Los efectos neurobiológicos del ejercicio físico son numerosos e involucran una amplia gama de efectos interrelacionados sobre la estructura cerebral, la función cerebral y la cognición . [1] [2] [3] [4] Una gran cantidad de investigación en humanos ha demostrado que el ejercicio aeróbico constante (por ejemplo, 30 minutos todos los días) induce mejoras persistentes en ciertas funciones cognitivas , alteraciones saludables en la expresión génica en el cerebro, y formas beneficiosas de neuroplasticidad y plasticidad conductual ; algunos de estos efectos a largo plazo incluyen: aumento del crecimiento de las neuronas, aumento de la actividad neurológica (p. ej., señalización de c-Fos y BDNF ), mejor afrontamiento del estrés, mejor control cognitivo del comportamiento , mejor memoria declarativa , espacial y de trabajo , y mejoras estructurales y funcionales en las estructuras y vías cerebrales asociadas con el control cognitivo y la memoria . [1] [2] [3] [4] [5] [6] [7] [8] [9] [10] Los efectos del ejercicio en la cognición tienen implicaciones importantes para mejorar el rendimiento académico en niños y estudiantes universitarios, mejorando productividad adulta, preservación de la función cognitiva en la vejez, prevención o tratamiento de determinados trastornos neurológicos y mejora de la calidad de vida en general . [1] [11] [12] [13]
Efectos neurobiológicos del ejercicio físico | |
---|---|
Terapia de ejercicios - intervención médica | |
![]() Una mujer realizando ejercicio aeróbico. | |
ICD-9-CM | 93,19 |
Malla | D005081 |
LOINC | 73986-2 |
eMedicina | 324583 |
En adultos sanos, se ha demostrado que el ejercicio aeróbico induce efectos transitorios sobre la cognición después de una sola sesión de ejercicio y efectos persistentes sobre la cognición después del ejercicio regular durante varios meses. [1] [10] [14] Las personas que realizan ejercicio aeróbico con regularidad (p. Ej., Correr, trotar , caminar a paso ligero, nadar y montar en bicicleta) tienen puntuaciones más altas en las pruebas de función y rendimiento neuropsicológicas que miden ciertas funciones cognitivas, como el control de la atención , control inhibitorio , flexibilidad cognitiva , capacidad y actualización de la memoria de trabajo , memoria declarativa , memoria espacial y velocidad de procesamiento de la información . [1] [5] [7] [9] [10] [14] Los efectos transitorios del ejercicio sobre la cognición incluyen mejoras en la mayoría de las funciones ejecutivas (p. Ej., Atención, memoria de trabajo, flexibilidad cognitiva, control inhibitorio, resolución de problemas y decisión elaboración) y velocidad de procesamiento de la información durante un período de hasta 2 horas después del ejercicio. [14]
El ejercicio aeróbico induce efectos a corto y largo plazo sobre el estado de ánimo y los estados emocionales al promover el afecto positivo , inhibir el afecto negativo y disminuir la respuesta biológica al estrés psicológico agudo . [14] A corto plazo, el ejercicio aeróbico funciona como antidepresivo y euforizante , [15] [16] [17] [18] mientras que el ejercicio constante produce mejoras generales en el estado de ánimo y la autoestima . [19] [20]
El ejercicio aeróbico regular mejora los síntomas asociados con una variedad de trastornos del sistema nervioso central y puede usarse como terapia complementaria para estos trastornos. Existe una clara evidencia de la eficacia del tratamiento con ejercicios para el trastorno depresivo mayor y el trastorno por déficit de atención con hiperactividad . [11] [17] [21] [22] [23] La Academia Americana de Neurología 's guía de práctica clínica para el deterioro cognitivo leve indica que los médicos deben recomendar el ejercicio regular (dos veces por semana) a individuos que han sido diagnosticados con esta condición. [24] Las revisiones de la evidencia clínica también apoyan el uso del ejercicio como terapia complementaria para ciertos trastornos neurodegenerativos , particularmente la enfermedad de Alzheimer y la enfermedad de Parkinson . [25] [26] [27] [28] [29] [30] El ejercicio regular también se asocia con un riesgo menor de desarrollar trastornos neurodegenerativos. [28] [31] Una gran cantidad de evidencia preclínica y evidencia clínica emergente respalda el uso del ejercicio como terapia complementaria para el tratamiento y la prevención de la adicción a las drogas . [32] [33] [34] [35] [36] También se ha propuesto el ejercicio regular como terapia complementaria para los cánceres de cerebro . [37]
Efectos a largo plazo
Neuroplasticidad
La neuroplasticidad es el proceso por el cual las neuronas se adaptan a una alteración con el tiempo y ocurre con mayor frecuencia en respuesta a la exposición repetida a estímulos. [38] El ejercicio aeróbico aumenta la producción de factores neurotróficos [nota 1] (p. Ej., BDNF , IGF-1 , VEGF ) que median mejoras en las funciones cognitivas y diversas formas de memoria al promover la formación de vasos sanguíneos en el cerebro, neurogénesis adulta , [ nota 2] y otras formas de neuroplasticidad. [40] [2] [5] [19] [41] [42] El ejercicio aeróbico constante durante un período de varios meses induce mejoras clínicamente significativas en las funciones ejecutivas y un aumento del volumen de materia gris en casi todas las regiones del cerebro, [43] con los aumentos más marcados que ocurren en las regiones del cerebro que dan lugar a funciones ejecutivas. [1] [5] [6] [7] [9] Las estructuras cerebrales que muestran las mayores mejoras en el volumen de materia gris en respuesta al ejercicio aeróbico son la corteza prefrontal , el núcleo caudado y el hipocampo ; [1] [5] [6] [8] se producen aumentos menos significativos en el volumen de materia gris en la corteza cingulada anterior , la corteza parietal , el cerebelo y el núcleo accumbens . [5] [6] [8] La corteza prefrontal, el núcleo caudado y la corteza cingulada anterior se encuentran entre las estructuras cerebrales más importantes de los sistemas de dopamina y norepinefrina que dan lugar al control cognitivo. [6] [44] La neurogénesis inducida por el ejercicio (es decir, los aumentos en el volumen de materia gris) en el hipocampo se asocia con mejoras mensurables en la memoria espacial . [6] [8] [20] [45] Los puntajes más altos de aptitud física , medidos por el VO 2 máx. , Se asocian con una mejor función ejecutiva, una velocidad de procesamiento de información más rápida y un mayor volumen de materia gris del hipocampo, el núcleo caudado y el núcleo accumbens. [1] [6] El ejercicio aeróbico a largo plazo también se asocia con cambios epigenéticos beneficiosos persistentes que resultan en un mejor manejo del estrés, una mejor función cognitiva y una mayor actividad neuronal ( señalización de c-Fos y BDNF ). [4] [46]
Crecimiento estructural
Las revisiones de los estudios de neuroimagen indican que el ejercicio aeróbico constante aumenta el volumen de materia gris en casi todas las regiones del cerebro, [43] con aumentos más pronunciados que ocurren en las regiones del cerebro asociadas con el procesamiento de la memoria, el control cognitivo, la función motora y la recompensa ; [1] [5] [6] [8] [43] las ganancias más prominentes en el volumen de materia gris se observan en la corteza prefrontal, el núcleo caudado y el hipocampo, que apoyan el control cognitivo y el procesamiento de la memoria, entre otras funciones cognitivas. [1] [6] [8] [9] Además, las mitades izquierda y derecha de la corteza prefrontal, el hipocampo y la corteza cingulada parecen estar más interconectadas funcionalmente en respuesta al ejercicio aeróbico constante. [1] [7] Tres revisiones indican que se producen mejoras marcadas en el volumen de materia gris prefrontal e hipocampal en adultos sanos que realizan regularmente ejercicio de intensidad media durante varios meses. [1] [6] [47] Otras regiones del cerebro que demuestran ganancias moderadas o menos significativas en el volumen de materia gris durante la obtención de imágenes neurológicas incluyen la corteza cingulada anterior , la corteza parietal , el cerebelo y el núcleo accumbens . [5] [6] [8] [48]
Se ha demostrado que el ejercicio regular contrarresta el encogimiento del hipocampo y el deterioro de la memoria que ocurre naturalmente al final de la edad adulta. [5] [6] [8] Los adultos sedentarios mayores de 55 años muestran una disminución anual de 1-2% en el volumen del hipocampo. [8] [49] Un estudio de neuroimagen con una muestra de 120 adultos reveló que la participación en ejercicio aeróbico regular aumentó el volumen del hipocampo izquierdo en un 2,12% y el hipocampo derecho en un 1,97% durante un período de un año. [8] [49] Los sujetos en el grupo de estiramiento de baja intensidad que tenían niveles más altos de condición física al inicio del estudio mostraron menos pérdida de volumen del hipocampo, lo que proporciona evidencia de que el ejercicio protege contra el deterioro cognitivo relacionado con la edad. [49] En general, las personas que hacen más ejercicio durante un período determinado tienen mayores volúmenes del hipocampo y una mejor función de la memoria. [5] [8] También se ha demostrado que el ejercicio aeróbico induce el crecimiento de los tractos de materia blanca en el cuerpo calloso anterior , que normalmente se encoge con la edad. [5] [47]
Las diversas funciones de las estructuras cerebrales que muestran aumentos en el volumen de materia gris inducidos por el ejercicio incluyen:
- Cortezas cinguladas prefrontales y anteriores : necesarias para el control cognitivo de la conducta, en particular: memoria de trabajo , control de la atención , toma de decisiones , flexibilidad cognitiva , cognición social y control inhibitorio de la conducta; [50] [51] implicados en el trastorno por déficit de atención con hiperactividad (TDAH) y la adicción [50]
- Nucleus accumbens : responsable de la prominencia de los incentivos ("querer" o deseo, la forma de motivación asociada con la recompensa ) y el refuerzo positivo ; implicado en la adicción [52]
- Hipocampo : responsable del almacenamiento y consolidación de la memoria declarativa y la memoria espacial ; [6] [53] implicados en la depresión [8]
- Cerebelo : responsable de la coordinación motora y el aprendizaje motor [54]
- Núcleo caudado : responsable del aprendizaje de respuesta al estímulo y del control inhibitorio; implicados en la enfermedad de Parkinson y el TDAH [50] [53]
- Corteza parietal : responsable de la percepción sensorial , la memoria de trabajo y la atención [50] [55]
Efectos persistentes sobre la cognición
En concordancia con las funciones funcionales de las estructuras cerebrales que exhiben mayores volúmenes de materia gris, se ha demostrado que el ejercicio regular durante un período de varios meses mejora de manera persistente numerosas funciones ejecutivas y varias formas de memoria. [5] [7] [9] [56] [57] [58] En particular, se ha demostrado que el ejercicio aeróbico constante mejora el control de la atención , [nota 3] velocidad de procesamiento de la información , flexibilidad cognitiva (p. Ej., Cambio de tareas ), inhibición control , [nota 4] actualización y capacidad de la memoria de trabajo , [nota 5] memoria declarativa , [nota 6] y memoria espacial . [5] [6] [7] [9] [10] [56] [57] En adultos jóvenes y de mediana edad sanos, los tamaños del efecto de las mejoras en la función cognitiva son mayores para los índices de funciones ejecutivas y de pequeños a moderados para aspectos de la memoria y la velocidad de procesamiento de la información. [1] [10] Es posible que en los adultos mayores, las personas se beneficien cognitivamente al participar en ejercicios aeróbicos y de resistencia de al menos una intensidad moderada. [60] Las personas que tienen un estilo de vida sedentario tienden a tener funciones ejecutivas deterioradas en comparación con otras personas que no hacen ejercicio más físicamente. [9] [56] También se ha observado una relación recíproca entre el ejercicio y las funciones ejecutivas: las mejoras en los procesos de control ejecutivo, como el control de la atención y el control inhibitorio, aumentan la tendencia del individuo al ejercicio. [9]
Mecanismo de efectos
Señalización BDNF
Uno de los efectos más importantes del ejercicio en el cerebro es el aumento de la síntesis y expresión de BDNF , un neuropéptido y hormona , en el cerebro y la periferia, lo que resulta en un aumento de la señalización a través de su receptor tirosina quinasa , el receptor de tropomiosina quinasa B (TrkB). [4] [63] [64] Dado que el BDNF es capaz de cruzar la barrera hematoencefálica , la síntesis de BDNF periférica más alta también aumenta la señalización del BDNF en el cerebro. [41] Los aumentos inducidos por el ejercicio en la señalización del BDNF se asocian con cambios epigenéticos beneficiosos , mejor función cognitiva, mejor estado de ánimo y mejor memoria. [4] [8] [19] [63] Además, la investigación ha proporcionado un gran apoyo al papel del BDNF en la neurogénesis del hipocampo, la plasticidad sináptica y la reparación neural. [5] [63] Realizar ejercicio aeróbico de intensidad moderada a alta, como correr, nadar y andar en bicicleta, aumenta la biosíntesis de BDNF a través de la señalización de mioquinas , lo que da como resultado un aumento de hasta tres veces en los niveles de plasma sanguíneo y de BDNF; [4] [63] [64] la intensidad del ejercicio se correlaciona positivamente con la magnitud del aumento de la biosíntesis y expresión de BDNF. [4] [63] [64] Un metaanálisis de estudios que involucran el efecto del ejercicio en los niveles de BDNF encontró que el ejercicio constante también aumenta modestamente los niveles de BDNF en reposo. [19] Esto tiene implicaciones importantes para el ejercicio como mecanismo para reducir el estrés, ya que el estrés está estrechamente relacionado con la disminución de los niveles de BDNF en el hipocampo. De hecho, los estudios sugieren que el BDNF contribuye a los efectos reductores de la ansiedad de los antidepresivos. El aumento de los niveles de BDNF causado por el ejercicio ayuda a revertir la disminución de BDNF inducida por el estrés que media el estrés a corto plazo y amortigua las enfermedades relacionadas con el estrés a largo plazo. [sesenta y cinco]
Señalización IGF-1
El IGF-1 es un péptido y un factor neurotrófico que media algunos de los efectos de la hormona del crecimiento ; [66] IGF-1 provoca sus efectos fisiológicos mediante la unión a una específica de la tirosina quinasa del receptor , el receptor de IGF-1 , para el crecimiento de tejido de control y remodelación. [66] En el cerebro, el IGF-1 funciona como un factor neurotrófico que, como el BDNF , juega un papel importante en la cognición, la neurogénesis y la supervivencia neuronal. [63] [67] [68] La actividad física se relaciona con niveles elevados de IGF-1 en el suero sanguíneo , que se sabe que contribuye a la neuroplasticidad en el cerebro debido a su capacidad para cruzar la barrera hematoencefálica y el líquido cefalorraquídeo barrera ; [5] [63] [66] [67] en consecuencia, una revisión señaló que el IGF-1 es un mediador clave de la neurogénesis en adultos inducida por el ejercicio, mientras que una segunda revisión lo caracterizó como un factor que vincula la "aptitud corporal" con el "cerebro aptitud física". [66] [67] La cantidad de IGF-1 liberada al plasma sanguíneo durante el ejercicio se correlaciona positivamente con la intensidad y duración del ejercicio. [69]
Señalización VEGF
VEGF es una proteína de señalización neurotrófica y angiogénica (es decir, que promueve el crecimiento de los vasos sanguíneos) que se une a dos receptores tirosina quinasas, VEGFR1 y VEGFR2 , que se expresan en neuronas y células gliales en el cerebro. [68] La hipoxia , o suministro de oxígeno celular inadecuado, regula fuertemente la expresión de VEGF y VEGF ejerce un efecto neuroprotector en las neuronas hipóxicas. [68] Al igual que el BDNF y el IGF-1 , se ha demostrado que el ejercicio aeróbico aumenta la biosíntesis de VEGF en el tejido periférico que posteriormente cruza la barrera hematoencefálica y promueve la neurogénesis y la formación de vasos sanguíneos en el sistema nervioso central . [41] [42] [70] Se ha demostrado que los aumentos de la señalización de VEGF inducidos por el ejercicio mejoran el volumen sanguíneo cerebral y contribuyen a la neurogénesis inducida por el ejercicio en el hipocampo. [5] [42] [70]
GPLD1
En julio de 2020, los científicos informaron que después de que los ratones hacen ejercicio, sus hígados secretan la proteína GPLD1 , que también está elevada en los seres humanos de edad avanzada que hacen ejercicio con regularidad, que esto se asocia con una función cognitiva mejorada en los ratones ancianos y que aumenta la cantidad de GPLD1 producida por el hígado del ratón en ratones viejos a través de la ingeniería genética podría producir muchos beneficios del ejercicio regular para sus cerebros, como un aumento de los niveles de BDNF, neurogénesis y un mejor funcionamiento cognitivo en las pruebas. [71] [72]
Efectos a corto plazo
Efectos transitorios sobre la cognición
Además de los efectos persistentes sobre la cognición que resultan de varios meses de ejercicio diario, se ha demostrado que el ejercicio intenso (es decir, una sola sesión de ejercicio) mejora transitoriamente varias funciones cognitivas. [14] [73] [74] Las revisiones y los metanálisis de la investigación sobre los efectos del ejercicio agudo en la cognición en adultos jóvenes y de mediana edad sanos han concluido que la velocidad de procesamiento de la información y una serie de funciones ejecutivas, incluida la atención, la memoria de trabajo , resolución de problemas, flexibilidad cognitiva, fluidez verbal, toma de decisiones y control inhibitorio, todo mejora durante un período de hasta 2 horas después del ejercicio. [14] [73] [74] Una revisión sistemática de estudios realizados en niños también sugirió que algunas de las mejoras inducidas por el ejercicio en la función ejecutiva son evidentes después de sesiones únicas de ejercicio, mientras que otros aspectos (p. Ej., Control de la atención) solo mejoran después ejercicio constante de forma regular. [57] Otra investigación ha sugerido mejoras de rendimiento inmediatas durante el ejercicio, como mejoras simultáneas con el ejercicio en la velocidad de procesamiento durante las tareas de la memoria de trabajo visual. [75]
Euforia inducida por el ejercicio
El ejercicio continuo puede producir un estado transitorio de euforia , un estado afectivo con valencia positiva que implica la experiencia de placer y sentimientos de profunda satisfacción, euforia y bienestar, que se conoce coloquialmente como "euforia del corredor " en carreras de distancia o " remero alto "en el remo . [15] [16] [76] [77] Las revisiones médicas actuales indican que varios euforizantes endógenos son responsables de producir euforia relacionada con el ejercicio, específicamente fenetilamina (un psicoestimulante endógeno ), β-endorfina (un opioide endógeno ) y anandamida (un cannabinoide endógeno ). [78] [79] [80] [81] [82]
Efectos sobre la neuroquímica
β-feniletilamina
Vías biosintéticas para catecolaminas y trazas de aminas en el cerebro humano [83] [84] [85] ![]() |
β-Phenylethylamine, commonly referred to as phenethylamine, is a human trace amine and potent catecholaminergic and glutamatergic neuromodulator that has similar psychostimulant and euphoriant effects and a similar chemical structure to amphetamine.[86] Thirty minutes of moderate to high intensity physical exercise has been shown to induce an enormous increase in urinary β-phenylacetic acid, the primary metabolite of phenethylamine.[78][79][80] Two reviews noted a study where the average 24 hour urinary β-phenylacetic acid concentration among participants following just 30 minutes of intense exercise increased by 77% relative to baseline concentrations in resting control subjects;[78][79][80] the reviews suggest that phenethylamine synthesis sharply increases while an individual is exercising, during which time it is rapidly metabolized due to its short half-life of roughly 30 seconds.[78][79][80][87] In a resting state, phenethylamine is synthesized in catecholamine neurons from L-phenylalanine by aromatic amino acid decarboxylase (AADC) at approximately the same rate at which dopamine is produced.[87]
In light of this observation, the original paper and both reviews suggest that phenethylamine plays a prominent role in mediating the mood-enhancing euphoric effects of a runner's high, as both phenethylamine and amphetamine are potent euphoriants.[78][79][80]
β-Endorphin
β-Endorphin (contracted from "endogenous morphine") is an endogenous opioid neuropeptide that binds to μ-opioid receptors, in turn producing euphoria and pain relief.[81] A meta-analytic review found that exercise significantly increases the secretion of β-endorphin and that this secretion is correlated with improved mood states.[81] Moderate intensity exercise produces the greatest increase in β-endorphin synthesis, while higher and lower intensity forms of exercise are associated with smaller increases in β-endorphin synthesis.[81] A review on β-endorphin and exercise noted that an individual's mood improves for the remainder of the day following physical exercise and that one's mood is positively correlated with overall daily physical activity level.[81] However, data from rodents and humans have shown that pharmacological blockade of endogenous endorphins does not prevent the development of a runner's high, while blockade of endocannabinoids does.[88][89]
Anandamide
Anandamide is an endogenous cannabinoid and retrograde neurotransmitter that binds to cannabinoid receptors (primarily CB1), in turn producing euphoria.[76][82] It has been shown that aerobic exercise causes an increase in plasma anandamide levels, where the magnitude of this increase is highest at moderate exercise intensity (i.e., exercising at ~70–80% maximum heart rate).[82] Increases in plasma anandamide levels are associated with psychoactive effects because anandamide is able to cross the blood–brain barrier and act within the central nervous system.[82] Thus, because anandamide is a euphoriant and aerobic exercise is associated with euphoric effects, it has been proposed that anandamide partly mediates the short-term mood-lifting effects of exercise (e.g., the euphoria of a runner's high) via exercise-induced increases in its synthesis.[76][82]
In mice it was demonstrated that certain features of a runner's high depend on cannabinoid receptors. Pharmacological or genetic disruption of cannabinoid signaling via cannabinoid receptors prevents the analgesic and anxiety-reducing effects of running.[88][non-primary source needed]
Cortisol and the psychological stress response
![Diagram of the HPA axis](http://wikiimg.tojsiabtv.com/wikipedia/commons/thumb/e/ee/HPA_Axis_Diagram_%28Brian_M_Sweis_2012%29.svg/325px-HPA_Axis_Diagram_%28Brian_M_Sweis_2012%29.svg.png)
The "stress hormone", cortisol, is a glucocorticoid that binds to glucocorticoid receptors.[90][91][92] Psychological stress induces the release of cortisol from the adrenal gland by activating the hypothalamic–pituitary–adrenal axis (HPA axis).[90][91][92] Short-term increases in cortisol levels are associated with adaptive cognitive improvements, such as enhanced inhibitory control;[42][91][92] however, excessively high exposure or prolonged exposure to high levels of cortisol causes impairments in cognitive control and has neurotoxic effects in the human brain.[42][56][92] For example, chronic psychological stress decreases BDNF expression, which has detrimental effects on hippocampal volume and can lead to depression.[42][90]
As a physical stressor, aerobic exercise stimulates cortisol secretion in an intensity-dependent manner;[91] however, it does not result in long-term increases in cortisol production since this exercise-induced effect on cortisol is a response to transient negative energy balance.[note 7][91] Individuals who have recently exercised exhibit improvements in stress coping behaviors.[4][42][46] Aerobic exercise increases physical fitness and lowers neuroendocrine (i.e., HPA axis) reactivity and therefore reduces the biological response to psychological stress in humans (e.g., reduced cortisol release and attenuated heart rate response).[14][42][93] Exercise also reverses stress-induced decreases in BDNF expression and signaling in the brain, thereby acting as a buffer against stress-related diseases like depression.[42][90][93]
Glutamate and GABA
Glutamate, one of the most common neurochemicals in the brain, is an excitatory neurotransmitter involved in many aspects of brain function, including learning and memory.[94] Based upon animal models, exercise appears to normalize the excessive levels of glutamate neurotransmission into the nucleus accumbens that occurs in drug addiction.[33] A review of the effects of exercise on neurocardiac function in preclinical models noted that exercise-induced neuroplasticity of the rostral ventrolateral medulla (RVLM) has an inhibitory effect on glutamatergic neurotransmission in this region, in turn reducing sympathetic activity;[95] the review hypothesized that this neuroplasticity in the RVLM is a mechanism by which regular exercise prevents inactivity-related cardiovascular disease.[95]
Monoamine neurotransmitters
Acetylcholine
Efectos en los niños
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![](http://wikiimg.tojsiabtv.com/wikipedia/en/thumb/f/f2/Kids_exercising.jpeg/220px-Kids_exercising.jpeg)
Sibley and Etnier (2003) performed a meta-analysis that looked at the relationship between physical activity and cognitive performance in children.[96] They reported a beneficial relationship in the categories of perceptual skills, intelligence quotient, achievement, verbal tests, mathematic tests, developmental level/academic readiness and other, with the exception of memory, that was found to be unrelated to physical activity.[96] The correlation was strongest for the age ranges of 4–7 and 11–13 years.[96] On the other hand, Chaddock and colleagues (2011) found results that contrasted Sibley and Etnier's meta-analysis. In their study, the hypothesis was that lower-fit children would perform poorly in executive control of memory and have smaller hippocampal volumes compared to higher-fit children.[97] Instead of physical activity being unrelated to memory in children between 4 and 18 years of age, it may be that preadolescents of higher fitness have larger hippocampal volumes, than preadolescents of lower fitness. According to a previous study done by Chaddock and colleagues (Chaddock et al. 2010), a larger hippocampal volume would result in better executive control of memory.[98] They concluded that hippocampal volume was positively associated with performance on relational memory tasks.[98] Their findings are the first to indicate that aerobic fitness may relate to the structure and function of the preadolescent human brain.[98] In Best’s (2010) meta-analysis of the effect of activity on children’s executive function, there are two distinct experimental designs used to assess aerobic exercise on cognition. The first is chronic exercise, in which children are randomly assigned to a schedule of aerobic exercise over several weeks and later assessed at the end.[99] The second is acute exercise, which examines the immediate changes in cognitive functioning after each session.[99] The results of both suggest that aerobic exercise may briefly aid children’s executive function and also influence more lasting improvements to executive function.[99] Other studies have suggested that exercise is unrelated to academic performance, perhaps due to the parameters used to determine exactly what academic achievement is.[100] This area of study has been a focus for education boards that make decisions on whether physical education should be implemented in the school curriculum, how much time should be dedicated to physical education, and its impact on other academic subjects.[96]
Another study found that sixth-graders who participated in vigorous physical activity at least three times a week had the highest scores compared to those who participated in moderate or no physical activity at all. The kids who participated in vigorous physical activity scored three points higher, on average, on their academic test, which consisted of math, science, English, and world studies.[101]
Animal studies have also shown that exercise can impact brain development early on in life. Mice that had access to running wheels and other such exercise equipment had better neuronal growth in the neural systems involved in learning and memory.[100] Neuroimaging of the human brain has yielded similar results, where exercise leads to changes in brain structure and function.[100] Some investigations have linked low levels of aerobic fitness in children with impaired executive function in older adults, but there is mounting evidence it may also be associated with a lack of selective attention, response inhibition, and interference control.[97]
Efectos sobre los trastornos del sistema nervioso central
Addiction
Clinical and preclinical evidence indicate that consistent aerobic exercise, especially endurance exercise (e.g., marathon running), actually prevents the development of certain drug addictions and is an effective adjunct treatment for drug addiction, and psychostimulant addiction in particular.[32][33][34][35][36] Consistent aerobic exercise magnitude-dependently (i.e., by duration and intensity) reduces drug addiction risk, which appears to occur through the reversal of drug-induced, addiction-related neuroplasticity.[33][34] One review noted that exercise may prevent the development of drug addiction by altering ΔFosB or c-Fos immunoreactivity in the striatum or other parts of the reward system.[36] Moreover, aerobic exercise decreases psychostimulant self-administration, reduces the reinstatement (i.e., relapse) of drug-seeking, and induces opposite effects on striatal dopamine receptor D2 (DRD2) signaling (increased DRD2 density) to those induced by pathological stimulant use (decreased DRD2 density).[33][34] Consequently, consistent aerobic exercise may lead to better treatment outcomes when used as an adjunct treatment for drug addiction.[33][35] As of 2016[update], more clinical research is still needed to understand the mechanisms and confirm the efficacy of exercise in drug addiction treatment and prevention.[32][36]
Form of neuroplasticity or behavioral plasticity | Type of reinforcer | Sources | |||||
---|---|---|---|---|---|---|---|
Opiates | Psychostimulants | High fat or sugar food | Sexual intercourse | Physical exercise (aerobic) | Environmentalenrichment | ||
ΔFosB expression in nucleus accumbens D1-type MSNs | ↑ | ↑ | ↑ | ↑ | ↑ | ↑ | [34] |
Behavioral plasticity | |||||||
Escalation of intake | Yes | Yes | Yes | [34] | |||
Psychostimulant cross-sensitization | Yes | Not applicable | Yes | Yes | Attenuated | Attenuated | [34] |
Psychostimulant self-administration | ↑ | ↑ | ↓ | ↓ | ↓ | [34] | |
Psychostimulant conditioned place preference | ↑ | ↑ | ↓ | ↑ | ↓ | ↑ | [34] |
Reinstatement of drug-seeking behavior | ↑ | ↑ | ↓ | ↓ | [34] | ||
Neurochemical plasticity | |||||||
CREB phosphorylation in the nucleus accumbens | ↓ | ↓ | ↓ | ↓ | ↓ | [34] | |
Sensitized dopamine response in the nucleus accumbens | No | Yes | No | Yes | [34] | ||
Altered striatal dopamine signaling | ↓DRD2, ↑DRD3 | ↑DRD1, ↓DRD2, ↑DRD3 | ↑DRD1, ↓DRD2, ↑DRD3 | ↑DRD2 | ↑DRD2 | [34] | |
Altered striatal opioid signaling | No change or ↑μ-opioid receptors | ↑μ-opioid receptors ↑κ-opioid receptors | ↑μ-opioid receptors | ↑μ-opioid receptors | No change | No change | [34] |
Changes in striatal opioid peptides | ↑dynorphin No change: enkephalin | ↑dynorphin | ↓enkephalin | ↑dynorphin | ↑dynorphin | [34] | |
Mesocorticolimbic synaptic plasticity | |||||||
Number of dendrites in the nucleus accumbens | ↓ | ↑ | ↑ | [34] | |||
Dendritic spine density in the nucleus accumbens | ↓ | ↑ | ↑ | [34] |
Attention deficit hyperactivity disorder
Regular physical exercise, particularly aerobic exercise, is an effective add-on treatment for ADHD in children and adults, particularly when combined with stimulant medication (i.e., amphetamine or methylphenidate), although the best intensity and type of aerobic exercise for improving symptoms are not currently known.[22][23][102] In particular, the long-term effects of regular aerobic exercise in ADHD individuals include better behavior and motor abilities, improved executive functions (including attention, inhibitory control, and planning, among other cognitive domains), faster information processing speed, and better memory.[22][23][102] Parent-teacher ratings of behavioral and socio-emotional outcomes in response to regular aerobic exercise include: better overall function, reduced ADHD symptoms, better self-esteem, reduced levels of anxiety and depression, fewer somatic complaints, better academic and classroom behavior, and improved social behavior.[22] Exercising while on stimulant medication augments the effect of stimulant medication on executive function.[22] It is believed that these short-term effects of exercise are mediated by an increased abundance of synaptic dopamine and norepinephrine in the brain.[22]
Major depressive disorder
A number of medical reviews have indicated that exercise has a marked and persistent antidepressant effect in humans,[5][17][18][21][103][104] an effect believed to be mediated through enhanced BDNF signaling in the brain.[8][21] Several systematic reviews have analyzed the potential for physical exercise in the treatment of depressive disorders. The 2013 Cochrane Collaboration review on physical exercise for depression noted that, based upon limited evidence, it is more effective than a control intervention and comparable to psychological or antidepressant drug therapies.[103] Three subsequent 2014 systematic reviews that included the Cochrane review in their analysis concluded with similar findings: one indicated that physical exercise is effective as an adjunct treatment (i.e., treatments that are used together) with antidepressant medication;[21] the other two indicated that physical exercise has marked antidepressant effects and recommended the inclusion of physical activity as an adjunct treatment for mild–moderate depression and mental illness in general.[17][18] One systematic review noted that yoga may be effective in alleviating symptoms of prenatal depression.[105] Another review asserted that evidence from clinical trials supports the efficacy of physical exercise as a treatment for depression over a 2–4 month period.[5] These benefits have also been noted in old age, with a review conducted in 2019 finding that exercise is an effective treatment for clinically diagnosed depression in older adults.[106]
A meta-analysis from July 2016 concluded that physical exercise improves overall quality of life in individuals with depression relative to controls.[11][107]
Brain cancers
Mild cognitive impairment
The American Academy of Neurology's January 2018 update of their clinical practice guideline for mild cognitive impairment states that clinicians should recommend regular exercise (two times per week) to individuals who have been diagnosed with this condition.[24] This guidance is based upon a moderate amount of high-quality evidence which supports the efficacy of regular physical exercise (twice weekly over a 6-month period) for improving cognitive symptoms in individuals with mild cognitive impairment.[24]
Neurodegenerative disorders
Alzheimer's disease
Alzheimer's Disease is a cortical neurodegenerative disorder and the most prevalent form of dementia, representing approximately 65% of all cases of dementia; it is characterized by impaired cognitive function, behavioral abnormalities, and a reduced capacity to perform basic activities of daily life.[25][26] Two meta-analytic systematic reviews of randomized controlled trials with durations of 3–12 months have examined the effects of physical exercise on the aforementioned characteristics of Alzheimer's disease.[25][26] The reviews found beneficial effects of physical exercise on cognitive function, the rate of cognitive decline, and the ability to perform activities of daily living in individuals with Alzheimer's disease.[25][26] One review suggested that, based upon transgenic mouse models, the cognitive effects of exercise on Alzheimer's disease may result from a reduction in the quantity of amyloid plaque.[25][108]
The Caerphilly Prospective study followed 2,375 male subjects over 30 years and examined the association between healthy lifestyles and dementia, among other factors.[109] Analyses of the Caerphilly study data have found that exercise is associated with a lower incidence of dementia and a reduction in cognitive impairment.[109][110] A subsequent systematic review of longitudinal studies also found higher levels of physical activity to be associated with a reduction in the risk of dementia and cognitive decline;[31] this review further asserted that increased physical activity appears to be causally related with these reduced risks.[31]
Parkinson's disease
Parkinson's disease (PD) is a movement disorder that produces symptoms such as bradykinesia, rigidity, shaking, and impaired gait.[111]
A review by Kramer and colleagues (2006) found that some neurotransmitter systems are affected by exercise in a positive way.[112] A few studies reported seeing an improvement in brain health and cognitive function due to exercise.[112][113] One particular study by Kramer and colleagues (1999) found that aerobic training improved executive control processes supported by frontal and prefrontal regions of the brain.[114] These regions are responsible for the cognitive deficits in PD patients, however there was speculation that the difference in the neurochemical environment in the frontal lobes of PD patients may inhibit the benefit of aerobic exercise.[115] Nocera and colleagues (2010) performed a case study based on this literature where they gave participants with early-to mid-staged PD, and the control group cognitive/language assessments with exercise regimens. Individuals performed 20 minutes of aerobic exercise three times a week for 8 weeks on a stationary exercise cycle. It was found that aerobic exercise improved several measures of cognitive function,[115] providing evidence that such exercise regimens may be beneficial to patients with PD.
Ver también
- Brain fitness
- Memory improvement
- Nootropic
- Exercise therapy
- Exercise is Medicine
- Exercise prescription
Notas
- ^ Neurotrophic factors are peptides or other small proteins that promote the growth, survival, and differentiation of neurons by binding to and activating their associated tyrosine kinases.[39]
- ^ Adult neurogenesis is the postnatal (after-birth) growth of new neurons, a beneficial form of neuroplasticity.[38]
- ^ Attentional control allows an individual to focus their attention on a specific source and ignore other stimuli that compete for one's attention,[44] such as in the cocktail party effect.
- ^ Inhibitory control is the process of altering one's learned behavioral responses, sometimes called "prepotent responses", in a way that makes it easier to complete a particular goal.[50][59] Inhibitory control allows individuals to control their impulses and habits when necessary or desired,[50][56][59] e.g., to overcome procrastination.
- ^ Working memory is the form of memory used by an individual at any given moment for active information processing,[44] such as when reading or writing an encyclopedia article. Working memory has a limited capacity and functions as an information buffer, analogous to a computer's data buffer, that permits the manipulation of information for comprehension, decision-making, and guidance of behavior.[50]
- ^ Declarative memory, also known as explicit memory, is the form of memory that pertains to facts and events.[53]
- ^ In healthy individuals, this energy deficit resolves simply from eating and drinking a sufficient amount of food and beverage after exercising.
Referencias
- ^ a b c d e f g h i j k l m 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. S2CID 54301951.
- ^ a b c 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.
- ^ a b 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.
- ^ a b c d e f g h Denham J, Marques FZ, O'Brien BJ, Charchar FJ (February 2014). "Exercise: putting action into our epigenome". Sports Med. 44 (2): 189–209. doi:10.1007/s40279-013-0114-1. PMID 24163284. S2CID 30210091.
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.
- ^ a b c d e f g h i j k l m n o p q r Gomez-Pinilla F, Hillman C (January 2013). "The influence of exercise on cognitive abilities". Comprehensive Physiology. Compr. Physiol. 3. pp. 403–428. doi:10.1002/cphy.c110063. ISBN 9780470650714. PMC 3951958. PMID 23720292.
- ^ a b c d e f g h i j k l m n Erickson KI, Leckie RL, Weinstein AM (September 2014). "Physical activity, fitness, and gray matter volume". Neurobiol. Aging. 35 Suppl 2: S20–528. doi:10.1016/j.neurobiolaging.2014.03.034. PMC 4094356. PMID 24952993.
- ^ a b c d e f Guiney H, Machado L (February 2013). "Benefits of regular aerobic exercise for executive functioning in healthy populations". Psychon Bull Rev. 20 (1): 73–86. doi:10.3758/s13423-012-0345-4. PMID 23229442. S2CID 24190840.
- ^ a b c d e f g h i j k l m n Erickson KI, Miller DL, Roecklein KA (2012). "The aging hippocampus: interactions between exercise, depression, and BDNF". Neuroscientist. 18 (1): 82–97. doi:10.1177/1073858410397054. PMC 3575139. PMID 21531985.
- ^ a b c d e f g h Buckley J, Cohen JD, Kramer AF, McAuley E, Mullen SP (2014). "Cognitive control in the self-regulation of physical activity and sedentary behavior". Front Hum Neurosci. 8: 747. doi:10.3389/fnhum.2014.00747. PMC 4179677. PMID 25324754.
- ^ a b c d e 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). ... 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. - ^ a b c Schuch FB, Vancampfort D, Rosenbaum S, Richards J, Ward PB, Stubbs B (July 2016). "Exercise improves physical and psychological quality of life in people with depression: A meta-analysis including the evaluation of control group response". Psychiatry Res. 241: 47–54. doi:10.1016/j.psychres.2016.04.054. PMID 27155287. S2CID 4787287.
Exercise has established efficacy as an antidepressant in people with depression. ... Exercise significantly improved physical and psychological domains and overall QoL. ... The lack of improvement among control groups reinforces the role of exercise as a treatment for depression with benefits to QoL.
- ^ Pratali L, Mastorci F, Vitiello N, Sironi A, Gastaldelli A, Gemignani A (November 2014). "Motor Activity in Aging: An Integrated Approach for Better Quality of Life". International Scholarly Research Notices. 2014: 257248. doi:10.1155/2014/257248. PMC 4897547. PMID 27351018.
Research investigating the effects of exercise on older adults has primarily focused on brain structural and functional changes with relation to cognitive improvement. In particular, several cross-sectional and intervention studies have shown a positive association between physical activity and cognition in older persons [86] and an inverse correlation with cognitive decline and dementia [87]. Older adults enrolled in a 6-month aerobic fitness intervention increased brain volume in both gray matter (anterior cingulate cortex, supplementary motor area, posterior middle frontal gyrus, and left superior temporal lobe) and white matter (anterior third of corpus callosum) [88]. In addition, Colcombe and colleagues showed that older adults with higher cardiovascular fitness levels are better at activating attentional resources, including decreased activation of the anterior cingulated cortex. One of the possible mechanisms by which physical activity may benefit cognition is that physical activity maintains brain plasticity, increases brain volume, stimulates neurogenesis and synaptogenesis, and increases neurotrophic factors in different areas of the brain, possibly providing reserve against later cognitive decline and dementia [89, 90].
- ^ Mandolesi, Laura; Polverino, Arianna; Montuori, Simone; Foti, Francesca; Ferraioli, Giampaolo; Sorrentino, Pierpaolo; Sorrentino, Giuseppe (27 April 2018). "Effects of Physical Exercise on Cognitive Functioning and Wellbeing: Biological and Psychological Benefits". Frontiers in Psychology. 9: 509. doi:10.3389/fpsyg.2018.00509. PMC 5934999. PMID 29755380.
- ^ a b c d e f g h i j 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. PMC 5928534. PMID 29765853. Lay summary – Can A Single Exercise Session Benefit Your Brain? (12 June 2017).
A large collection of research in humans has shown that a single bout of exercise alters behavior at the level of affective state and cognitive functioning in several key ways. In terms of affective state, acute exercise decreases negative affect, increases positive affect, and decreases the psychological and physiological response to acute stress [28]. These effects have been reported to persist for up to 24 hours after exercise cessation [28, 29, 53]. In terms of cognitive functioning, acute exercise primarily enhances executive functions dependent on the prefrontal cortex including attention, working memory, problem solving, cognitive flexibility, verbal fluency, decision making, and inhibitory control [9]. These positive changes have been demonstrated to occur with very low to very high exercise intensities [9], with effects lasting for up to two hours after the end of the exercise bout (Fig. 1A) [27]. Moreover, many of these neuropsychological assessments measure several aspects of behavior including both accuracy of performance and speed of processing. McMorris and Hale performed a meta-analysis examining the effects of acute exercise on both accuracy and speed of processing, revealing that speed significantly improved post-exercise, with minimal or no effect on accuracy [17]. These authors concluded that increasing task difficulty or complexity may help to augment the effect of acute exercise on accuracy. ... However, in a comprehensive meta-analysis, Chang and colleagues found that exercise intensities ranging from very light (<50% MHR) to very hard (>93% MHR) have all been reported to improve cognitive functioning [9].
- ^ a b Cunha GS, Ribeiro JL, Oliveira AR (June 2008). "[Levels of beta-endorphin in response to exercise and overtraining]". Arq Bras Endocrinol Metabol (in Portuguese). 52 (4): 589–598. doi:10.1590/S0004-27302008000400004. PMID 18604371.
Interestingly, some symptoms of OT are related to beta-endorphin (beta-end(1-31)) effects. Some of its effects, such as analgesia, increasing lactate tolerance, and exercise-induced euphoria, are important for training.
- ^ a b Boecker H, Sprenger T, Spilker ME, Henriksen G, Koppenhoefer M, Wagner KJ, Valet M, Berthele A, Tolle TR (2008). "The runner's high: opioidergic mechanisms in the human brain". Cereb. Cortex. 18 (11): 2523–2531. doi:10.1093/cercor/bhn013. PMID 18296435.
The runner's high describes a euphoric state resulting from long-distance running.
- ^ a b c d 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. S2CID 29351791.
- ^ a b c 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. - ^ a b c d Szuhany KL, Bugatti M, Otto MW (October 2014). "A meta-analytic review of the effects of exercise on brain-derived neurotrophic factor". J Psychiatr Res. 60C: 56–64. doi:10.1016/j.jpsychires.2014.10.003. PMC 4314337. PMID 25455510.
Consistent evidence indicates that exercise improves cognition and mood, with preliminary evidence suggesting that brain-derived neurotrophic factor (BDNF) may mediate these effects. The aim of the current meta-analysis was to provide an estimate of the strength of the association between exercise and increased BDNF levels in humans across multiple exercise paradigms. We conducted a meta-analysis of 29 studies (N = 1111 participants) examining the effect of exercise on BDNF levels in three exercise paradigms: (1) a single session of exercise, (2) a session of exercise following a program of regular exercise, and (3) resting BDNF levels following a program of regular exercise. Moderators of this effect were also examined. Results demonstrated a moderate effect size for increases in BDNF following a single session of exercise (Hedges' g = 0.46, p < 0.001). Further, regular exercise intensified the effect of a session of exercise on BDNF levels (Hedges' g = 0.59, p = 0.02). Finally, results indicated a small effect of regular exercise on resting BDNF levels (Hedges' g = 0.27, p = 0.005). ... Effect size analysis supports the role of exercise as a strategy for enhancing BDNF activity in humans.
- ^ a b 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 [aerobic physical activity (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.
- ^ a b c d 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. - ^ a b c d e f Den Heijer AE, Groen Y, Tucha L, Fuermaier AB, Koerts J, Lange KW, Thome J, Tucha O (July 2016). "Sweat it out? The effects of physical exercise on cognition and behavior in children and adults with ADHD: a systematic literature review". J. Neural Transm. (Vienna). 124 (Suppl 1): 3–26. doi:10.1007/s00702-016-1593-7. PMC 5281644. PMID 27400928.
- ^ a b c Kamp CF, Sperlich B, Holmberg HC (July 2014). "Exercise reduces the symptoms of attention-deficit/hyperactivity disorder and improves social behaviour, motor skills, strength and neuropsychological parameters". Acta Paediatr. 103 (7): 709–14. doi:10.1111/apa.12628. PMID 24612421. S2CID 45881887.
The present review summarises the impact of exercise interventions (1–10 weeks in duration with at least two sessions each week) on parameters related to ADHD in 7-to 13-year-old children. We may conclude that all different types of exercise (here yoga, active games with and without the involvement of balls, walking and athletic training) attenuate the characteristic symptoms of ADHD and improve social behaviour, motor skills, strength and neuropsychological parameters without any undesirable side effects. Available reports do not reveal which type, intensity, duration and frequency of exercise is most effective in this respect and future research focusing on this question with randomised and controlled long-term interventions is warranted.
- ^ a b c Petersen RC, Lopez O, Armstrong MJ, Getchius T, Ganguli M, Gloss D, Gronseth GS, Marson D, Pringsheim T, Day GS, Sager M, Stevens J, Rae-Grant A (January 2018). "Practice guideline update summary: Mild cognitive impairment – Report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology". Neurology. Special article. 90 (3): 126–135. doi:10.1212/WNL.0000000000004826. PMC 5772157. PMID 29282327. Lay summary – Exercise may improve thinking ability and memory (27 December 2017).
In patients with MCI, exercise training (6 months) is likely to improve cognitive measures and cognitive training may improve cognitive measures. ... Clinicians should recommend regular exercise (Level B). ... Recommendation
For patients diagnosed with MCI, clinicians should recommend regular exercise (twice/week) as part of an overall approach to management (Level B). - ^ a b c d e 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.
- ^ a b c d 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. PMC 5360200. 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).
- ^ a b 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.
- ^ a b c 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. S2CID 33890283.
- ^ a b 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. S2CID 22822120.
- ^ a b 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 (9): CD002817. doi:10.1002/14651858.CD002817.pub4. PMC 7120224. PMID 24018704.
- ^ a b c Blondell SJ, Hammersley-Mather R, Veerman JL (May 2014). "Does physical activity prevent cognitive decline and dementia?: A systematic review and meta-analysis of longitudinal studies". BMC Public Health. 14: 510. doi:10.1186/1471-2458-14-510. PMC 4064273. PMID 24885250.
Longitudinal observational studies show an association between higher levels of physical activity and a reduced risk of cognitive decline and dementia. A case can be made for a causal interpretation. Future research should use objective measures of physical activity, adjust for the full range of confounders and have adequate follow-up length. Ideally, randomised controlled trials will be conducted. ... On the whole the results do, however, lend support to the notion of a causal relationship between physical activity, cognitive decline and dementia, according to the established criteria for causal inference.
- ^ a b c Carroll ME, Smethells JR (February 2016). "Sex Differences in Behavioral Dyscontrol: Role in Drug Addiction and Novel Treatments". Front. Psychiatry. 6: 175. doi:10.3389/fpsyt.2015.00175. PMC 4745113. PMID 26903885.
There is accelerating evidence that physical exercise is a useful treatment for preventing and reducing drug addiction ... In some individuals, exercise has its own rewarding effects, and a behavioral economic interaction may occur, such that physical and social rewards of exercise can substitute for the rewarding effects of drug abuse. ... The value of this form of treatment for drug addiction in laboratory animals and humans is that exercise, if it can substitute for the rewarding effects of drugs, could be self-maintained over an extended period of time. Work to date in [laboratory animals and humans] regarding exercise as a treatment for drug addiction supports this hypothesis. ... However, a RTC study was recently reported by Rawson et al. (226), whereby they used 8 weeks of exercise as a post-residential treatment for METH addiction, showed a significant reduction in use (confirmed by urine screens) in participants who had been using meth 18 days or less a month. ... Animal and human research on physical exercise as a treatment for stimulant addiction indicates that this is one of the most promising treatments on the horizon. [emphasis added]
- ^ a b c d e f Lynch WJ, Peterson AB, Sanchez V, Abel J, Smith MA (September 2013). "Exercise as a novel treatment for drug addiction: a neurobiological and stage-dependent hypothesis". Neurosci Biobehav Rev. 37 (8): 1622–1644. doi:10.1016/j.neubiorev.2013.06.011. PMC 3788047. PMID 23806439.
- ^ a b c d e f g h i j k l m n o p q Olsen CM (December 2011). "Natural rewards, neuroplasticity, and non-drug addictions". Neuropharmacology. 61 (7): 1109–1122. doi:10.1016/j.neuropharm.2011.03.010. PMC 3139704. PMID 21459101.
Similar to environmental enrichment, studies have found that exercise reduces self-administration and relapse to drugs of abuse (Cosgrove et al., 2002; Zlebnik et al., 2010). There is also some evidence that these preclinical findings translate to human populations, as exercise reduces withdrawal symptoms and relapse in abstinent smokers (Daniel et al., 2006; Prochaska et al., 2008), and one drug recovery program has seen success in participants that train for and compete in a marathon as part of the program (Butler, 2005). ... In humans, the role of dopamine signaling in incentive-sensitization processes has recently been highlighted by the observation of a dopamine dysregulation syndrome in some patients taking dopaminergic drugs. This syndrome is characterized by a medication-induced increase in (or compulsive) engagement in non-drug rewards such as gambling, shopping, or sex (Evans et al., 2006; Aiken, 2007; Lader, 2008).
- ^ a b c Linke SE, Ussher M (2015). "Exercise-based treatments for substance use disorders: evidence, theory, and practicality". Am J Drug Alcohol Abuse. 41 (1): 7–15. doi:10.3109/00952990.2014.976708. PMC 4831948. PMID 25397661.
The limited research conducted suggests that exercise may be an effective adjunctive treatment for SUDs. In contrast to the scarce intervention trials to date, a relative abundance of literature on the theoretical and practical reasons supporting the investigation of this topic has been published. ... numerous theoretical and practical reasons support exercise-based treatments for SUDs, including psychological, behavioral, neurobiological, nearly universal safety profile, and overall positive health effects.
- ^ a b c d Zhou Y, Zhao M, Zhou C, Li R (July 2015). "Sex differences in drug addiction and response to exercise intervention: From human to animal studies". Front. Neuroendocrinol. 40: 24–41. doi:10.1016/j.yfrne.2015.07.001. PMC 4712120. PMID 26182835.
Collectively, these findings demonstrate that exercise may serve as a substitute or competition for drug abuse by changing ΔFosB or cFos immunoreactivity in the reward system to protect against later or previous drug use. ... As briefly reviewed above, a large number of human and rodent studies clearly show that there are sex differences in drug addiction and exercise. The sex differences are also found in the effectiveness of exercise on drug addiction prevention and treatment, as well as underlying neurobiological mechanisms. The postulate that exercise serves as an ideal intervention for drug addiction has been widely recognized and used in human and animal rehabilitation. ... In particular, more studies on the neurobiological mechanism of exercise and its roles in preventing and treating drug addiction are needed.
- ^ a b 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.
- ^ a b Malenka RC, Nestler EJ, Hyman SE (2009). Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 5, 351. ISBN 9780071481274.
The clinical actions of fluoxetine, like those of many neuropharmacologic agents, reflect drug-induced neural plasticity, which is the process by which neurons adapt over time in response to chronic disturbance. ... For example, evidence indicates that prolonged increases in cortisol may be damaging to hippocampal neurons and can suppress hippocampal neurogenesis (the generation of new neurons postnatally).
- ^ Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 8:Atypical Neurotransmitters". In Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 199, 215. ISBN 9780071481274.
Neurotrophic factors are polypeptides or small proteins that support the growth, differentiation, and survival of neurons. They produce their effects by activation of tyrosine kinases.
- ^ "Neuroplasticity", Wikipedia, 23 October 2020, retrieved 28 October 2020
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Exercise-related improvements in brain function and structure may be conferred by the concurrent adaptations in vascular function and structure. Aerobic exercise increases the peripheral levels of growth factors (e.g., BDNF, IFG-1, and VEGF) which cross the blood-brain barrier (BBB) and stimulate neurogenesis and angiogenesis (Trejo et al., 2001; Lee et al., 2002; Fabel et al., 2003; Lopez-Lopez et al., 2004).
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- ^ a b c 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. S2CID 205895178.
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.
- ^ a b c Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 6: Widely Projecting Systems: Monoamines, Acetylcholine, and Orexin". In Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 147–148, 154–157. ISBN 9780071481274.
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Alterations in epigenetic modification patterns have been demonstrated to be dependent on exercise and growth hormone (GH), insulin-like growth factor 1 (IGF-1), and steroid administration. ... the authors observed improved stress coping in exercised subjects. Investigating the dentate gyrus, a brain region which is involved in learning and coping with stressful and traumatic events, they could show that this effect is mediated by increased 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).
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Control group: Active
Intervention: Aerobic exercise
[Increased GMV in:] Lobes (dorsal anterior cingulate cortex, supplementary motor area, middle frontal gyrus bilaterally); R inferior frontal gyrus, middle frontal gyrus and L superior temporal lobe; increase in the volume of anterior white matter tracts ... ↑GMV anterior hippocampus - ^ Ruscheweyh R, Willemer C, Krüger K, Duning T, Warnecke T, Sommer J, Völker K, Ho HV, Mooren F, Knecht S, Flöel A (July 2011). "Physical activity and memory functions: an interventional study". Neurobiol. Aging. 32 (7): 1304–19. doi:10.1016/j.neurobiolaging.2009.08.001. PMID 19716631. S2CID 22238883.
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- ^ a b c d e f g Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 13: Higher Cognitive Function and Behavioral Control". In Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 313–321. ISBN 9780071481274.
- ^ Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 13: Higher Cognitive Function and Behavioral Control". In Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. p. 315. ISBN 9780071481274.
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.
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There is weak evidence for the effect of acute bouts of physical activity on attention. ... Fortunately, the literature-base on the acute effect of PA on the underlying cognitive processes of academic performance is growing. Hillman et al. (2011) found in their review a positive effect of acute PA on brain health and cognition in children, but concluded it was complicated to compare the different studies due to the different outcome measures (e.g. memory, response time and accuracy, attention, and comprehension). Therefore, this review focuses on the sole outcome measure ‘attention’ as a mediator for cognition and achievement.
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- ^ Anderson, Elizabeth; Shivakumar, Geetha (2013). "Effects of Exercise and Physical Activity on Anxiety". Frontiers in Psychiatry. 4: 27. doi:10.3389/fpsyt.2013.00027. PMC 3632802. PMID 23630504.
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- ^ a b c Malenka RC, Nestler EJ, Hyman SE (2009). Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 221, 412. ISBN 9780071481274.
- ^ Gatti R, De Palo EF, Antonelli G, Spinella P (July 2012). "IGF-I/IGFBP system: metabolism outline and physical exercise". J. Endocrinol. Invest. 35 (7): 699–707. doi:10.3275/8456. PMID 22714057. S2CID 22974661.
Copeland et al. (90) studied the effect of a moderate-intensity exercise and a high-intensity equal duration intervalled exercise in healthy males. IGF-I and IGFBP-3 increased during both exercise trials, but only the IGFBP-3 area under curve was significantly greater during high-intensity exercise than resting control session. ... Decreased IGF-I and increased IGFBP-1 levels, observed by Rarick et al. (100) after mild aerobic training, might be an adaptive physiological response to prevent hypoglycemia following insulin-sensitizing training. In fact the decrease of circulating IGF-I during short-term training seems to be reflective of favorable neuromuscular anabolic adaptation and is a normal adaptive response to increased physical activity. The potential for exercise-induced increases in circulating IGF-I seems to require longer training duration (100).
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- ^ a b McMorris T, Hale BJ (December 2012). "Differential effects of differing intensities of acute exercise on speed and accuracy of cognition: a meta-analytical investigation". Brain and Cognition. 80 (3): 338–351. doi:10.1016/j.bandc.2012.09.001. PMID 23064033. S2CID 8320775.
- ^ Dodwell, Gordon; Müller, Hermann J.; Töllner, Thomas (May 2019). "Electroencephalographic evidence for improved visual working memory performance during standing and exercise". British Journal of Psychology. 110 (2): 400–427. doi:10.1111/bjop.12352. PMID 30311188.
- ^ a b c Raichlen DA, Foster AD, Gerdeman GL, Seillier A, Giuffrida A (2012). "Wired to run: exercise-induced endocannabinoid signaling in humans and cursorial mammals with implications for the 'runner's high'". J. Exp. Biol. 215 (Pt 8): 1331–1336. doi:10.1242/jeb.063677. PMID 22442371. S2CID 5129200.
Humans report a wide range of neurobiological rewards following moderate and intense aerobic activity, popularly referred to as the 'runner's high', which may function to encourage habitual aerobic exercise. ... Thus, a neurobiological reward for endurance exercise may explain why humans and other cursorial mammals habitually engage in aerobic exercise despite the higher associated energy costs and injury risks
- ^ Cohen EE, Ejsmond-Frey R, Knight N, Dunbar RI (2010). "Rowers' high: behavioural synchrony is correlated with elevated pain thresholds". Biol. Lett. 6 (1): 106–108. doi:10.1098/rsbl.2009.0670. PMC 2817271. PMID 19755532.
- ^ a b c d e Szabo A, Billett E, Turner J (2001). "Phenylethylamine, a possible link to the antidepressant effects of exercise?". Br J Sports Med. 35 (5): 342–343. doi:10.1136/bjsm.35.5.342. PMC 1724404. PMID 11579070.
The 24 hour mean urinary concentration of phenylacetic acid was increased by 77% after exercise. ... As phenylacetic acid reflects phenylethylamine levels3, and the latter has antidepressant effects, the antidepressant effects of exercise appear to be linked to increased phenylethylamine concentrations. Furthermore, considering the structural and pharmacological analogy between amphetamines and phenylethylamine, it is conceivable that phenylethylamine plays a role in the commonly reported "runners high" thought to be linked to cerebral β-endorphin activity. The substantial increase in phenylacetic acid excretion in this study implies that phenylethylamine levels are affected by exercise. ... A 30 minute bout of moderate to high intensity aerobic exercise increases phenylacetic acid levels in healthy regularly exercising men.
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The pharmacology of TAs might also contribute to a molecular understanding of the well-recognized antidepressant effect of physical exercise [51]. In addition to the various beneficial effects for brain function mainly attributed to an upregulation of peptide growth factors [52,53], exercise induces a rapidly enhanced excretion of the main β-PEA metabolite β-phenylacetic acid (b-PAA) by on average 77%, compared with resting control subjects [54], which mirrors increased β-PEA synthesis in view of its limited endogenous pool half-life of ~30 s [18,55].
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It has also been suggested that the antidepressant effects of exercise are due to an exercise-induced elevation of PE [151].
- ^ a b c d e 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. S2CID 40951545.
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- ^ Berry MD, Gainetdinov RR, Hoener MC, Shahid M (December 2017). "Pharmacology of human trace amine-associated receptors: Therapeutic opportunities and challenges". Pharmacology & Therapeutics. 180: 161–180. doi:10.1016/j.pharmthera.2017.07.002. PMID 28723415. S2CID 207366162.
As initial trace amine research focussed largely on p-tyramine, 2-phenylethylamine, and to a lesser extent tryptamine and p-octopamine, the term subsequently became synonymous with these compounds. These initial research efforts stalled, however, through a combination of a focus on the “false neurotransmitter”, amphetamine-like, indirect sympathomimetic action of p-tyramine and 2-phenylethylamine at plasma membrane monoamine transporters, and the lack of a receptor target for other effects.
- ^ a b Broadley KJ (March 2010). "The vascular effects of trace amines and amphetamines". Pharmacol. Ther. 125 (3): 363–375. doi:10.1016/j.pharmthera.2009.11.005. PMID 19948186.
Trace amines are metabolized in the mammalian body via monoamine oxidase (MAO; EC 1.4.3.4) (Berry, 2004) (Fig. 2) ... It deaminates primary and secondary amines that are free in the neuronal cytoplasm but not those bound in storage vesicles of the sympathetic neurone ... Similarly, β-PEA would not be deaminated in the gut as it is a selective substrate for MAO-B which is not found in the gut ...
Brain levels of endogenous trace amines are several hundred-fold below those for the classical neurotransmitters noradrenaline, dopamine and serotonin but their rates of synthesis are equivalent to those of noradrenaline and dopamine and they have a very rapid turnover rate (Berry, 2004). Endogenous extracellular tissue levels of trace amines measured in the brain are in the low nanomolar range. These low concentrations arise because of their very short half-life ... - ^ a b Fuss J, Steinle J, Bindila L, Auer MK, Kirchherr H, Lutz B, and Gass P (2015). "A runner's high depends on cannabinoid receptors in mice". PNAS. 112 (42): 13105–13108. Bibcode:2015PNAS..11213105F. doi:10.1073/pnas.1514996112. PMC 4620874. PMID 26438875.
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The excessive release of stress hormones, such as cortisol, which occurs in many individuals with mood disorders, may result from hyperfunctioning of the PVN of the hypothalamus, hyperfunctioning of the amygdala (which activates the PVN), or hypofunctioning of the hippocampus (which exerts a potent inhibitory influence on the PVN). ... Chronic stress decreases the expression of brain-derived neurotrophic factor (BDNF) in the hippocampus, which in turn may contribute to the atrophy of CA3 neurons and their increased vulnerability to a variety of neuronal insults. Chronic elevation of glucocorticoid levels is also known to decrease the survival of these neurons. Such activity may increase the dendritic arborizations and survival of the neurons, or help repair or protect the neurons from further damage. ... Stress and glucocorticoids inhibit, and a wide variety of antidepressant drugs, exercise, and enriched environments activate hippocampal neurogenesis.
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In psychiatric patients, different mechanisms of action for PA and EX have been discussed: On a neurochemical and physiological level, a number of acute changes occur during and following bouts of EX, and several long-term adaptations are related to regular EX training. For instance, EX has been found to normalize reduced levels of brain-derived neurotrophic factor (BDNF) and therefore has neuroprotective or even neurotrophic effects [7–9]. Animal studies found EX-induced changes in different neurotransmitters such as serotonin and endorphins [10,11], which relate to mood, and positive effects of EX on stress reactivity (e.g., the hypothalamus-pituitary-adrenal axis [12,13]). Finally, anxiolytic effects of EX mediated by atrial natriuretic peptide have been reported [14]. Potential psychological mechanisms of action include learning and extinction, changes in body scheme and health attitudes/behaviors, social reinforcement, experience of mastery, shift of external to more internal locus of control, improved coping strategies, or simple distraction [15,16].
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• The major excitatory neurotransmitter in the brain is glutamate; the major inhibitory neurotransmitter is GABA. ...
• The most extensively studied form of synaptic plasticity is long-term potentiation (LTP) in the hippocampus, which is triggered by strong activation of NMDA receptors and the consequent large rise in postsynaptic calcium concentration.
• Long-term depression (LTD), a long-lasting decrease in synaptic strength, also occurs at most excitatory and some inhibitory synapses in the brain. ... The bidirectional control of synaptic strength by LTP and LTD is believed to underlie some forms of learning and memory in the mammalian brain. - ^ a b 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. PMC 4504968. PMID 25957223.
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As exercise has been found to enhance neural growth and development, and improve cognitive and behavioural functioning in [healthy] individuals and animal studies, we reviewed the literature on the effects of exercise in children and adolescents with ADHD and animal models of ADHD behaviours.
A limited number of undersized non-randomized, retrospective and cross-sectional studies have investigated the impact of exercise on ADHD and the emotional, behavioural and neuropsychological problems associated with the disorder. The findings from these studies provide some support for the notion that exercise has the potential to act as a protective factor for ADHD. ... Although it remains unclear which role, if any, BDNF plays in the pathophysiology of ADHD, enhanced neural functioning has been suggested to be associated with the reduction of remission of ADHD symptoms.49,50,72 As exercise can elicit gene expression changes mediated by alterations in DNA methylation38, the possibility emerges that some of the positive effects of exercise could be caused by epigenetic mechanisms, which may set off a cascade of processes instigated by altered gene expression that could ultimately link to a change in brain function. - ^ a b Cooney GM, Dwan K, Greig CA, Lawlor DA, Rimer J, Waugh FR, McMurdo M, Mead GE (September 2013). "Exercise for depression". Cochrane Database Syst. Rev. 9 (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.
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