Adaptive Capacity: An Evolutionary Neuroscience Model Linking Exercise, Cognition, and Brain Health - PubMed (original) (raw)
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Adaptive Capacity: An Evolutionary Neuroscience Model Linking Exercise, Cognition, and Brain Health
David A Raichlen et al. Trends Neurosci. 2017 Jul.
Abstract
The field of cognitive neuroscience was transformed by the discovery that exercise induces neurogenesis in the adult brain, with the potential to improve brain health and stave off the effects of neurodegenerative disease. However, the basic mechanisms underlying exercise-brain connections are not well understood. We use an evolutionary neuroscience approach to develop the adaptive capacity model (ACM), detailing how and why physical activity improves brain function based on an energy-minimizing strategy. Building on studies showing a combined benefit of exercise and cognitive challenge to enhance neuroplasticity, our ACM addresses two fundamental questions: (i) what are the proximate and ultimate mechanisms underlying age-related brain atrophy, and (ii) how do lifestyle changes influence the trajectory of healthy and pathological aging?
Copyright © 2017 Elsevier Ltd. All rights reserved.
Figures
Figure 1
The Adaptive Capacity Model (ACM). Dotted lines indicate adult lifespan prior to detectable cognitive decline due to aging or neurodegenerative disease. Solid lines indicate periods of potentially observable cognitive decline. Peach lines represent individuals with low risk for late-life neurodegenerative disease (e.g., Alzheimer’s disease or cerebrovascular disease), while blue lines represent those with high risk for neurodegenerative disease. It is expected that individual differences in early life development, such as with early access to healthcare, in utero exposures, nutrition, genetics (e.g., apolipoprotein E ε4 alleles), and other early lifestyle and health factors can alter the start point for the adult trajectory of risk for developing age-related cognitive decline or late-life neurodegenerative disease. The ACM predicts that individuals who engage in cognitively challenging aerobic exercise (E&C) will maintain brain structure across much of their lifespan, as this represents the brain’s natural state, consistent with our evolutionary history. When met with periods of inactivity during adult aging, the brain responds adaptively by diminishing capacity to reduce energy costs, leading to decreased structure and associated function, as reflected by age-related regional brain atrophy. Individuals with reduced brain structure due to chronic inactivity experience greater vulnerability to either age-related cognitive decline (low risk) or developing neurodegenerative disease (high risk). Importantly, the ACM suggests that engaging in late-life E&C after extended periods of inactivity can adaptively increase capacity, altering the trajectory of brain changes to reduce the impacts of cognitive aging and the risk for dementia during the adult lifespan. It is expected that cognitive decline becomes evident when the combination of reduced capacity and level of risk for neurodegenerative disease is sufficient to overcome an individual’s constellation of lifelong developed capabilities, leading to observable effects of cognitive aging or neurodegenerative disease. Thus, for a young adult, diminished regional brain morphology due to inactivity can be offset by driving existing task-related networks to capacity, engaging alternative brain networks, or using a combination of both to maintain levels of cognitive performance. For an older adult with adaptively reduced brain capacity due to chronic inactivity, as reflected by regional brain atrophy, and especially for those with higher risk for developing late-life neurodegenerative disease pathology, the use of such existing task-related and/or alternative brain networks are no longer sufficient to hold off the expression of cognitive decline related to aging or neurodegenerative disease. In turn, the ACM predicts that the course of cognitive decline and the associated lifelong trajectory can be altered by engagement in E&C during the adult lifespan.
Figure 2
Mechanisms underlying the ACM. A. Cognitively challenging physical activity, traditionally experienced during foraging, represents the evolutionary origins of the ACM. During foraging bouts, individuals must combine aerobic activity with control of motor systems, spatial navigation and memory, executive functions including decision making and planning, and control of sensory and attentional systems. This combination makes foraging a cognitively complex behavior, requiring an adaptive neural response to processing demands that can be further amplified when moving through novel environments and at increasing speeds. B. Acute effects of aerobic exercise. At the acute level, cognitively challenging aerobic activity (e.g., during foraging) begins with a neurogenic trigger (physical movement). Movement initiates the upregulation of neurotrophins and increased brain perfusion. In turn, the effects may induce hippocampal neurogenesis, as well as synaptogenesis and myelin remodeling with associated white matter (WM) and cortical brain effects. These non-specific effects are referred to as on-demand potential that may be realized when combined with cognitive challenges during or immediately following the aerobic activity. If these challenges occur, the acute effects of cognitively challenging exercise lead to neuron survival in the hippocampus and strengthened connections and myelination in key white matter tracts and associated cortical brain regions. C. Lifetime effects of cognitively challenging exercise. Combining aerobic exercise and cognitive challenges across the lifespan leads to the maintenance of brain structure and associated function during aging. Inactivity over the lifespan leads to an adaptive brain response that reduces structure (i.e., brain atrophy), potentially leading to the expression of cognitive decline or neurodegenerative disease. However, increasing cognitively challenging physical activity (Ex + Cog) after a lifetime of inactivity can alter the trajectory of cognitive aging and potentially reduce risks for the development of neurodegenerative disease.
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