Exercise and Brain Repair

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Physical activity is essential in maintaining a healthy lifestyle and is associated with reducing the likelihood of many diseases. Increasing evidence points towards the benefits of exercise on brain structure and function and could even delay or prevent the onset of many neurological conditions including Alzheimer’s and stroke.

Physical Activity

Physical Activity. Image Credit: Halfpoint/Shutterstock.com

Regular aerobic exercise and/or moderate physical activity (such as brisk walking) is associated with better overall health compared to those who have a sedentary lifestyle. In combination with a healthy balanced diet, exercise promotes improved cardiovascular, metabolic, and immune health and therefore is associated with a reduced likelihood of developing cardiovascular diseases and metabolic diseases such as diabetes mellitus.

Since the brain is a highly metabolically active organ with intricate links to the cardiovascular system, any susceptibilities to systemic diseases also have a negative impact on the brain, for example, cardiovascular diseases and stroke. Therefore, promoting a healthy lifestyle with exercise also has a beneficial impact on the brain’s health by enhancing neurovascular, neuroimmune, and neurometabolic function.

Cognitive Function

Many studies have found that adults (especially >65 years of age) who regularly exercise or perform some form of physical activity (walking, gardening, swimming, etc) tend to perform better in cognitive tests and as such are at a reduced risk of cognitive impairment and dementia compared to those who do not regularly perform some form of physical activity. Furthermore, performing physical activity and exercise can improve some level of cognitive and executive functions in patients with earlier stages of dementia.

One of the main neuroprotective chemicals found in the brain are called neurotrophic factors which support neuronal and synaptic health and can improve cognition and mood. Reduction in neurotrophic factors can be detrimental to neuronal health and synaptic plasticity and may be implicated in the onset of neurodegenerative disorders. Even mild physical activity such as walking through to intense aerobic exercise all increase the levels of neurotrophic factors such as BDNF, and higher levels due to higher intensity exercise is positively correlated with better neural health and function.

Rodent studies have given us mechanistic insights into how exercise is able to confer neuroprotective properties. For example, one month of voluntary wheel running in mice reduced the pathological and behavioral deficits associated with aging by increasing levels of BDNF as well as enhancing neurogenesis in the hippocampus. In addition, voluntary wheel running also led to the upregulation of nerve growth factor (NGF), insulin-like growth factor (IGF-1), and tight junction proteins in maintaining the blood-brain barrier.

Physical exercise has a direct effect not only on levels of BDNF and other neurotrophic factors but also upregulates levels of p75NTR and CREB – both involved in synaptic plasticity. Improving synaptic plasticity mechanisms directly leads to improvements in memory and cognition, whereas normal aging suppresses these mechanisms. Furthermore, aerobic exercise e.g., treadmill, increases the expression of pNDMA, PSD 95 & decreases DNA damage all contributing to stabilizing and preventing cognitive decline in healthy aging. However, it is important to note that “over-training” can lead to negative consequences with more DNA damage, for example.

Together, these maintain the cerebrovasculature preventing the infiltration of toxic compounds and chemokines that promote neuroinflammation, as well as enhancing both neuronal and synaptic function. Furthermore, the activation of microglia (the brain's immune cells) was reduced by exercise thus protecting key brain regions from insult. Interestingly, exercise in mice modeling Alzheimer’s has been shown to reduce the levels of soluble beta-amyloid by enhancing glymphatic clearance as well as reducing white matter pathology leading to enhanced cognitive performance. These preclinical findings mirror clinical findings described earlier and provide a mechanism by which exercise can protect the brain, but also enhance its function, even in disease.


Many of the above findings not only protect the brain but are able to repair and stabilize neurological damage such as through the increased production of neurotrophic factors for example. As such, exercise in the early stages of dementia can slow down and even reverse some of the damage.

Depending on the severity and location of a stroke, different challenges can present including impairments to activities of daily living. As areas of the brain are damaged, it is important to rehabilitate and repair some of the reversible damage as soon as possible for a better prognosis. Aerobic exercise has been shown to reduce the lesion size (volume) and protect the surrounding perilesional tissue from oxidative damage and inflammation in addition to increasing neurogenesis in the short term. This can be achieved by moderate forced exercise of around 10 minutes a day 5-7 times a week initiated within 48 hours after stroke. The earlier the better when it comes to forced exercise in the short-term outlook. The higher the intensity of exercise, the better the recovery and higher levels of angiogenesis within the perilesional area to support recovery.

In summary, exercise has a profound neuroprotective effect on the brain and regular exercise (especially aerobic) not only can improve brain function and enhance cognitive function and mood, but also delay, improve, or prevent the onset of neurological disorders such as stroke and dementia. In addition, performing regular exercise in earlier stages of the disease has also been shown to improve pathological and clinical outcomes.


Further Reading

Last Updated: Jul 19, 2021

Dr. Osman Shabir

Written by

Dr. Osman Shabir

Osman is a Postdoctoral Research Associate at the University of Sheffield studying the impact of cardiovascular disease (atherosclerosis) on neurovascular function in vascular dementia and Alzheimer's disease using pre-clinical models and neuroimaging techniques. He is based in the Department of Infection, Immunity & Cardiovascular Disease in the Faculty of Medicine at Sheffield.


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