, nutrition, and obesity to cognition and scholastic performance across the human lifespan. Adv. Nutr. Int. Rev. J. 2, 201S−206S.

    Not in our library10.3945/an.111.000331

  20. 20.

    Cabral D. A. da Costa K. G. Okano A. H. Elsangedy H. M. Rachetti V. P. Fontes E. B. (2017 ). Improving cerebral oxygenation, cognition and autonomic nervous system control of a chronic alcohol abuser through a three-month running program. Addict. Behav. Rep. 6, 83–89.

    Not in our library10.1016/j.abrep.2017.08.004

  21. 21.

    Carek P. J. Laibstain S. E. Carek S. M. (2011 ). Exercise for the treatment of depression and anxiety. Int. J. Psychiatry Med. 41, 15–28.

    Not in our library10.2190/pm.41.1.c

  22. 22.

    Cataldo A. M. McPhie D. L. Lange N. T. Punzell S. Elmiligy S. Ye N. Z.. (2010 ). Abnormalities in mitochondrial structure in cells from patients with bipolar disorder. Am. J. Pathol. 177, 575–585.

    Not in our library10.2353/ajpath.2010.081068

  23. 23.

    Cechinel L. R. Basso C. G. Bertoldi K. Schallenberger B. de Meireles L. C. F. Siqueira I. R. (2016 ). Treadmill exercise induces age and protocol-dependent epigenetic changes in prefrontal cortex of Wistar rats. Behav. Brain Res. 313, 82–87.

    Not in our library10.1016/j.bbr.2016.07.016

  24. 24.
  25. 25.

    Chang M. Jonsson P. V. Snaedal J. Bjornsson S. Saczynski J. S. Aspelund T. (2010 ). The effect of midlife physical activity on cognitive function among older adults: ages—Reykjavik study. J. Gerontol. Ser. A 65A, 1369–1374.

    Not in our library10.1093/gerona/glq152

  26. 26.

    Chang Y. K. Etnier J. L. (2009 ). Exploring the dose-response relationship between resistance exercise intensity and cognitive function. J. Sport Exerc. Psychol. 31, 640–656.

    Not in our library10.1123/jsep.31.5.640

  27. 27.

    Chang Y. K. Labban J. D. Gapin J. I. Etnier J. L. (2012 ). The effects of acute exercise on cognitive performance: a meta-analysis. Brain Res. 1453, 87–101.

    Not in our library10.1016/j.brainres.2012.02.068

  28. 28.

    Chang Y. K. Tsai C. L. Hung T. M. So E. C. Chen F. T. Etnier J. L. (2011 ). Effects of acute exercise on executive function: a study with a tower of London task. J. Sport Exerc. Psychol. 33, 847–865.

    Not in our library10.1123/jsep.33.6.847

  29. 29.

    Chieffi S. Messina G. Villano I. Messina A. Valenzano A. Moscatelli F.. (2017 ). Neuroprotective effects of physical activity: evidence from human and animal studies. Front. Neurol. 8:188.

    Not in our library10.3389/fneur.2017.00188

  30. 30.

    Coelho F. G. de Gobbi S. Andreatto C. A. A. Corazza D. I. Pedroso R. V. Santos-Galduróz R. F. (2013 ). Physical exercise modulates peripheral levels of brain-derived neurotrophic factor (BDNF): a systematic review of experimental studies in the elderly. Arch. Gerontol. Geriatr. 56, 10–15.

    Not in our library10.1016/j.archger.2012.06.003

  31. 31.

    Colberg S. R. Somma C. T. Sechrist S. R. (2008 ). Physical activity participation may offset some of the negative impact of diabetes on cognitive function. J. Am. Med. Dir. Assoc. 9, 434–438.

    Not in our library10.1016/j.jamda.2008.03.014

  32. 32.

    Colcombe S. J. Erickson K. I. Scalf P. E. Kim J. S. Prakash R. McAuley E.. (2006 ). Aerobic exercise training increases brain volume in aging humans. J. Gerontol. A Biol. Sci. Med. Sci. 61, 1166–1170.

    Not in our library10.1093/gerona/61.11.1166

  33. 33.

    Colcombe S. Kramer A. F. (2003 ). Fitness effects on the cognitive function of older adults. Psychol. Sci. 14, 125–130.

    Not in our library10.1111/1467-9280.t01-1-01430

  34. 34.

    Craft L. L. (2005 ). Exercise and clinical depression: examining two psychological mechanisms. Psychol. Sport Exerc. 6, 151–171.

    Not in our library10.1016/j.psychsport.2003.11.003

  35. 35.

    Craft L. L. Perna F. M. (2004 ). The benefits of exercise for the clinically depressed. Prim. Care Companion J. Clin. Psychiatry 6, 104–111.

    Not in our library10.4088/pcc.v06n0301

  36. 36.

    Cutuli D. Berretta E. Caporali P. Sampedro-Piquero P. De Bartolo P. Laricchiuta D.. (2018 ). Effects of pre-reproductive maternal enrichment on maternal care, offspring's play behavior and oxytocinergic neurons. Neuropharmacology. [Epub ahead of print].

    Not in our library10.1016/j.neuropharm.2018.02.015

  37. 37.
  38. 38.

    DeBoer L. B. Powers M. B. Utschig A. C. Otto M. W. Smits J. A. J. (2012 ). Exploring exercise as an avenue for the treatment of anxiety disorders. Expert Rev. Neurother. 12, 1011–1022.

    Not in our library10.1586/ern.12.73

  39. 39.

    Deeny S. P. Poeppel D. Zimmerman J. B. Roth S. M. Brandauer J. Witkowski S.. (2008 ). Exercise, APOE, and working memory: MEG and behavioral evidence for benefit of exercise in epsilon4 carriers. Biol. Psychol. 78, 179–187.

    Not in our library10.1016/j.biopsycho.2008.02.007

  40. 40.

    Deibel S. H. Zelinski E. L. Keeley R. J. Kovalchuk O. McDonald R. J. (2015 ). Epigenetic alterations in the suprachiasmatic nucleus and hippocampus contribute to age-related cognitive decline. Oncotarget 6, 23181–23203.

    Not in our library10.18632/oncotarget.4036

  41. 41.

    De Moor M. H. Beem A. L. Stubbe J. H. Boomsma D. I. De Geus E. J. C. (2006 ). Regular exercise, anxiety, depression and personality: a population-based study. Prev. Med. 42, 273–279.

    Not in our library10.1016/j.ypmed.2005.12.002

  42. 42.

    de Souza Moura A. M. Lamego M. K. Paes F. Rocha N. B. F. Simoes-Silva V. Rocha S. A.. (2015 ). Comparison among aerobic exercise and other types of interventions to treat depression: a systematic review. CNS Neurol. Disord. Drug Targets 14, 1171–1183.

    Not in our library10.2174/1871527315666151111120714

  43. 43.

    Dietrich A. McDaniel W. F. (2004 ). Endocannabinoids and exercise. Br. J. Sports Med. 38, 536–541.

    Not in our library10.1136/bjsm.2004.011718

  44. 44.

    Ding Q. Vaynman S. Akhavan M. Ying Z. Gomez-Pinilla F. (2006 ). Insulin-like growth factor I interfaces with brain-derived neurotrophic factor-mediated synaptic plasticity to modulate aspects of exercise-induced cognitive function. Neuroscience 140, 823–833.

    Not in our library10.1016/j.neuroscience.2006.02.084

  45. 45.

    Donnelly J. E. Hillman C. H. Castelli D. Etnier J. L. Lee S. Tomporowski P. (2016 ). Physical activity, fitness, cognitive function, and academic achievement in children. Med. Sci. Sport. Exerc. 48, 1197–1222.

    Not in our library10.1249/mss.0000000000000901

  46. 46.

    Douw L. Nieboer D. van Dijk B. W. Stam C. J. Twisk J. W. (2014 ). A healthy brain in a healthy body: brain network correlates of physical and mental fitness. PLoS ONE 9:e88202.

    Not in our library10.1371/journal.pone.0088202

  47. 47.

    Ehninger D. Kempermann G. (2003 ). Regional effects of wheel running and environmental enrichment on cell genesis and microglia proliferation in the adult murine neocortex. Cereb. Cortex 13, 845–851.

    Not in our library10.1093/cercor/13.8.845

  48. 48.

    Ekstrand J. Hellsten J. Tingström A. (2008 ). Environmental enrichment, exercise and corticosterone affect endothelial cell proliferation in adult rat hippocampus and prefrontal cortex. Neurosci. Lett. 442, 203–207.

    Not in our library10.1016/j.neulet.2008.06.085

  49. 49.

    Erickson K. I. Miller D. L. Weinstein A. M. Akl S. L. Banducci S. (2012 ). Physical activity and brain plasticity in late adulthood: a conceptual and comprehensive review. Ageing Res. 3, 34–47.

    Not in our library10.4081/ar.2012.e6

  50. 50.

    Erickson K. I. Prakash R. S. Voss M. W. Chaddock L. Hu L. Morris K. S.. (2009 ). Aerobic fitness is associated with hippocampal volume in elderly humans. Hippocampus 19, 1030–1039.

    Not in our library10.1002/hipo.20547

  51. 51.

    Erickson K. I. Voss M. W. Prakash R. S. Basak C. Szabo A. Chaddock L.. (2011 ). Exercise training increases size of hippocampus and improves memory. Proc. Natl. Acad. Sci. U.S.A. 108, 3017–3022.

    Not in our library10.1073/pnas.1015950108

  52. 52.

    Farioli-Vecchioli S. Sacchetti S. di Robilant N. V. Cutuli D. (2018 ). The role of physical exercise and omega-3 fatty acids in depressive illness in the elderly. Curr. Neuropharmacol. 16, 308–326.

    Not in our library10.2174/1570159x15666170912113852

  53. 53.

    Fernandes J. Arida R. M. Gomez-Pinilla F. (2017 ). Physical exercise as an epigenetic modulator of brain plasticity and cognition. Neurosci. Biobehav. Rev. 80, 443–456.

    Not in our library10.1016/j.neubiorev.2017.06.012

  54. 54.

    Ferreira-Vieira T. H. Bastos C. P. Pereira G. S. Moreira F. A. Massensini A. R. (2014 ). A role for the endocannabinoid system in exercise-induced spatial memory enhancement in mice. Hippocampus 24, 79–88.

    Not in our library10.1002/hipo.22206

  55. 55.

    Foster P. P. (2015 ). Role of physical and mental training in brain network configuration. Front. Aging Neurosci. 7:117.

    Not in our library10.3389/fnagi.2015.00117

  56. 56.

    Fox K. R. (2000 ). Self-esteem, self-perceptions and exercise. Int. J. Sport Psychol. 31, 228–240.

    Not in our library

  57. 57.

    Fuss J. Steinle J. Bindila L. Auer M. K. Kirchherr H. Lutz B.. (2015 ). A runner's high depends on cannabinoid receptors in mice. Proc. Natl. Acad. Sci. U.S.A. 112, 13105–13108.

    Not in our library10.1073/pnas.1514996112

  58. 58.

    Gelfo F. Mandolesi L. Serra L. Sorrentino G. Caltagirone C. (2018 ). The neuroprotective effects of experience on cognitive functions: evidence from animal studies on the neurobiological bases of brain reserve. Neuroscience 370, 218–235.

    Not in our library10.1016/j.neuroscience.2017.07.065

  59. 59.

    Giesen E. S. Deimel H. Bloch W. (2015 ). Clinical exercise interventions in alcohol use disorders: a systematic review. J. Subst. Abuse Treat. 52, 1–9.

    Not in our library10.1016/j.jsat.2014.12.001

  60. 60.

    Gomes da Silva S. Araujo B. H. S. Cossa A. C. Scorza F. A. Cavalheiro E. A. Naffah-Mazzacoratti Mda G.. (2010 ). Physical exercise in adolescence changes CB1 cannabinoid receptor expression in the rat brain. Neurochem. Int. 57, 492–496.

    Not in our library10.1016/j.neuint.2010.07.001

  61. 61.
  62. 62.

    Grego F. Vallier J. M. Collardeau M. Rousseu C. Cremieux J. Brisswalter J. (2005 ). Influence of exercise duration and hydration status on cognitive function during prolonged cycling exercise. Int. J. Sports Med. 26, 27–33.

    Not in our library10.1055/s-2004-817915

  63. 63.

    Haasova M. Warren F. C. Ussher M. Janse Van Rensburg K. Faulkner G. Cropley M.. (2013 ). The acute effects of physical activity on cigarette cravings: systematic review and meta-analysis with individual participant data. Addiction 108, 26–37.

    Not in our library10.1111/j.1360-0443.2012.04034.x

  64. 64.

    Hillman C. H. Erickson K. I. Kramer A. F. (2008 ). Be smart, exercise your heart: exercise effects on brain and cognition. Nat. Rev. Neurosci. 9, 58–65.

    Not in our library10.1038/nrn2298

  65. 65.

    Hirase H. Shinohara Y. (2014 ). Transformation of cortical and hippocampal neural circuit by environmental enrichment. Neuroscience 280, 282–298.

    Not in our library10.1016/j.neuroscience.2014.09.031

  66. 66.
  67. 67.

    Hötting K. Röder B. (2013 ). Beneficial effects of physical exercise on neuroplasticity and cognition. Neurosci. Biobehav. Rev. 37, 2243–2257.

    Not in our library10.1016/j.neubiorev.2013.04.005

  68. 68.

    Hötting K. Schickert N. Kaiser J. Röder B. Schmidt-Kassow M. (2016 ). The effects of acute physical exercise on memory, peripheral bdnf, and cortisol in young adults. Neural Plast. 2016, 1–12.

    Not in our library10.1155/2016/6860573

  69. 69.

    Hu T. Zhou F. J. Chang Y. F. Li Y. S. Liu G. C. Hong Y.. (2015 ). miR21 is associated with the cognitive improvement following voluntary running wheel exercise in TBI mice. J. Mol. Neurosci. 57, 114–122.

    Not in our library10.1007/s12031-015-0584-8

  70. 70.

    Huang P. Fang R. Li B. Y. Chen S.-D. (2016 ). Exercise-related changes of networks in aging and mild cognitive impairment brain. Front. Aging Neurosci. 8:47.

    Not in our library10.3389/fnagi.2016.00047

  71. 71.

    Ieraci A. Mallei A. Musazzi L. Popoli M. (2015 ). Physical exercise and acute restraint stress differentially modulate hippocampal brain-derived neurotrophic factor transcripts and epigenetic mechanisms in mice. Hippocampus 25, 1380–1392.

    Not in our library10.1002/hipo.22458

  72. 72.

    Isaacs K. R. Anderson B. J. Alcantara A. A. Black J. E. Greenough W. T. (1992 ). Exercise and the brain: angiogenesis in the adult rat cerebellum after vigorous physical activity and motor skill learning. J. Cereb. Blood Flow Metab. 12, 110–119.

    Not in our library10.1038/jcbfm.1992.14

  73. 73.

    Ji E. S. Kim Y. M. Shin M. S. Kim C. J. Lee K. S. Kim K.. (2015 ). Treadmill exercise enhances spatial learning ability through suppressing hippocampal apoptosis in Huntington's disease rats. J. Exerc. Rehabil. 11, 133–139.

    Not in our library10.12965/jer.150212

  74. 74.

    Kim S. Kaang B.-K. (2017 ). Epigenetic regulation and chromatin remodeling in learning and memory. Exp. Mol. Med. 49:e281.

    Not in our library10.1038/emm.2016.140

  75. 75.

    Kleim J. A. Cooper N. R. VandenBerg P. M. (2002 ). Exercise induces angiogenesis but does not alter movement representations within rat motor cortex. Brain Res. 934, 1–6.

    Not in our library10.1016/s0006-8993(02)02239-4

  76. 76.

    Knapen J. Sommerijns E. Vancampfort D. Sienaert P. Pieters G. Haake P.. (2009 ). State anxiety and subjective well-being responses to acute bouts of aerobic exercise in patients with depressive and anxiety disorders. Br. J. Sports Med. 43, 756–759.

    Not in our library10.1136/bjsm.2008.052654

  77. 77.

    Korb A. Bonetti L. V. Da Silva S. A. Marcuzzo S. Ilha J. Bertagnolli M.. (2010 ). Effect of treadmill exercise on serotonin immunoreactivity in medullary raphe nuclei and spinal cord following sciatic nerve transection in rats. Neurochem. Res. 35, 380–389.

    Not in our library10.1007/s11064-009-0066-x

  78. 78.

    Kou X. Li J. Liu X. Chang J. Zhao Q. Jia S.. (2017 ). Swimming attenuates d-galactose-induced brain aging via suppressing miR-34a-mediated autophagy impairment and abnormal mitochondrial dynamics. J. Appl. Physiol. 122, 1462–1469.

    Not in our library10.1152/japplphysiol.00018.2017

  79. 79.

    Kramer A. F. Hahn S. Cohen N. J. Banich M. T. McAuley E. Harrison C. R.. (1999 ). Ageing, fitness and neurocognitive function. Nature 400, 418–419.

    Not in our library10.1038/22682

  80. 80.

    Kronenberg G. Bick-Sander A. Bunk E. Wolf C. Ehninger D. Kempermann G. (2006 ). Physical exercise prevents age-related decline in precursor cell activity in the mouse dentate gyrus. Neurobiol. Aging 27, 1505–1513.

    Not in our library10.1016/j.neurobiolaging.2005.09.016

  81. 81.

    Lafenetre P. Leske O. Wahle P. Heumann R. (2011 ). The beneficial effects of physical activity on impaired adult neurogenesis and cognitive performance. Front. Neurosci. 5:51.

    Not in our library10.3389/fnins.2011.00051

  82. 82.

    Lambourne K. Tomporowski P. (2010 ). The effect of exercise-induced arousal on cognitive task performance: a meta-regression analysis. Brain Res. 1341, 12–24.

    Not in our library10.1016/j.brainres.2010.03.091

  83. 83.

    Landers D. M. Arent S. M. (2001 ). Physical activity and mental health, in Handbook of Sport Psychology, eds Singer R. N. Hausenblas H. A. Janelle C. (New York, NY: Wiley), 740–765.

    Not in our library

  84. 84.

    Langdon K. D. Corbett D. (2012 ). Improved working memory following novel combinations of physical and cognitive activity. Neurorehabil. Neural Repair 26, 523–532.

    Not in our library10.1177/1545968311425919

  85. 85.
  86. 86.
  87. 87.

    Lin T. W. Shih Y. H. Chen S. J. Lien C. H. Chang C. Y. Huang T. Y.. (2015 ). Running exercise delays neurodegeneration in amygdala and hippocampus of Alzheimer's disease (APP/PS1) transgenic mice. Neurobiol. Learn. Mem. 118, 189–197.

    Not in our library10.1016/j.nlm.2014.12.005

  88. 88.

    Lista I. Sorrentino G. (2010 ). Biological mechanisms of physical activity in preventing cognitive decline. Cell. Mol. Neurobiol. 30, 493–503.

    Not in our library10.1007/s10571-009-9488-x

  89. 89.

    Loprinzi P. D. Frith E. Edwards M. K. Sng E. Ashpole N. (2018 ). The effects of exercise on memory function among young to middle-aged adults: systematic review and recommendations for future research. Am. J. Heal. Promot. 32, 691–704.

    Not in our library10.1177/0890117117737409

  90. 90.

    Ludyga S. Gerber M. Brand S. Holsboer-Trachsler E. Pühse U. (2016 ). Acute effects of moderate aerobic exercise on specific aspects of executive function in different age and fitness groups: a meta-analysis. Psychophysiology 53, 1611–1626.

    Not in our library10.1111/psyp.12736

  91. 91.

    Maejima H. Kanemura N. Kokubun T. Murata K. Takayanagi K. (2018 ). Exercise enhances cognitive function and neurotrophin expression in the hippocampus accompanied by changes in epigenetic programming in senescence-accelerated mice. Neurosci. Lett. 665, 67–73.

    Not in our library10.1016/j.neulet.2017.11.023

  92. 92.

    Mammen G. Faulkner G. (2013 ). Physical activity and the prevention of depression: a systematic review of prospective studies. Am. J. Prev. Med. 45, 649–657.

    Not in our library10.1016/j.amepre.2013.08.001

  93. 93.

    Mandolesi L. Gelfo F. Serra L. Montuori S. Polverino A. Curcio G.. (2017 ). Environmental factors promoting neural plasticity: insights from animal and human studies. Neural Plast. 2017, 1–10.

    Not in our library10.1155/2017/7219461

  94. 94.

    Marsh H. W. Sonstroem R. J. (1995 ). Importance ratings and specific components of physical self-concept: relevance to predicting global components of self-concept and exercise. J. Sport Exerc. Psychol. 17, 84–104.

    Not in our library10.1123/jsep.17.1.84

  95. 95.

    Martinsen E. W. (1990 ). Benefits of exercise for the treatment of depression. Sports Med. 9, 380–389.

    Not in our library10.2165/00007256-199009060-00006

  96. 96.

    Meyer J. D. Ellingson L. D. Koltyn K. F. Stegner A. J. Kim J. S. Cook D. B. (2016a ). Psychobiological responses to preferred and prescribed intensity exercise in major depressive disorder. Med. Sci. Sports Exerc. 48, 2207–2215.

    Not in our library10.1249/mss.0000000000001022

  97. 97.

    Meyer J. D. Koltyn K. F. Stegner A. J. Kim J.-S. Cook D. B. (2016b ). Relationships between serum BDNF and the antidepressant effect of acute exercise in depressed women. Psychoneuroendocrinology 74, 286–294.

    Not in our library10.1016/j.psyneuen.2016.09.022

  98. 98.

    Molteni R. Ying Z. Gómez-Pinilla F. (2002 ). Differential effects of acute and chronic exercise on plasticity-related genes in the rat hippocampus revealed by microarray. Eur. J. Neurosci. 16, 1107–1116.

    Not in our library10.1046/j.1460-9568.2002.02158.x

  99. 99.

    Niemann C. Godde B. Staudinger U. M. Voelcker-Rehage C. (2014 ). Exercise-induced changes in basal ganglia volume and cognition in older adults. Neuroscience 281, 147–163.

    Not in our library10.1016/j.neuroscience.2014.09.033

  100. 100.

    Nithianantharajah J. Hannan A. J. (2006 ). Enriched environments, experience-dependent plasticity and disorders of the nervous system. Nat. Rev. Neurosci. 7, 697–709.

    Not in our library10.1038/nrn1970

  101. 101.

    Pahng A. R. McGinn M. A. Paulsen R. I. (2017 ). The prefrontal cortex as a critical gate of negative affect and motivation in alcohol use disorder. Curr. Opin. Behav. Sci. 13, 139–143.

    Not in our library10.1016/j.cobeha.2016.11.004

  102. 102.

    Pan-Vazquez A. Rye N. Ameri M. McSparron B. Smallwood G. Bickerdyke J.. (2015 ). Impact of voluntary exercise and housing conditions on hippocampal glucocorticoid receptor, miR-124 and anxiety. Mol. Brain 8:40.

    Not in our library10.1186/s13041-015-0128-8

  103. 103.

    Pedrinolla A. Schena F. Venturelli M. (2017 ). Resilience to Alzheimer's disease: the role of physical activity. Curr. Alzheimer Res. 14, 546–553.

    Not in our library10.2174/1567205014666170111145817

  104. 104.

    Penedo F. J. Dahn J. R. (2005 ). Exercise and well-being: a review of mental and physical health benefits associated with physical activity. Curr. Opin. Psychiatry 18, 189–193.

    Not in our library10.1097/00001504-200503000-00013

  105. 105.

    Pereira A. C. Huddleston D. E. Brickman A. M. Sosunov A. A. Hen R. McKhann G. M.. (2007 ). An in vivo correlate of exercise-induced neurogenesis in the adult dentate gyrus. Proc. Natl. Acad. Sci. U.S.A. 104, 5638–5643.

    Not in our library10.1073/pnas.0611721104

  106. 106.

    Petrosini L. De Bartolo P. Foti F. Gelfo F. Cutuli D. Leggio M. G.. (2009 ). On whether the environmental enrichment may provide cognitive and brain reserves. Brain Res. Rev. 61, 221–239.

    Not in our library10.1016/j.brainresrev.2009.07.002

  107. 107.

    Querido J. S. Sheel A. W. (2007 ). Regulation of cerebral blood flow during exercise. Sport. Med. 37, 765–782.

    Not in our library10.2165/00007256-200737090-00002

  108. 108.

    Raedeke T. D. (2007 ). The relationship between enjoyment and affective responses to exercise. J. Appl. Sport Psychol. 19, 105–115.

    Not in our library10.1080/10413200601113638

  109. 109.

    Richter H. Ambrée O. Lewejohann L. Herring A. Keyvani K. Paulus W. (2008 ). Wheel-running in a transgenic mouse model of Alzheimer's disease: protection or symptom? Behav. Brain Res. 190, 74–84.

    Not in our library10.1016/j.bbr.2008.02.005

  110. 110.

    Robinson A. M. Eggleston R. L. Bucci D. J. (2012 ). Physical exercise and catecholamine reuptake inhibitors affect orienting behavior and social interaction in a rat model of attention-deficit/hyperactivity disorder. Behav. Neurosci. 126, 762–771.

    Not in our library10.1037/a0030488

  111. 111.

    Rodgers W. M. Markland D. Selzler A. M. Murray T. C. Wilson P. M. (2014 ). Distinguishing perceived competence and self-efficacy: an example from exercise. Res. Q. Exerc. Sport 85, 527–539.

    Not in our library10.1080/02701367.2014.961050

  112. 112.

    Saab B. J. Mansuy I. M. (2014 ). Neuroepigenetics of memory formation and impairment: the role of microRNAs. Neuropharmacology 80, 61–69.

    Not in our library10.1016/j.neuropharm.2014.01.026

  113. 113.

    Sachs M. L. (1981 ). Running addiction, in Psychology of Running, eds Sachs M. H. Sachs M. L. (Champaign, IL: Human Kinetics), 116–127.

    Not in our library

  114. 114.

    Schwellnus M. Soligard T. Alonso J.-M. Bahr R. Clarsen B. Dijkstra H. P.. (2016 ). How much is too much? (Part 2) International Olympic Committee consensus statement on load in sport and risk of illness. Br. J. Sports Med. 50, 1043–1052.

    Not in our library10.1136/bjsports-2016-096572

  115. 115.

    Scully D. Kremer J. Meade M. M. Graham R. Dudgeon K. (1998 ). Physical exercise and psychological well being: a critical review. Br. J. Sports Med. 32, 111–120.

    Not in our library10.1136/bjsm.32.2.111

  116. 116.

    Serra L. Cercignani M. Petrosini L. Basile B. Perri R. Fadda L.. (2011 ). Neuroanatomical correlates of cognitive reserve in alzheimer disease. Rejuvenation Res. 14, 143–151.

    Not in our library10.1089/rej.2010.1103

  117. 117.
  118. 118.

    Sibley B. A. Etnier J. L. (2003 ). The relationship between physical activity and cognition in children: a meta-analysis. Pediatr. Exerc. Sci. 15, 243–256.

    Not in our library10.1123/pes.15.3.243

  119. 119.

    Sim Y. J. (2014 ). Treadmill exercise alleviates impairment of spatial learning ability through enhancing cell proliferation in the streptozotocin-induced Alzheimer's disease rats. J. Exerc. Rehabil. 10, 81–88.

    Not in our library10.12965/jer.140102

  120. 120.

    Snigdha S. de Rivera C. Milgram N. W. Cotman C. W. (2014 ). Exercise enhances memory consolidation in the aging brain. Front. Aging Neurosci. 6:3.

    Not in our library10.3389/fnagi.2014.00003

  121. 121.

    Steiner B. Kronenberg G. Jessberger S. Brandt M. D. Reuter K. Kempermann G. (2004 ). Differential regulation of gliogenesis in the context of adult hippocampal neurogenesis in mice. Glia 46, 41–52.

    Not in our library10.1002/glia.10337

  122. 122.

    Stern Y. (2002 ). What is cognitive reserve? Theory and research application of the reserve concept. J. Int. Neuropsychol. Soc. 8, 448–460.

    Not in our library10.1017/s1355617702813248

  123. 123.

    Stern Y. (2009 ). Cognitive reserve. Neuropsychologia 47, 2015–2028.

    Not in our library10.1016/j.neuropsychologia.2009.03.004

  124. 124.

    Stern Y. (2012 ). Cognitive reserve in ageing and Alzheimer's disease. Lancet Neurol. 11, 1006–1012.

    Not in our library10.1016/s1474-4422(12)70191-6

  125. 125.

    Stessman J. Hammerman-Rozenberg R. Cohen A. Ein-Mor E. Jacobs J. M. (2009 ). Physical activity, function, and longevity among the very old. Arch. Intern. Med. 169, 1476–1483.

    Not in our library10.1001/archinternmed.2009.248

  126. 126.

    Swain R. A. Harris A. B. Wiener E. C. Dutka M. V. Morris H. D. Theien B. E.. (2003 ). Prolonged exercise induces angiogenesis and increases cerebral blood volume in primary motor cortex of the rat. Neuroscience 117, 1037–1046.

    Not in our library10.1016/s0306-4522(02)00664-4

  127. 127.

    Thomas S. N. Schroeder T. Secher N. H. Mitchell J. H. (1989 ). Cerebral blood flow during submaximal and maximal dynamic exercise in humans. J. Appl. Physiol. 67, 744–748.

    Not in our library10.1152/jappl.1989.67.2.744

  128. 128.

    Thomson D. Turner A. Lauder S. Gigler M. E. Berk L. Singh A. B.. (2015 ). A brief review of exercise, bipolar disorder, and mechanistic pathways. Front. Psychol. 6:147.

    Not in our library10.3389/fpsyg.2015.00147

  129. 129.

    Tiryaki-Sonmez G. Vatansever S. Olcucu B. Schoenfeld B. (2015 ). Obesity, food intake and exercise: relationship with ghrelin. Biomed. Hum. Kinet. 7, 116–124.

    Not in our library10.1515/bhk-2015-0018

  130. 130.

    Tomporowski P. D. (2003 ). Effects of acute bouts of exercise on cognition. Acta Psychol. 112, 297–324.

    Not in our library10.1016/s0001-6918(02)00134-8

  131. 131.

    Urso M. L. Clarkson P. M. (2003 ). Oxidative stress, exercise, and antioxidant supplementation. Toxicology 189, 41–54.

    Not in our library10.1016/s0300-483x(03)00151-3

  132. 132.

    van Praag H. (2009 ). Exercise and the brain: something to chew on. Trends Neurosci. 32, 283–290.

    Not in our library10.1016/j.tins.2008.12.007

  133. 133.

    van Praag H. Christie B. R. Sejnowski T. J. Gage F. H. (1999a ). Running enhances neurogenesis, learning, and long-term potentiation in mice. Proc. Natl. Acad. Sci. U.S.A. 96, 13427–13431.

    Not in our library10.1073/pnas.96.23.13427

  134. 134.

    van Praag H. Kempermann G. Gage F. H. (1999b ). Running increases cell proliferation and neurogenesis in the adult mouse dentate gyrus. Nat. Neurosci. 2, 266–270.

    Not in our library10.1038/6368

  135. 135.

    van Praag H. Shubert T. Zhao C. Gage F. H. (2005 ). Exercise enhances learning and hippocampal neurogenesis in aged mice. J. Neurosci. 25, 8680–8685.

    Not in our library10.1523/jneurosci.1731-05.2005

  136. 136.

    Vatansever-Ozen S. Tiryaki-Sonmez G. Bugdayci G. Ozen G. (2011 ). The effects of exercise on food intake and hunger: relationship with acylated ghrelin and leptin. J. Sports Sci. Med. 10, 283–291.

    Not in our library

  137. 137.

    Vaynman S. Ying Z. Gomez-Pinilla F. (2004 ). Hippocampal BDNF mediates the efficacy of exercise on synaptic plasticity and cognition. Eur. J. Neurosci. 20, 2580–2590.

    Not in our library10.1111/j.1460-9568.2004.03720.x

  138. 138.

    Voss M. W. Chaddock L. Kim J. S. VanPatter M. Pontifex M. B. Raine L. B.. (2011 ). Aerobic fitness is associated with greater efficiency of the network underlying cognitive control in preadolescent children. Neuroscience 199, 166–176.

    Not in our library10.1016/j.neuroscience.2011.10.009

  139. 139.

    Waddington C. H. (1939 ). An Introduction to Modern Genetics. London: George Allen and Unwin Ltd.

    Not in our library

  140. 140.

    Wang J. Fan Y. Dong Y. Ma M. Ma Y. Dong Y.. (2016 ). Alterations in brain structure and functional connectivity in alcohol dependent patients and possible association with impulsivity. PLoS ONE 11:e0161956.

    Not in our library10.1371/journal.pone.0161956

  141. 141.

    Weinberg R. S. Gould D. (2015 ). Foundations of sport and exercise psychology, 6th Edn. Champaign, IL: Human Kinetics.

    Not in our library

  142. 142.

    Windle G. Hughes D. Linck P. Russell I. Woods B. (2010 ). Is exercise effective in promoting mental well-being in older age? A systematic review. Aging Ment. Health 14, 652–669.

    Not in our library10.1080/13607861003713232

  143. 143.

    Winter B. Breitenstein C. Mooren F. C. Voelker K. Fobker M. Lechtermann A.. (2007 ). High impact running improves learning. Neurobiol. Learn. Mem. 87, 597–609.

    Not in our library10.1016/j.nlm.2006.11.003

  144. 144.

    World Health Organization (2010 ). Global Recommendations on Physical Activity for Health. Geneva: WHO Press.

    Not in our library

  145. 145.

    Yaffe K. Fiocco A. J. Lindquist K. Vittinghoff E. Simonsick E. M. Newman A. B.. (2009 ). Predictors of maintaining cognitive function in older adults: the Health ABC study. Neurology 72, 2029–2035.

    Not in our library10.1212/wnl.0b013e3181a92c36

  146. 146.

    Young S. N. (2007 ). How to increase serotonin in the human brain without drugs. J. Psychiatry Neurosci. 32, 394–399.

    Not in our library

  147. 147.

    Zamani Sani S. H. Fathirezaie Z. Brand S. Pühse U. Holsboer-Trachsler E. Gerber M.. (2016 ). Physical activity and self-esteem: testing direct and indirect relationships associated with psychological and physical mechanisms. Neuropsychiatr. Dis. Treat. 12, 2617–2625.

    Not in our library10.2147/ndt.s116811

  148. 148.

    Zanetti M. Shigaeff N. Menzes A. H. T. Takahashi A. A. (2017 ). Cognitive reserve: evidence of delayed of dementia - a case report. J. Dement. 1:101.

    Not in our library

  149. 149.

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