Talk:Neurobiological effects of physical exercise/Archive 2

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Work in progress

I've decided to focus on this article for GA, so I'm going to recite the vast majority of the article; hopefully I won't have to delete anything, because I don't want to do so. If anyone would like to help improve the article to the WP:MEDRS standard, feel free to do so. Seppi333 (Insert 2¢ | Maintained) 06:29, 8 December 2014 (UTC)

This article is my #1 priority now, so I'll add this content fix all the citation issues over the next 1-3 months, depending on how much time I have outside WP. Seppi333 (Insert 2¢ | Maintained) 10:47, 4 February 2015 (UTC)

Refs to use in the article

1

Antidepressant reviews from Talk:Antidepressant/Archive 2#Exercise:

Antidepressant reflist

References

  1. ^ Cooney GM, Dwan K, Greig CA, Lawlor DA, Rimer J, Waugh FR, McMurdo M, Mead GE (2013). "Exercise for depression". Cochrane Database Syst Rev. 9: CD004366. doi:10.1002/14651858.CD004366.pub6. PMID 24026850. Exercise is moderately more effective than a control intervention for reducing symptoms of depression, but analysis of methodologically robust trials only shows a smaller effect in favour of exercise. When compared to psychological or pharmacological therapies, exercise appears to be no more effective, though this conclusion is based on a few small trials.
  2. ^ Mura G, Moro MF, Patten SB, Carta MG (2014). "Exercise as an add-on strategy for the treatment of major depressive disorder: a systematic review". CNS Spectr. 19 (6): 496–508. doi:10.1017/S1092852913000953. PMID 24589012. Considered overall, the studies included in the present review showed a strong effectiveness of exercise combined with antidepressants. ... Conclusions
    This is the first review to have focused on exercise as an add-on strategy in the treatment of MDD. Our findings corroborate some previous observations that were based on few studies and which were difficult to generalize.41,51,73,92,93 Given the results of the present article, it seems that exercise might be an effective strategy to enhance the antidepressant effect of medication treatments. Moreover, we hypothesize that the main role of exercise on treatment-resistant depression is in inducing neurogenesis by increasing BDNF expression, as was demonstrated by several recent studies.
  3. ^ Josefsson T, Lindwall M, Archer T (2014). "Physical exercise intervention in depressive disorders: meta-analysis and systematic review". Scand J Med Sci Sports. 24 (2): 259–272. doi:10.1111/sms.12050. PMID 23362828. Physical activity has also become increasingly and firmly associated with improvements in mental health and psychological well-being (Mutrie, 2000; Landers & Arent, 2007). In particular, exercise is believed to be effective in preventing depression and also to significantly reduce depressive symptoms in clinical as well as in nonclinical populations (O'Neal et al., 2000; Landers & Arent, 2007). Several correlational studies show that exercise is negatively related to depressive symptoms (e.g., Galper et al., 2006; Hassmén et al., 2000). Moreover, a considerably large number of intervention studies have by now investigated the effect of various exercise programs on depression and the vast majority of them indicate that exercise significantly reduces depression (e.g., Blumenthal et al., 2007; Martinsen et al., 1985; Singh et al., 1997). ... To date, it is not possible to determine exactly how effective exercise is in reducing depression symptoms in clinical and nonclinical depressed populations, respectively. However, the results from the present meta-analysis as well as from seven earlier meta-analyses (North et al., 1990; Craft & Landers, 1998; Lawlor & Hopker, 2001; Stathopoulou et al., 2006; Mead et al., 2009; Rethorst et al., 2009; Krogh et al., 2011) indicate that exercise has a moderate to large antidepressant effect. Some meta-analytic results (e.g., Rethorst et al., 2009) suggest that exercise may be even more efficacious for clinically depressed people. ... In short, our final conclusion is that exercise may well be recommended for people with mild and moderate depression who are willing, motivated, and physically healthy enough to engage in such a program.
  4. ^ Rosenbaum S, Tiedemann A, Sherrington C, Curtis J, Ward PB (2014). "Physical activity interventions for people with mental illness: a systematic review and meta-analysis". J Clin Psychiatry. 75 (9): 964–974. doi:10.4088/JCP.13r08765. PMID 24813261. This systematic review and meta-analysis found that physical activity reduced depressive symptoms among people with a psychiatric illness. The current meta-analysis differs from previous studies, as it included participants with depressive symptoms with a variety of psychiatric diagnoses (except dysthymia and eating disorders). ... This review provides strong evidence for the antidepressant effect of physical activity; however, the optimal exercise modality, volume, and intensity remain to be determined. ... Conclusion
    Few interventions exist whereby patients can hope to achieve improvements in both psychiatric symptoms and physical health simultaneously without significant risks of adverse effects. Physical activity offers substantial promise for improving outcomes for people living with mental illness, and the inclusion of physical activity and exercise programs within treatment facilities is warranted given the results of this review.
  5. ^ Bentley SM, Pagalilauan GL, Simpson SA (2014). "Major depression". Med. Clin. North Am. 98 (5): 981–1005. doi:10.1016/j.mcna.2014.06.013. PMID 25134869.
  6. ^ Sarris J, O'Neil A, Coulson CE, Schweitzer I, Berk M (2014). "Lifestyle medicine for depression". BMC Psychiatry. 14: 107. doi:10.1186/1471-244X-14-107. PMC 3998225. PMID 24721040.{{cite journal}}: CS1 maint: unflagged free DOI (link)

2

Formatted current medical review citations with filled quote parameters:

  • Exercise epigenetics reviews: [1][2]plus Added
  • Increased gray matter volume from aerobic exercise: [3]plus Added
  • Measurable improvements in attention do not arise as an acute response to exercise, but as a response to consistent exercise: [4]plus Added
  • Exercise and trophic factors: [5]plus Added
  • Exercise - bidirectional interactions with cognitive control/executive function: [6][7][8]plus Added (Describe components of cognitive control and corresponding structures in the article.[9]plus Added)
    Also cover clinical significance/relation of cognitive control in addiction & ADHD[10] Partly done
  • Organ-specific response to exercise (acute and long-term): [11] Partly done

3

Formatted review citations, pending quotes:

  • Exercise/cognition[12]plus Added
  • Exercise, older adults, and aging: [13]
  • Exercise - biological mechanisms in health/resilience: [14]plus Added
  • Exercise effects upon stroke recovery and neuroprotection: [15]
  • Exercise effects upon mental disorders: [16]plus Added
  • Exercise in child cognition and academic performance: [17]

Effects on receptor ligands

  • Beta-Endorphin[18]plus Added
  • Endocannabinoids[19]plus Added
  • Exercise endocrinology[20] (monoamines again)

4

  • Summary ref for citing lead[21] plus Added
  • General age-related cognitive decline[22]


Neurodegenerative disorders

  • IGF-1 resistance in all 3 disorders[32]
Massive reflist

References

  1. ^ "Epigenetics in sports". Sports Med. 43 (2): 93–110. February 2013. doi:10.1007/s40279-012-0012-y. PMID 23329609. Alterations in epigenetic modification patterns have been demonstrated to be dependent on exercise and growth hormone (GH), insulin-like growth factor 1 (IGF-1), and steroid administration. ... the authors observed improved stress coping in exercised subjects. Investigating the dentate gyrus, a brain region which is involved in learning and coping with stressful and traumatic events, they could show that this effect is mediated by increased phosphorylation of serine 10 combined with H3K14 acetylation, which is associated with local opening of condensed chromatin. Consequently, they found increased immediate early gene expression as shown for c-FOS (FBJ murine osteosarcoma viral oncogene homologue). {{cite journal}}: Unknown parameter |vauthor= ignored (help)
  2. ^ "Exercise: putting action into our epigenome". Sports Med. 44 (2): 189–209. February 2014. doi:10.1007/s40279-013-0114-1. PMID 24163284. Aerobic physical exercise produces numerous health benefits in the brain. Regular engagement in physical exercise enhances cognitive functioning, increases brain neurotrophic proteins, such as brain-derived neurotrophic factor (BDNF), and prevents cognitive diseases [76–78]. Recent findings highlight a role for aerobic exercise in modulating chromatin remodelers [21, 79–82]. ... These results were the first to demonstrate that acute and relatively short aerobic exercise modulates epigenetic modifications. The transient epigenetic modifications observed due to chronic running training have also been associated with improved learning and stress-coping strategies, epigenetic changes and increased c-Fos-positive neurons ... Nonetheless, these studies demonstrate the existence of epigenetic changes after acute and chronic exercise and show they are associated with improved cognitive function and elevated markers of neurotrophic factors and neuronal activity (BDNF and c-Fos). ... The aerobic exercise training-induced changes to miRNA profile in the brain seem to be intensity-dependent [164]. These few studies provide a basis for further exploration into potential miRNAs involved in brain and neuronal development and recovery via aerobic exercise. {{cite journal}}: Unknown parameter |vauthor= ignored (help)
  3. ^ "Physical activity, fitness, and gray matter volume". Neurobiol. Aging. 35 Suppl 2: S20–528. September 2014. doi:10.1016/j.neurobiolaging.2014.03.034. PMID 24952993. Retrieved 9 December 2014. We conclude that higher cardiorespiratory fitness levels are routinely associated with greater gray matter volume in the prefrontal cortex and hippocampus and less consistently in other regions. We also conclude that physical activity is associated with greater gray matter volume in the same regions that are associated with cardiorespiratory fitness including the prefrontal cortex and hippocampus. ... Meta-analyses (Colcombe and Kramer, 2003; Smith et al., 2010) suggest that the effects of exercise on the brain might not be uniform across all regions and that some brain areas, specifically those areas supporting executive functions, might be more influenced by participation in exercise than areas not as critically involved in executive functions. ... The effects appear to be general in the sense that many different cognitive domains are improved after several months of aerobic exercise, but specific in the sense that executive functions are improved more than other cognitive domains. ... physical activity and exercise may reduce the risk for AD (Barnes and Yaffe, 2011; Podewils et al., 2005; Sofi et al., 2011) ... Erickson et al. (2010) reported that greater amounts of physical activity were associated with greater gray matter volume 9-years later in the prefrontal cortex, anterior cingulate, parietal cortex, cerebellum, and hippocampus. ... Verstynen et al. (2012) found that higher fitness levels were associated with greater volume of the caudate nucleus and nucleus accumbens, and in turn, greater volumes were associated with better performance on a task-switching paradigm. {{cite journal}}: Unknown parameter |vauthor= ignored (help)
  4. ^ "Effects of acute bouts of physical activity on children's attention: a systematic review of the literature". Springerplus. 3: 410. 2014. doi:10.1186/2193-1801-3-410. PMC 4132441. PMID 25133092. There is weak evidence for the effect of acute bouts of physical activity on attention. {{cite journal}}: Unknown parameter |vauthor= ignored (help)CS1 maint: unflagged free DOI (link)
  5. ^ "Neuroprotective effects of physical activity on the brain: a closer look at trophic factor signaling". Front Cell Neurosci. 8: 170. 2014. doi:10.3389/fncel.2014.00170. PMC 4064707. PMID 24999318. Moreover, recent evidence suggests that myokines released by exercising muscles affect the expression of brain-derived neurotrophic factor synthesis in the dentate gyrus of the hippocampus, a finding that could lead to the identification of new and therapeutically important mediating factors. ... Studies have demonstrated the intensity of exercise training is positively correlated with BDNF plasma levels in young, healthy individuals (Ferris et al., 2007). Resistance exercise has also been shown to elevate serum BDNF levels in young individuals (Yarrow et al., 2010). Moreover, it has been shown that moderate levels of physical activity in people with AD significantly increased plasma levels of BDNF (Coelho et al., 2014). ... In humans, it has been shown that 4 h of rowing activity leads to increased levels of plasma BDNF from the internal jugular (an indicator of central release from the brain) and radial artery (an indicator of peripheral release; Rasmussen et al., 2009). Seifert et al. (2010) reported that basal release of BDNF increases following 3 months endurance training in young and healthy individuals, as measured from the jugular vein. These trends are augmented by rodent studies showing that endurance training leads to increased synthesis of BDNF in the hippocampal formation (Neeper et al., 1995, 1996). ... Both BDNF and IGF-1 play a significant role in cognition and motor function in humans. ... Multiple large-scale studies in humans have shown that serum levels of IGF-1 are correlated with fitness and as well as body mass indices (Poehlman and Copeland, 1990). Furthermore, animal studies have shown that exercise in rats is associated with increased amounts of IGF-1 in the CSF. {{cite journal}}: Unknown parameter |vauthor= ignored (help)CS1 maint: unflagged free DOI (link)
  6. ^ "Benefits of regular aerobic exercise for executive functioning in healthy populations". Psychon Bull Rev. 20 (1): 73–86. February 2013. doi:10.3758/s13423-012-0345-4. PMID 23229442. Executive functions are strategic in nature and depend on higher-order cognitive processes that underpin planning, sustained attention, selective attention, resistance to interference, volitional inhibition, working memory, and mental flexibility ... Data to date from studies of aging provide strong evidence of exercise-linked benefits related to task switching, selective attention, inhibition of prepotent responses, and working memory capacity; furthermore, cross-sectional fitness data suggest that working memory updating could potentially benefit as well. In young adults, working memory updating is the main executive function shown to benefit from regular exercise, but cross-sectional data further suggest that task-switching and post-error performance may also benefit. In children, working memory capacity has been shown to benefit, and cross-sectional data suggest potential benefits for selective attention and inhibitory control. ... Support for the idea that higher levels of aerobic activity may be associated with superior brain structure has been gained through cross-sectional studies in older adults and children (for a recent review, see Voss, Nagamatsu, et al., 2011). ... only those in the aerobic exercise group exhibited improved connectivity between the left and right prefrontal cortices, two areas that are crucial to the effective functioning of the fronto-executive network. ... Together, these studies provide evidence that regular aerobic exercise benefits control over responses during selective attention in older adults. ... aerobic fitness is a good predictor of performance on tasks that rely relatively heavily on inhibitory control over prepotent responses (e.g., Colcombe et al., 2004, Study 1; Prakash et al., 2011) and also that regular aerobic exercise improves performance on such tasks ... Overall, the results from the span and Sternberg tasks suggest that regular exercise can also confer benefits for the volume of information that children and older adults can hold in mind at one time. {{cite journal}}: Unknown parameter |vauthor= ignored (help)
  7. ^ "Cognitive control in the self-regulation of physical activity and sedentary behavior". Front Hum Neurosci. 8: 747. 2014. doi:10.3389/fnhum.2014.00747. PMC 4179677. PMID 25324754. Recent theory (e.g., Temporal Self-Regulation Theory; Hall and Fong, 2007, 2010, 2013) and evidence suggest that the relation between physical activity and cognitive control is reciprocal (Daly et al., 2013). Most research has focused on the beneficial effects of regular physical activity on executive functions-the set of neural processes that define cognitive control. Considerable evidence shows that regular physical activity is associated with enhanced cognitive functions, including attention, processing speed, task switching, inhibition of prepotent responses and declarative memory (for reviews see Colcombe and Kramer, 2003; Smith et al., 2010; Guiney and Machado, 2013; McAuley et al., 2013). Recent research demonstrates a dose-response relationship between fitness and spatial memory (Erickson et al., 2011) ... The effects of physical activity on cognitive control appear to be underpinned by a variety of brain processes including: increased hippocampal volume, increased gray matter density in the prefrontal cortex (PFC), upregulation of neurotrophins and greater microvascular density ... Together, this research suggests that an improvement in control processes, such as attention and inhibition or interference control, is associated with an improvement in self-regulation of physical activity. ... Increasingly, research shows that cognitive control abilities are malleable, and that cognitive training can produce positive cognitive outcomes and improvements in daily function (Willis et al., 2006; Hertzog et al., 2008) that can have long-lasting effects (Rebok et al., 2014). Approaches to cognitive training are numerous and varied; however, the relative superiority of different approaches with regard to training and transfer continue to be debated. {{cite journal}}: Unknown parameter |vauthor= ignored (help)CS1 maint: unflagged free DOI (link)
  8. ^ "Executive functions". Annu Rev Psychol. 64: 135–168. 2013. doi:10.1146/annurev-psych-113011-143750. PMC 4084861. PMID 23020641. Core EFs are inhibition [response inhibition (self-control—resisting temptations and resisting acting impulsively) and interference control (selective attention and cognitive inhibition)], working memory, and cognitive flexibility (including creatively thinking "outside the box," seeing anything from different perspectives, and quickly and flexibly adapting to changed circumstances). ... EFs and prefrontal cortex are the first to suffer, and suffer disproportionately, if something is not right in your life. They suffer first, and most, if you are stressed (Arnsten 1998, Liston et al. 2009, Oaten & Cheng 2005), sad (Hirt et al. 2008, von Hecker & Meiser 2005), lonely (Baumeister et al. 2002, Cacioppo & Patrick 2008, Campbell et al. 2006, Tun et al. 2012), sleep deprived (Barnes et al. 2012, Huang et al. 2007), or not physically fit (Best 2010, Chaddock et al. 2011, Hillman et al. 2008). Any of these can cause you to appear to have a disorder of EFs, such as ADHD, when you do not. You can see the deleterious effects of stress, sadness, loneliness, and lack of physical health or fitness at the physiological and neuroanatomical level in prefrontal cortex and at the behavioral level in worse EFs (poorer reasoning and problem solving, forgetting things, and impaired ability to exercise discipline and self-control). ...
    EFs can be improved (Diamond & Lee 2011, Klingberg 2010). ... At any age across the life cycle EFs can be improved, including in the elderly and in infants. There has been much work with excellent results on improving EFs in the elderly by improving physical fitness (Erickson & Kramer 2009, Voss et al. 2011) ... Inhibitory control (one of the core EFs) involves being able to control one's attention, behavior, thoughts, and/or emotions to override a strong internal predisposition or external lure, and instead do what's more appropriate or needed. Without inhibitory control we would be at the mercy of impulses, old habits of thought or action (conditioned responses), and/or stimuli in the environment that pull us this way or that. Thus, inhibitory control makes it possible for us to change and for us to choose how we react and how we behave rather than being unthinking creatures of habit. It doesn't make it easy. Indeed, we usually are creatures of habit and our behavior is under the control of environmental stimuli far more than we usually realize, but having the ability to exercise inhibitory control creates the possibility of change and choice.     {{cite journal}}: Unknown parameter |vauthor= ignored (help)
  9. ^ Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 13: Higher Cognitive Function and Behavioral Control". In Sydor A, Brown RY (ed.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. p. 315. ISBN 9780071481274. Several subregions of the prefrontal cortex have been implicated in partly distinct aspects of cognitive control, although these distinctions remain somewhat vaguely defined. The anterior cingulate cortex is involved in processes that require correct decision-making, as seen in conflict resolution (eg, the Stroop test, see in Chapter 16), or cortical inhibition (eg, stopping one task and switching to another). The medial prefrontal cortex is involved in supervisory attentional functions (eg, action-outcome rules) and behavioral flexibility (the ability to switch strategies). The dorsolateral prefrontal cortex, the last brain area to undergo myelination during development in late adolescence, is implicated in matching sensory inputs with planned motor responses. The ventromedial prefrontal cortex seems to regulate social cognition, including empathy. The orbitofrontal cortex is involved in social decision making and in representing the valuations assigned to different experiences. It is also implicated in impulsive and compulsive behaviors.{{cite book}}: CS1 maint: multiple names: authors list (link)
  10. ^ Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 13: Higher Cognitive Function and Behavioral Control". In Sydor A, Brown RY (ed.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 313–321. ISBN 9780071481274.
     • Executive function, the cognitive control of behavior, depends on the prefrontal cortex, which is highly developed in higher primates and especially humans.
     • Working memory is a short-term, capacitylimited cognitive buffer that stores information and permits its manipulation to guide decisionmaking and behavior. ...
     • Attention depends on working memory and on mechanisms that filter sensory inputs for access to working memory.
     • Attention and working memory are modulated by drugs that directly or indirectly stimulate dopamine D1 receptors and noradrenergic receptors. ...
     • Structures in the medial temporal lobe, such as the hippocampus, are particularly important for the temporary storage of declarative memories.
     • The striatum plays a central role in procedural and habit memory. ...
    These diverse inputs and back projections to both cortical and subcortical structures put the prefrontal cortex in a position to exert what is often called "top-down" control or cognitive control of behavior. ... The prefrontal cortex receives inputs not only from other cortical regions, including association cortex, but also, via the thalamus, inputs from subcortical structures subserving emotion and motivation, such as the amygdala (Chapter 14) and ventral striatum (or nucleus accumbens; Chapter 15). ...

    Adaptive responses depend on the ability to inhibit automatic or prepotent responses (eg, to ravenously eat the dessert or run from the snake) given certain social or environmental contexts or chosen goals and, in those circumstances, to select more appropriate responses. In conditions in which prepotent responses tend to dominate behavior, such as in drug addiction, where drug cues can elicit drug seeking (Chapter 15), or in attention deficit hyperactivity disorder (ADHD; described below), significant negative consequences can result. ... ADHD can be conceptualized as a disorder of executive function; specifically, ADHD is characterized by reduced ability to exert and maintain cognitive control of behavior. Compared with healthy individuals, those with ADHD have diminished ability to suppress inappropriate prepotent responses to stimuli (impaired response inhibition) and diminished ability to inhibit responses to irrelevant stimuli (impaired interference suppression). ... Functional neuroimaging in humans demonstrates activation of the prefrontal cortex and caudate nucleus (part of the striatum) in tasks that demand inhibitory control of behavior. Subjects with ADHD exhibit less activation of the medial prefrontal cortex than healthy controls even when they succeed in such tasks and utilize different circuits.    {{cite book}}: CS1 maint: multiple names: authors list (link)
  11. ^ Heinonen I, Kalliokoski KK, Hannukainen JC, Duncker DJ, Nuutila P, Knuuti J (November 2014). "Organ-Specific Physiological Responses to Acute Physical Exercise and Long-Term Training in Humans". Physiology (Bethesda). 29 (6): 421–436. doi:10.1152/physiol.00067.2013. PMID 25362636. The Effects of Acute Exercise
    Studies in humans and animals have shown that brain blood flow remains largely unchanged in response to acute exercise[,] ... does not increase with increasing exercise intensity[, and] ... increased metabolic demands of active brain parts are mostly met by redistributing oxygen supply, although changes in oxygen extraction may also contribute. During exercise, blood flow is directed to the areas controlling locomotor, vestibular, cardiorespiratory, and visual functions (8, 91), facilitated by direct communication of neurons and vascular cells (94, 134). ... with increasing exercise intensity, brain glucose uptake decreases (75) as the uptake and utilization of lactate is enhanced (65, 139, 182). Regional differences in brain glucose uptake are also evident, which is furthermore influenced by the level of physical fitness. Thus the decrease in glucose uptake in the dorsal part of the anterior cingulate cortex during exercise is significantly more pronounced in subjects with higher exercise capacity (75) ...
    The Effects of Long-Term Exercise Training
    ... [A] physically active lifestyle has been shown to lead to higher cognitive performance and delayed or prevented neurological conditions in humans (71, 101, 143, 191). ... The production of brain-derived neurotrophic factor (BDNF), a key protein regulating maintenance and growth of neurons, is known to be stimulated by acute exercise (145), which may contribute to learning and memory. BDNF is released from brain already at rest but increases two- to threefold during exercise, which contributes 70–80% of circulating BDNF (145).    {{cite journal}}: CS1 maint: multiple names: authors list (link)
  12. ^ Gomez-Pinilla F, Hillman C (January 2013). "The influence of exercise on cognitive abilities". Compr Physiol. 3 (1): 403–428. doi:10.1002/cphy.c110063. PMC 3951958. PMID 23720292. Normal aging results in the loss of brain tissue (31), with markedly larger tissue loss evidenced in the frontal, temporal, and parietal cortices (16, 58, 149). As such, cognitive functions subserved by these brain regions (such as those involved in cognitive control and memory) are expected to decay more dramatically than other aspects of cognition. Specifically, age-related decreases in gray matter volume have been associated with decrements in a variety of cognitive control processes. ... Decreases in gray matter volume may result from several factors including loss in the number of neurons, neuronal shrinkage, reduction in dendritic arborization, and alterations in glia (158). Further, decreases in white matter (brain tissue composed primarily of myelinated nerve fibers) volume, which represent changes in connectivity between neurons, also occur as a result of aging. Loss of white matter volume further relates to performance decrements on a host of cognitive tasks (41, 131, 167) and may result from the demyelination of axons, reducing the rapid and effective conduction of electrical signals through the nervous system. However, based on studies of non-human animals outlined within this paper, and the aerobic fitness-induced benefits to cognitive control observed in behavioral studies in humans, scientists have speculated that an active lifestyle may serve to spare age-related loss in regions of the brain that support top-down cognitive control. ... Specifically, those assigned to the aerobic training group demonstrated increases in gray matter in the frontal lobes, including the dorsal anterior cingulate cortex (ACC), supplementary motor area, middle frontal gyrus, dorsolateral region of the right inferior frontal gyrus, and the left superior temporal lobe (32). White matter volume changes were also evidenced for the aerobic fitness group with increases in white matter tracts within the anterior third of the corpus callosum (32). ... In addition, aerobic fitness has been shown to promote better functioning of brain, especially in neural networks involved in cognitive control of inhibition and attention (33). ... a picture has emerged suggesting that more active or higher fit individuals are capable of allocating greater attentional resources toward the environment and process perceived information more quickly. ... In addition to BDNF, the actions of IGF-1 and vascular endothelial growth factor (VEGF) (54) are considered essential for the angiogenic and neurogenic effects of exercise in the brain.
  13. ^ Bherer L, Erickson KI, Liu-Ambrose T (2013). "A review of the effects of physical activity and exercise on cognitive and brain functions in older adults". J Aging Res. 2013: 657508. doi:10.1155/2013/657508. PMC 3786463. PMID 24102028.{{cite journal}}: CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
  14. ^ Silverman MN, Deuster PA (October 2014). "Biological mechanisms underlying the role of physical fitness in health and resilience". Interface Focus. 4 (5): 20140040. doi:10.1098/rsfs.2014.0040. PMID 25285199. In this review, we discuss the biological mechanisms underlying the beneficial effects of physical fitness on mental and physical health. Physical fitness appears to buffer against stress-related disease owing to its blunting/optimizing effects on hormonal stress responsive systems, such as the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. This blunting appears to contribute to reduced emotional, physiological and metabolic reactivity as well as increased positive mood and well-being. Another mechanism whereby regular exercise and/or physical fitness may confer resilience is through minimizing excessive inflammation. Chronic psychological stress, physical inactivity and abdominal adiposity have been associated with persistent, systemic, low-grade inflammation and exert adverse effects on mental and physical health. ... Importantly, physical fitness, whether achieved through spontaneous physical activity or regular exercise, can confer resilience, defined as 'the ability to withstand, recover, and grow in the face of stressors and changing demands' [20], and serves as a stress resistance resource in a variety of ways [21–25]. The biological pathways whereby regular physical activity might confer resilience include (i) serving as a buffer against stress and stress-related disorders/chronic diseases, (ii) optimizing neuroendocrine and physiological responses to physical and psychosocial stressors, (iii) promoting an anti-inflammatory state, and (iv) enhancing neuroplasticity and growth factor expression [15–19,26–35].
  15. ^ Austin MW, Ploughman M, Glynn L, Corbett D (October 2014). "Aerobic exercise effects on neuroprotection and brain repair following stroke: A systematic review and perspective". Neurosci. Res. 87C: 8–15. doi:10.1016/j.neures.2014.06.007. PMID 24997243.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  16. ^ Zschucke E, Gaudlitz K, Ströhle A (January 2013). "Exercise and physical activity in mental disorders: clinical and experimental evidence". J Prev Med Public Health. 46 Suppl 1: S12–521. doi:10.3961/jpmph.2013.46.S.S12. PMC 3567313. PMID 23412549.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  17. ^ Lees C, Hopkins J (2013). "Effect of aerobic exercise on cognition, academic achievement, and psychosocial function in children: a systematic review of randomized control trials". Prev Chronic Dis. 10: E174. doi:10.5888/pcd10.130010. PMC 3809922. PMID 24157077. This omission is relevant, given the evidence that aerobic-based physical activity generates structural changes in the brain, such as neurogenesis, angiogenesis, increased hippocampal volume, and connectivity (12,13). In children, a positive relationship between aerobic fitness, hippocampal volume, and memory has been found (12,13). ... Mental health outcomes included reduced depression and increased self-esteem, although no change was found in anxiety levels (18). ... This systematic review of the literature found that APA is positively associated with cognition, academic achievement, behavior, and psychosocial functioning outcomes. Importantly, Shephard also showed that curriculum time reassigned to APA still results in a measurable, albeit small, improvement in academic performance (24).  ... The actual aerobic-based activity does not appear to be a major factor; interventions used many different types of APA and found similar associations. In positive association studies, intensity of the aerobic activity was moderate to vigorous. The amount of time spent in APA varied significantly between studies; however, even as little as 45 minutes per week appeared to have a benefit.
  18. ^ Dinas PC, Koutedakis Y, Flouris AD (2011). "Effects of exercise and physical activity on depression". Ir J Med Sci. 180 (2): 319–325. doi:10.1007/s11845-010-0633-9. PMID 21076975. According to the 'endorphins hypothesis', exercise augments the secretion of endogenous opioid peptides in the brain, reducing pain and causing general euphoria. ... Based upon a large effect size, the results confirmed the endorphins hypothesis demonstrating that exercise leads to an increased secretion of endorphins which, in turn, improved mood states.
    β-Endorphin, an endogenous μ-opioid receptor selective ligand, has received much attention in the literature linking endorphins and depression or mood states. ... exercise of sufficient intensity and duration can increase circulating β-endorphin levels. ... Moreover, a recent study demonstrated that exercise and physical activity increased β-endorphin levels in plasma with positive effects on mood. Interestingly, the researchers reported that, independently of sex and age, dynamic anaerobic exercises increased β-endorphin, while resistance and aerobic exercises seem to only have small effects on β-endorphins. ... The results showed that mood tends to be higher in a day an individual exercises as well as that daily activity and exercise overall are strongly linked with mood states. In line with these findings, a recent study showed that exercise significantly improved mood states in non-exercises, recreational exercisers, as well as marathon runners. More importantly, the effects of exercise on mood were twofold in recreational exercisers and marathon runners.
  19. ^ Tantimonaco M, Ceci R, Sabatini S, Catani MV, Rossi A, Gasperi V, Maccarrone M (2014). "Physical activity and the endocannabinoid system: an overview". Cell. Mol. Life Sci. 71 (14): 2681–2698. doi:10.1007/s00018-014-1575-6. PMID 24526057. The traditional view that PA engages the monoaminergic and endorphinergic systems has been challenged by the discovery of the endocannabinoid system (ECS), composed of endogenous lipids, their target receptors, and metabolic enzymes. Indeed, direct and indirect evidence suggests that the ECS might mediate some of the PA-triggered effects throughout the body. ... the evidence that PA induces some of the psychotropic effects elicited by the Cannabis sativa active ingredient Δ9-tetrahydrocannabinol (Δ9-THC, Fig. 1), like bliss, euphoria, and peacefulness, strengthened the hypothesis that endocannabinoids (eCBs) might mediate, at least in part, the central and peripheral effects of exercise [14]. ... To our knowledge, the first experimental study aimed at investigating the influence of PA on ECS in humans was carried out in 2003 by Sparling and coworkers [63], who showed increased plasma AEA content after 45 min of moderate intensity exercise on a treadmill or cycle ergometer. Since then, other human studies have shown increased blood concentrations of AEA ... A dependence of the increase of AEA concentration on exercise intensity has also been documented. Plasma levels of AEA significantly increased upon 30 min of moderate exercise (heart rate of 72 and 83 %), but not at lower and significantly higher exercise intensities, where the age-adjusted maximal heart rate was 44 and 92 %, respectively ... Several experimental data support the hypothesis that ECS might, at least in part, explain PA effects on brain functions, because: (1) CB1 is the most abundant GPCR in the brain participating in neuronal plasticity [18]; (2) eCBs are involved in several brain responses that greatly overlap with the positive effects of exercise; (3) eCBs are able to cross the blood–brain barrier [95]; and (4) exercise increases eCB plasma levels [64–67].
  20. ^ Bergman D (2013). "The endocrinology of exercise". Intern Emerg Med. 8 Suppl 1: S17–21. doi:10.1007/s11739-013-0921-2. PMID 23475807.
  21. ^ McKee AC, Daneshvar DH, Alvarez VE, Stein TD (January 2014). "The neuropathology of sport". Acta Neuropathol. 127 (1): 29–51. doi:10.1007/s00401-013-1230-6. PMC 4255282. PMID 24366527. The benefits of regular exercise, physical fitness and sports participation on cardiovascular and brain health are undeniable ... Exercise also enhances psychological health, reduces age-related loss of brain volume, improves cognition, reduces the risk of developing dementia, and impedes neurodegeneration.
  22. ^ Farina N, Rusted J, Tabet N (January 2014). "The effect of exercise interventions on cognitive outcome in Alzheimer's disease: a systematic review". Int Psychogeriatr. 26 (1): 9–18. doi:10.1017/S1041610213001385. PMID 23962667. Six RCTs were identified that exclusively considered the effect of exercise in AD patients. Exercise generally had a positive effect on rate of cognitive decline in AD. A meta-analysis found that exercise interventions have a positive effect on global cognitive function, 0.75 (95% CI = 0.32–1.17). ... The most prevalent subtype of dementia is Alzheimer's disease (AD), accounting for up to 65.0% of all dementia cases ... Cognitive decline in AD is attributable at least in part to the buildup of amyloid and tau proteins, which promote neuronal dysfunction and death (Hardy and Selkoe, 2002; Karran et al., 2011). Evidence in transgenic mouse models of AD, in which the mice have artificially elevated amyloid load, suggests that exercise programs are able to improve cognitive function (Adlard et al., 2005; Nichol et al., 2007). Adlard and colleagues also determined that the improvement in cognitive performance occurred in conjunction with a reduced amyloid load. Research that includes direct indices of change in such biomarkers will help to determine the mechanisms by which exercise may act on cognition in AD.
  23. ^ Rao AK, Chou A, Bursley B, Smulofsky J, Jezequel J (January 2014). "Systematic review of the effects of exercise on activities of daily living in people with Alzheimer's disease". Am J Occup Ther. 68 (1): 50–56. doi:10.5014/ajot.2014.009035. PMID 24367955. Alzheimer's disease (AD) is a progressive neurological disorder characterized by loss in cognitive function, abnormal behavior, and decreased ability to perform basic activities of daily living [(ADLs)] ... All studies included people with AD who completed an exercise program consisting of aerobic, strength, or balance training or any combination of the three. The length of the exercise programs varied from 12 weeks to 12 months. ... Six studies involving 446 participants tested the effect of exercise on ADL performance ... exercise had a large and significant effect on ADL performance (z = 4.07, p < .0001; average effect size = 0.80). ... These positive effects were apparent with programs ranging in length from 12 wk (Santana-Sosa et al., 2008; Teri et al., 2003) and intermediate length of 16 wk (Roach et al., 2011; Vreugdenhil et al., 2012) to 6 mo (Venturelli et al., 2011) and 12 mo (Rolland et al., 2007). Furthermore, the positive effects of a 3-mo intervention lasted 24 mo (Teri et al., 2003). ... No adverse effects of exercise on ADL performance were noted. ... The study with the largest effect size implemented a walking and aerobic program of only 30 min four times a week (Venturelli et al., 2011). ... The findings of this review have the following implications for occupational therapy practice:
     • Physical training, which is often included in occupational therapy practice, can help improve ADL performance in people with Alzheimer's disease. Occupational therapy practitioners may be involved in planning and delivering physical training, identifying and correcting compensatory mechanisms, and providing support to minimize adverse events such as falls. The studies reviewed highlight the clinical feasibility of an exercise program for people with AD.
     • Intervention should include components of aerobic, strength, balance, and coordination training.
     • Physical training was equally effective in long-term care facilities and in home-based settings.
     • Occupational therapy practitioners may enlist the help of caregivers or trained assistants (e.g., aides) in improving adherence to physical training programs. However, interventions should be structured so as not to increase caregiver burden.
     • Although physical training is not routinely recommended for people with AD, this review provides evidence to support inclusion of aerobic exercise and strength, balance, and coordination training in occupational therapy practice. Physical training is a reimbursable service and may be included in occupational therapy practice.
    In addition, the findings of this review have the following implications for occupational therapy research:
     • Well-designed randomized controlled trials with large sample sizes are needed to assess the effects of exercise on ADL performance in people with AD.
     • Additional studies are needed to clarify the specific components of physical training that are most effective and clinically feasible.
     • Research is needed to examine optimal length and intensity of intervention to develop clinical guidelines for exercise in this population.
  24. ^ Mattson MP (2014). "Interventions that improve body and brain bioenergetics for Parkinson's disease risk reduction and therapy". J Parkinsons Dis. 4 (1): 1–13. doi:10.3233/JPD-130335. PMID 24473219.
  25. ^ Grazina R, Massano J (2013). "Physical exercise and Parkinson's disease: influence on symptoms, disease course and prevention". Rev Neurosci. 24 (2): 139–152. doi:10.1515/revneuro-2012-0087. PMID 23492553.
  26. ^ van der Kolk NM, King LA (September 2013). "Effects of exercise on mobility in people with Parkinson's disease". Mov. Disord. 28 (11): 1587–1596. doi:10.1002/mds.25658. PMID 24132847.
  27. ^ Tomlinson CL, Patel S, Meek C, Herd CP, Clarke CE, Stowe R, Shah L, Sackley CM, Deane KH, Wheatley K, Ives N (September 2013). "Physiotherapy versus placebo or no intervention in Parkinson's disease". Cochrane Database Syst Rev. 9: CD002817. doi:10.1002/14651858.CD002817.pub4. PMID 24018704.
  28. ^ a b Schapira AH, Olanow CW, Greenamyre JT, Bezard E (August 2014). "Slowing of neurodegeneration in Parkinson's disease and Huntington's disease: future therapeutic perspectives". Lancet. 384 (9942): 545–555. doi:10.1016/S0140-6736(14)61010-2. PMID 24954676.
  29. ^ a b Quinn L, Busse M, Dal Bello-Haas V (April 2013). "Management of upper extremity dysfunction in people with Parkinson disease and Huntington disease: facilitating outcomes across the disease lifespan". J Hand Ther. 26 (2): 148–154, quiz 155. doi:10.1016/j.jht.2012.11.001. PMID 23231827.
  30. ^ Iversen MD, Hammond A, Betteridge N (June 2010). "Self-management of rheumatic diseases: state of the art and future perspectives". Ann. Rheum. Dis. 69 (6): 955–963. doi:10.1136/ard.2010.129270. PMID 20448289.
  31. ^ Spielman LJ, Little JP, Klegeris A (August 2014). "Inflammation and insulin/IGF-1 resistance as the possible link between obesity and neurodegeneration". J. Neuroimmunol. 273 (1–2): 8–21. doi:10.1016/j.jneuroim.2014.06.004. PMID 24969117. Obesity is a growing epidemic that contributes to several brain disorders including Alzheimer's, Parkinson's, and Huntington's diseases. Obesity could promote these diseases through several different mechanisms. Here we review evidence supporting the involvement of two recently recognized factors linking obesity with neurodegeneration: the induction of pro-inflammatory cytokines and onset of insulin and insulin-like growth factor 1 (IGF-1) resistance. ... IGF-1 resistance leads to weakening of neuroprotective signaling by these molecules and can contribute to onset of neurodegenerative diseases.

Notable reviews - mostly from 2015/2016

  • Brain glucose mid- and post-exercise responses during prolonged/endurance exercise[1]
  • Effect of CNS monoamines on central fatigue + body temperature limit during exercise [2]
  • Erickson review from 2015[3] plus Added
  • Neurooncology (brain cancer) - entire review on the topic[4] plus Added
  • Regional CNS effects and associated mechanisms[5]
    • Supplemental review for writing the monoamines section[6] [NEED TO ADD THIS REVIEW]
  • Clinical guidelines for depression[7] plus Added
  • Neurocardiac plasticity of the rostral ventrolateral medulla[8] plus Added
  • Cochrane dementia review[9] plus Added
  • GDNF[10][11] - need more reviews on this
  • Effect on the basal ganglia [NEED TO ADD THESE REVIEWS - PARTICULARLY THE SECOND]
  • Astrocytes[12]
  • Effects on cognition in healthy young-middle aged adults[13] plus Added

References

  1. ^ Rattray B, Argus C, Martin K, Northey J, Driller M (March 2015). "Is it time to turn our attention toward central mechanisms for post-exertional recovery strategies and performance?". Front. Physiol. 6: 79. doi:10.3389/fphys.2015.00079. PMC 4362407. PMID 25852568.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  2. ^ Roelands B, De Pauw K, Meeusen R (June 2015). "Neurophysiological effects of exercise in the heat". Scand. J. Med. Sci. Sports. 25 Suppl 1: 65–78. doi:10.1111/sms.12350. PMID 25943657.
  3. ^ Erickson KI, Hillman CH, Kramer AF (August 2015). "Physical activity, brain, and cognition". Current Opinion in Behavioral Sciences. 4: 27–32. doi:10.1016/j.cobeha.2015.01.005. Research in children finds that higher fit and more active preadolescent children show greater hippocampal and basal ganglia volume, greater white matter integrity, elevated and more efficient patterns of brain activity, and superior cognitive performance and scholastic achievement. Higher fit and more physically active older adults show greater hippocampal, prefrontal cortex, and basal ganglia volume, greater functional brain connectivity, greater white matter integrity, more efficient brain activity, and superior executive and memory function. ...
    Cognitive performance: Cross-sectional, observational, and randomized clinical trials of PA in late adulthood have demonstrated that engaging in PA may preserve and/or enhance cognitive function even in cognitively impaired individuals (e.g., [18]). Summaries of these studies can now be found in several meta-analyses, most of which confirm that PA positively influences cognitive function in late adulthood with small to moderate sized effects [19]. In a meta-analysis of 18 randomized PA trials, engaging in moderate intensity PA resulted in enhanced cognitive function across all cognitive domains examined, but with the largest effect sizes for indices of executive function [20]. Meta-analyses of longitudinal observational studies have also confirmed that self-reported engagement in PA is associated with nearly a 40% reduced risk of experiencing cognitive decline over several years [21]. These, and other studies, make a convincing argument that both continuing to engage in, and starting to engage in, PA in late adulthood may have a profound effect on maintaining cognitive health, improving function, and reducing the risk of developing cognitive impairment.
    Brain structure: There have been now more than 30 published studies of PA or fitness on brain structure in older adults (>60 years) with the majority showing positive associations (see [22]). Such effects are important since increasing age is associated with brain atrophy and loss of volume, which precedes and predicts conversion to dementia. Higher aerobic fitness levels have been associated with larger gray matter volumes in older adults in several areas including the frontal cortex [23,24], hippocampus [25,26], and caudate nucleus [27]. Longitudinal observational studies have also shown that greater amounts of PA are associated with larger gray matter volumes in these regions, and greater volume is, in turn, associated with a reduced risk of cognitive impairment [28]. These cross-sectional and observational results in older adults are further supported by clinical trials that have shown that six-months to one-year of regular PA is associated with an increase in both frontal cortex [29••,30] and hippocampal volume ... These effects on gray matter volume are accompanied by differences found in white matter integrity. For example, several studies have reported that higher cardiorespiratory fitness levels and PA are associated with greater white matter integrity along several tracts linking frontal and subcortical areas [34–36] and that greater changes in fitness after an intervention was associated with an increase in white matter integrity [37]. In sum, there is now convincing evidence that PA and fitness influence brain structure, characterized by both gray matter volume and white matter integrity, in late adulthood.
  4. ^ Cormie P, Nowak AK, Chambers SK, Galvão DA, Newton RU (April 2015). "The potential role of exercise in neuro-oncology". Front. Oncol. 5: 85. doi:10.3389/fonc.2015.00085. PMC 4389372. PMID 25905043.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  5. ^ a b Morgan JA, Corrigan F, Baune BT (April 2015). "Effects of physical exercise on central nervous system functions: a review of brain region specific adaptations". J Mol Psychiatry. 3 (1): 3. doi:10.1186/s40303-015-0010-8. PMC 4461979. PMID 26064521.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  6. ^ Lin TW, Kuo YM (2013). "Exercise benefits brain function: the monoamine connection". Brain Sci. 3 (1): 39–53. doi:10.3390/brainsci3010039. PMC 4061837. PMID 24961306. Regular physical exercise has been proved to have therapeutic benefit [1], such as treating psychiatric illnesses [2,3,4,5,6,7], supporting brain injury recovery [8,9,10,11,12], and resisting neurodegenerative diseases [13,14,15,16,17,18]. ... Furthermore, regulations of the secretion of neurotrophic factors, vasculotropic factors, inflammatory mediators, and neurotransmitters are also involved in exercise's influence on brain function [21,22,23,24,25]. Among these effects, secretion of neurotransmitters, especially monoamines, have been linked to the exercise-induced neuronal adaptation. ... Upregulation of DA in the brain has been linked to exercise-induced higher levels of serum calcium, which is transported into the brain and affects calcium/calmodulin-dependent DA synthesis by activating the tyrosine hydroxylase enzyme [77]. ... Studies of patients with PD suggest that exercise may provide preventive and non-pharmaceutical therapeutic approach for PD. Six months of aerobics exercise significantly improves the executive movement of simple and complex motions in patients diagnosed with mild to moderate PD [90]. Additionally, in an epidemiological evaluation of physical activity in a cohort of more than 200,000 participants, exercise at moderate to vigorous levels is found to protect against PD [91]. Altogether, exercise not only modulates the direct action of DA system, but also protects DA neuron against toxic assaults. ... the levels of plasma galanin are also increased in humans after acute exercise [101]. ... Similarly, the levels of NE in brain regions that are linked to cognitive function, including hippocampus and central and medial amygdala, are elevated by chronic treadmill exercise [108]. Blockade of β-adrenoreceptors with various antagonists inhibits the chronic exercise-induced improvement of learning and memory in contextual fear conditioning and water maze tasks [100,109]. The memory performance in both amnestic mild cognitive impairment patients and control subjects is significantly enhanced if a single bout of aerobic exercise is given immediately after learning [110]. Meanwhile, the endogenous activity of NE is also increased by exercise, suggesting a potential linkage between NE and exercise-enhanced cognitive function. ... The stimulation of the monoamine system is dependent on exercise intensity.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  7. ^ Ranjbar E, Memari AH, Hafizi S, Shayestehfar M, Mirfazeli FS, Eshghi MA (June 2015). "Depression and Exercise: A Clinical Review and Management Guideline". Asian J Sports Med. 6 (2): e24055. doi:10.5812/asjsm.6(2)2015.24055. PMC 4592762. PMID 26448838.
  8. ^ Mischel NA, Subramanian M, Dombrowski MD, Llewellyn-Smith IJ, Mueller PJ (May 2015). "(In)activity-related neuroplasticity in brainstem control of sympathetic outflow: unraveling underlying molecular, cellular, and anatomical mechanisms". Am. J. Physiol. Heart Circ. Physiol. 309 (2): H235–43. doi:10.1152/ajpheart.00929.2014. PMID 25957223.
  9. ^ Forbes D, Forbes SC, Blake CM, Thiessen EJ, Forbes S (April 2015). "Exercise programs for people with dementia". Cochrane Database Syst Rev. 4: CD006489. doi:10.1002/14651858.CD006489.pub4. PMID 25874613.
  10. ^ Zigmond MJ, Cameron JL, Hoffer BJ, Smeyne RJ (2012). "Neurorestoration by physical exercise: moving forward". Parkinsonism Relat. Disord. 18 Suppl 1: S147–50. doi:10.1016/S1353-8020(11)70046-3. PMID 22166417. Using toxins that induce a deficiency of dopamine, we have affirmed that physical exercise can reduce behavioral and neurobiological deficits induced by such toxins, and suggest that these neuroprotective effects are likely to involve the activation of signaling cascades by neurotrophic factors such as glial cell line derived neurotrophic factor.
  11. ^ a b Paillard T, Rolland Y, de Souto Barreto P (July 2015). "Protective Effects of Physical Exercise in Alzheimer's Disease and Parkinson's Disease: A Narrative Review". J Clin Neurol. 11 (3): 212–219. doi:10.3988/jcn.2015.11.3.212. PMC 4507374. PMID 26174783. Aerobic physical exercise (PE) activates the release of neurotrophic factors and promotes angiogenesis, thereby facilitating neurogenesis and synaptogenesis, which in turn improve memory and cognitive functions. ... Exercise limits the alteration in dopaminergic neurons in the substantia nigra and contributes to optimal functioning of the basal ganglia involved in motor commands and control by adaptive mechanisms involving dopamine and glutamate neurotransmission.
  12. ^ Tsai SF, Chen PC, Calkins MJ, Wu SY, Kuo YM (March 2016). "Exercise Counteracts Aging-Related Memory Impairment: A Potential Role for the Astrocytic Metabolic Shuttle". Front Aging Neurosci. 8: 57. doi:10.3389/fnagi.2016.00057. PMC 4801859. PMID 27047373.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  13. ^ Cox EP, O'Dwyer N, Cook R, Vetter M, Cheng HL, Rooney K, O'Connor H (August 2016). "Relationship between physical activity and cognitive function in apparently healthy young to middle-aged adults: A systematic review". J. Sci. Med. Sport. 19 (8): 616–628. doi:10.1016/j.jsams.2015.09.003. PMID 26552574. A range of validated platforms assessed CF across three domains: executive function (12 studies), memory (four studies) and processing speed (seven studies). Habitual PA was assessed via questionnaire/self-report methods (n=13, 8 validated) or accelerometers (n=1). In studies of executive function, five found a significant ES in favour of higher PA, ranging from small to large. Although three of four studies in the memory domain reported a significant benefit of higher PA, there was only one significant ES, which favoured low PA. Only one study examining processing speed had a significant ES, favouring higher PA.
    CONCLUSIONS: A limited body of evidence supports a positive effect of PA on CF in young to middle-aged adults. Further research into this relationship at this age stage is warranted. ...
    Significant positive effects of PA on cognitive function were found in 12 of the 14 included manuscripts, the relationship being most consistent for executive function, intermediate for memory and weak for processing speed.

Seppi333 (Insert 2¢) 22:56, 27 July 2016 (UTC)

Sept 2016 study - cognitive effects in healthy young adults

New review

I came across this[1] March 2017 review on the acute effects of exercise on cognition, affect, neurophysiology, and neurochemical/myokine signaling from a "Neuroscience news" story on my facebook news feed. Could probably use the news piece as a laysummary parameter in the citation. It makes some very interesting/notable assertions about the effects of acute exercise on executive functions/cognitive control and cognitive processing speed.

And oh my god, I have so much work to do on updating this article with the MASSIVE deluge of reviews and meta-analyses that have been published since I last worked on it 12 months ago (75 reviews, systematic reviews, and meta-analyses from using very specific filters for relevance). It seems like a lot more researchers have actually taken notice of the fact that aerobic exercise induces both acute and chronic psychostimulant-like effects on cognition and marked neuroplasticity in healthy adults and those with CNS disorders.

A couple of templated review/meta-analysis citations to add soonish:

  • Review from above with lay summary (not pubmed indexed)[1] – need to cover the content on myokines (BDNF, IGF-1, VEGF), epigenetic/HDAC inhibitor effects of beta-hydroxybutyrate, monoamines, glutamate, acetylcholine, cortisol, HPA-axis, the PFC, executive functions, memory, information processing speed, and a number of other details.  Partly done - the transient cognitive effects of acute exercise were added
    • Source they cited about acute exercise-induced PFC-dependent effects on cognitive control in healthy adults[2]
  • Meta-analysis on the effects of exercise on resting peripheral BDNF levels: PMID 27658238[3]
  • Meta-analysis on the effects of acute exercise on peripheral BDNF in healthy adults: PMID 28493624[4]
  • "At least eighty percent of brain grey matter is modifiable by physical activity: A review study"[5]  Partly done - there's a lot from this review that could still be added Seppi333 (Insert 2¢) 20:11, 6 November 2017 (UTC)

Seppi333 (Insert 2¢) 12:54, 16 June 2017 (UTC)

References

  1. ^ a b Basso JC, Suzuki WA (March 2017). "The Effects of Acute Exercise on Mood, Cognition, Neurophysiology, and Neurochemical Pathways: A Review". Brain Plasticity. 2 (2): 127–152. doi:10.3233/BPL-160040. {{cite journal}}: Unknown parameter |lay-date= ignored (help); Unknown parameter |lay-source= ignored (help); Unknown parameter |lay-url= ignored (help)
  2. ^ Basso JC, Shang A, Elman M, Karmouta R, Suzuki WA (November 2015). "Acute Exercise Improves Prefrontal Cortex but not Hippocampal Function in Healthy Adults". Journal of the International Neuropsychological Society : JINS. 21 (10): 791–801. doi:10.1017/S135561771500106X. PMID 26581791.
  3. ^ Dinoff A, Herrmann N, Swardfager W, Liu CS, Sherman C, Chan S, Lanctôt KL (September 2016). "The Effect of Exercise Training on Resting Concentrations of Peripheral Brain-Derived Neurotrophic Factor (BDNF): A Meta-Analysis". Plos One. 11 (9): e0163037. doi:10.1371/journal.pone.0163037. PMC 5033477. PMID 27658238.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  4. ^ Dinoff A, Herrmann N, Swardfager W, Lanctôt KL (May 2017). "The effect of acute exercise on blood concentrations of brain-derived neurotrophic factor (BDNF) in healthy adults: A meta-analysis". The European Journal of Neuroscience. doi:10.1111/ejn.13603. PMID 28493624.
  5. ^ Batouli SH, Saba V (June 2017). "At least eighty percent of brain grey matter is modifiable by physical activity: A review study". Behavioural Brain Research. 332: 204–217. doi:10.1016/j.bbr.2017.06.002. PMID 28600001. The results of this study showed that a large network of brain areas, equal to 82% of the total grey matter volume, were associated with PA. This finding has important implications in utilizing PA as a mediator factor for educational purposes in children, rehabilitation applications in patients, improving the cognitive abilities of the human brain such as in learning or memory, and preventing age-related brain deteriorations. ... There is a significant association between the volume of the brain areas and their corresponding functions. Examples include the association of total and regional brain volumes (BV) with executive function and speed of processing, intelligence, working, verbal and spatial memory, and skill acquisition performance [27–29]. The connections between brain function and structure is due to the neural information processing being dependent on the size, arrangement, and configuration of the neurons, the number and type of the synaptic connections of the neurons, on the quality of their connection with distant neurons, and on the properties of non-neuronal cells such as glia [30]. ... This study showed that PA is positively associating with nearly all brain regions.

Interesting review (IMO) on gender-dependent differences in motivation to engage in physical exercise

I've only read a few scattered paragraphs of this review;[1] I intend to finish reading it later. I've haven't read most of the material relevant to molecular neurobiology and neuropharmacology (NB: some of that may be worth covering). Out of the parts I read, I came across a few significant excerpts that should be added to/paraphrased in the article:

Extended quote

Screening of US college students in two studies (n = 621 for one and n = 2199 for another) suggest that motivation to engage in LTPA is primarily governed by internal factors, such as intention, strength, competition, and challenge, in males, but primarily extrinsic factors, including attitude, self-efficacy, body mass index/weight management, physical appearance, i.e. slenderness, and sports participation influence this decision in females (Beville et al. 2014; Egli et al. 2011). Further studies support the notion that motivation drivers for LTPA differ between the sexes in both young and middle age adults (Molanorouzi et al. 2015). ...

It is more difficult to pinpoint individual factors that influence PA in humans, where motivation to engage in PA comes under strong social influences. It is possible that conspecifics, especially those of the same sex, may also affect voluntary PA in rodents, although to date, there does not appear to be any studies comparing spontaneous activity levels in socially-housed vs. isolated rodents. In humans, similar patterns across studies with children to elderly individuals emerge in terms of sex differences in PA levels and differential reasons why each sex remain active. At almost all ages studied, human males are more PA than females (Barnekow-Bergkvist et al. 1996; Butt et al. 2011; Deaner et al. 2012; Gardner and Montgomery 2008; Lee 2005; Marquez and McAuley 2006; Sirard et al. 2006; Sukys et al. 2014; Yli-Piipari et al. 2012). For human males, the motivators tend to be more intrinsic, such as improving health, preventing NCD, enhancing body shape, and being competitive (Beville et al. 2014; Butt et al. 2011; Caperchione et al. 2015; Cole and Maeda 2015; Egli et al. 2011; Jonason 2007; Marquez and McAuley 2006; Molanorouzi et al. 2015; Sirard et al. 2006; Yli-Piipari et al. 2012). In contrast, a combination of extrinsic and intrinsic factors, simultaneously listening to music, emotional support, social aspects, sense of well-being, and positive body image, appear to guide PA in females of varying age ranges. ...

The current rodent studies suggest that the striatum region, especially the NAc, is a primary regulator of spontaneous PA in both sexes. ...

Rodents models, such as transgenic mice, those with pharmacologically-induced neural lesions, and those selectively bred to engage in high or low amount of wheel running or other PA, have helped elucidate the brain regions and molecular mechanisms regulating PA. Because of the strong conservation in brain structure and physiology between rodents and humans (Howdeshell 2002; Rice and Barone 2000), the same brain areas likely facilitate PA in humans. The brain regions in rodents that are essential in modulating this behavior include the striatum, NAc, hypothalamus, amygdala, hippocampus, prefrontal cortex, locus coeruleus, cerebellum, and pons (Ambrogi Lorenzini et al. 1991; Andrzejewski et al. 2004; Basso and Morrell 2015; Beninger et al. 2009; Bronikowski et al. 2004; Cahill et al. 2015; Dubreucq et al. 2010; Kolb et al. 2013; Korczynski and Fonberg 1979; Monroe et al. 2014; Nonneman and Corwin 1981; Rhodes et al. 2003; Roberts et al. 2014; Ruegsegger et al. 2016; Ruegsegger et al. 2015; Tarr et al. 2004; Teske et al. 2013; Werme et al. 2002; Yim and Mogenson 1989).
— PMID 27870424

Seppi333 (Insert 2¢) 01:10, 12 August 2017 (UTC)

References

  1. ^ Rosenfeld CS (January 2017). "Sex-dependent differences in voluntary physical activity". Journal of Neuroscience Research. 95 (1–2): 279–290. doi:10.1002/jnr.23896. PMC 5120617. PMID 27870424.


Look for review that covers this primary source and related research

Seppi333 (Insert 2¢) 23:55, 21 December 2017 (UTC)

2018 review to add

Long-term effects needs to be sorted by body components

See also: Neuroscience and Nervous system

The section on Long-term effects could be sorted by body segments, ie. brain, skin, muscles etc. It appears that the entire Long-term section is basically about brain development. prokaryotes (talk) 21:27, 6 November 2017 (UTC)

Sounds like a reasonable approach; I'll look into doing this when I work on restructuring the article later. Thanks for the feedback. Seppi333 (Insert 2¢) 07:12, 9 November 2017 (UTC)
There are also way too many references occasionally (overlinkage). prokaryotes (talk) 09:30, 10 November 2017 (UTC)
That's sometimes unavoidable when an extremely broad or varied list of medical claims in included in an article. Seppi333 (Insert 2¢) 23:37, 10 November 2017 (UTC)
I ended up restructuring the long-term effects section based upon topical hierarchy; the neuroplasticity subsection covers structural neuroplasticity and cognitive plasticity while the "mechanism of effects" section covers (or rather, will eventually cover) how repeated skeletal muscle contraction releases myokines into the blood stream, which then circulate to the brain via the cardiovascular system, and bind to receptors located on neurons. Before adding that content though, I need to identify which of the sources I cited that covers how regular exercise leads to repeated activation of neurotrophic signaling pathways through the release of myokines, thereby producing lasting changes to neural structure/function. It's been a while since I worked on this article. Seppi333 (Insert 2¢) 20:55, 12 March 2019 (UTC)

Statements in the lead/body about clinical effects

@Zefr: I rewrote almost every sentence in this article in the lead and body sections that do not contain a maintenance banner; I don't exaggerate the conclusions of sources that I cite. However, if you feel that there's an issue with how existing article text is worded in relation to the statements in the sources, it would be best to discuss this at WP:NPOV/Noticeboard instead of argue about it with me here since that will generate external/third-party feedback on this content.

I would prefer not to get into an edit war over this. Seppi333 (Insert 2¢) 19:07, 13 May 2018 (UTC)

Indeed not. However, the lead should not be supporting statements with 6 (even 10) citations which are repeated in the main text (it looks like OR when all that is needed is a summary and one or two refs - indeed, in uncontested (hm, unmedical) leads, none is the best number). I shan't touch it but it sure looks ott. Chiswick Chap (talk)
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