Exercise, Brain, and Cognition Across the Lifespan

Beckman Institute for Advanced Science and Technology, Dept. of Psychology, Univ. of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.
Journal of Applied Physiology (Impact Factor: 3.06). 04/2011; 111(5):1505-13. DOI: 10.1152/japplphysiol.00210.2011
Source: PubMed


This is a brief review of current evidence for the relationships between physical activity and exercise and the brain and cognition throughout the life span in non-pathological populations. We focus on the effects of both aerobic and resistance training and provide a brief overview of potential neurobiological mechanisms derived from non-human animal models. Whereas research has focused primarily on the benefits of aerobic exercise in youth and young adult populations, there is growing evidence that both aerobic and resistance training are important for maintaining cognitive and brain health in old age. Finally, in these contexts, we point out gaps in the literature and future directions that will help advance the field of exercise neuroscience, including more studies that explicitly examine the effect of exercise type and intensity on cognition, the brain, and clinically significant outcomes. There is also a need for human neuroimaging studies to adopt a more unified multi-modal framework and for greater interaction between human and animal models of exercise effects on brain and cognition across the life span.

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Available from: Teresa Liu-Ambrose, Jun 26, 2015
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    • "It is well accepted that motor recovery after stroke is achieved through cortical reorganization, in which the brain and central nervous system (CNS) adapt in response to environmental and behavioral change to acquire novel information by modifying neural connectivity and function (Knaepen, Goekint, Heyman, & Meeusen, 2010; Mang, Campbell, Ross, & Boyd, 2013). Although the exact mechanism for cortical reorganization is not known, neurotrophins are thought to play a major role by enabling neuronal survival, potentiation, and differentiation; promoting dendritic growth and remodeling; and promoting synaptic plasticity (Lin & Kuo, 2013; Voss, Nagamatsu, Liu-Ambrose, & Kramer, 2011). Brain-derived neurotrophic factor (BDNF) is of particular interest in basic science and rehabilitation research because of its responsiveness to physical activity and exercise (Knaepen et al., 2010). "
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    ABSTRACT: Previously, we demonstrated that forced aerobic exercise (FE) increases the pattern of neural activation in Parkinson's disease. We sought to evaluate whether FE, when coupled with repetitive task practice, could promote motor recovery poststroke. A 46-yr-old man with ischemic stroke exhibited chronic residual upper-extremity deficits, scoring 35/66 on the Fugl-Meyer Assessment (FMA) at baseline. He completed 24 training sessions comprising 45 min of FE on a motorized stationary bicycle followed by 45 min of upper-extremity repetitive task practice. From baseline to end of treatment, the FMA score improved by 20 points, perceived level of recovery on the Stroke Impact Scale increased by 20 percentage points, and cardiovascular function measured by peak oxygen uptake improved 30%. These improvements persisted 4 wk after the intervention ceased. FE may be a safe and feasible rehabilitation approach to augment recovery of motor and nonmotor function while improving aerobic fitness in people with chronic stroke. Copyright © 2015 by the American Occupational Therapy Association, Inc.
    07/2015; 69(4):6904210010p1-6904210010p8. DOI:10.5014/ajot.2015.015636
    • "Importantly, there are no published studies examining the effects of aerobic exercise training on inhibitory control, using a modified flanker paradigm in persons with MS. Based on the similar associations between aerobic fitness and inhibitory control in the MS and control samples, future studies should carefully examine exercise training effects on inhibitory control in adults of the general population (Colcombe & Kramer, 2003; Voss et al., 2011) that might be applicable for designing similar interventions in persons with MS. "
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    ABSTRACT: Cognitive impairment is highly prevalent, disabling, and poorly managed in persons with multiple sclerosis (MS). Aerobic fitness might be a target of exercise training interventions for improving cognition in this population. It is unknown if the well-established pattern of associations between higher aerobic fitness and better inhibitory control in the general population exists among persons with MS. The current cross-sectional study examined the effects of aerobic fitness (VO2peak) on inhibitory control, using a modified flanker task, in 28 persons with MS and 28 healthy controls matched by age, sex, and body mass index. This involved performing bivariate correlations and hierarchical linear regression analyses on measures of aerobic fitness and inhibitory control. Persons with MS demonstrated lower VO2peak (d = -0.45), slower (d = 0.62-0.84), and less accurate (d = -0.60 to 0.71) performance on the flanker task than controls. VO2peak was similarly associated with reaction time measures of inhibitory control in the MS and control samples (ρ = -0.40 to 0.54). VO2peak (p < .01), but not group (p ≥ .08) (MS vs. control), predicted reaction time on the flanker task, irrespective of age, sex, and education. This supports the development of aerobic exercise interventions for improving reaction time on tasks of inhibitory control in persons with MS, much like what has been successfully undertaken in the general population. © The Author 2015. Published by Oxford University Press. All rights reserved. For permissions, please e-mail:
    Archives of Clinical Neuropsychology 04/2015; 30(4). DOI:10.1093/arclin/acv022 · 1.99 Impact Factor
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    • "IGF-1 is often considered as the central node of a complex system of homeostatic regulation [12], and as the mediator of exercise-induced benefits on the brain [1], [3]. However, studies explored mainly the effect of exercise on cognition and hippocampus, more rarely the consequences of physical activity on the sensorimotor system. "
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    ABSTRACT: A chronic reduction in neuromuscular activity through prolonged body immobilization in human alters motor task performance through a combination of peripheral and central factors. Studies performed in a rat model of sensorimotor restriction have shown functional and biochemical changes in sensorimotor cortex. However, the underlying mechanisms are still unclear. Interest was turned towards a possible implication of Insulin-like Growth Factor 1 (IGF-1), a growth factor known to mediate neuronal excitability and synaptic plasticity by inducing phosphorylation cascades which include the PI3K-AKT pathway. In order to better understand the influence of IGF-1 in cortical plasticity in rats submitted to a sensorimotor restriction, we analyzed the effect of hindlimb unloading on IGF-1 and its main molecular pathway in structures implied in motor control (sensorimotor cortex, striatum, cerebellum). IGF-1 level was determined by ELISA, and phosphorylation of its receptor and proteins of the PI3K-AKT pathway by immunoblot. In the sensorimotor cortex, our results indicate that HU induces a decrease in IGF-1 level; this alteration is associated to a decrease in activation of PI3K-AKT pathway. The same effect was observed in the striatum, although to a lower extent. No variation was noticed in the cerebellum. These results suggest that IGF-1 might contribute to cortical and striatal plasticity induced by a chronic sensorimotor restriction.
    PLoS ONE 09/2014; 9(9):e107631. DOI:10.1371/journal.pone.0107631 · 3.23 Impact Factor
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