Neuroplasticity was a relatively unknown term until the 1970s when scientists began accepting the notion that our brain is a not a physiologically static organ, becoming fixed shortly after birth with approximately 100 billion neurons (nerve cells) (1, 2). Over the past 15 to 20 years, this field of study has expanded dramatically given the discovery of various compounds capable of changing both brain structure and function throughout life and how each is positively impacted by exercise, physical activity and even mental exercises (3, 4).
Perhaps the most impressive success story connecting exercise to improved brain function is the Learning Readiness Physical Education Program, founded as the Zero Hour PE program at Naperville Central High School in Chicago in the 1990s (5). The original purpose of the program was to examine whether working out before school would improve a student’s learning capacity in the classroom. Since the program’s inception and through its evolution, students in this school district now rank among the fittest and smartest in the nation. In fact, this district’s eighth graders have outperformed the US national average on the Trends in International Math and Science Study (TIMMS), even beating out many students in China, Japan and Singapore who have traditionally outranked American students. So what is going on?
Daniel Lieberman, a paleoanthropologist at Harvard University, has been researching human evolution and has demonstrated how our brain and skull have evolved over time in order to preserve our survival as a species (6). Our need to think, process, strategise, hunt in teams, and function and communicate within social groups has spurred growth within various regions of our brain and improved our overall brain function. This growth of our brain, especially specific regions like the frontal lobe which is connected to conscious thinking, decision-making, planning, judgment, analysis and inhibition, continues into our modern era.
Our brain can also suffer losses and shrink in the form of decreased mental efficiency and memory decline as we age. In fact, memory loss is cited as a primary cognitive complaint in older adults. It is estimated that approximately 10% of adults over the age of 65 years have some form of cognitive impairment and this statistic increases to approximately 50% of adults over the age of 80 years (7). Although this decline is generally attributed to overall physiological losses within our brain cells, the potential impact of disease (e.g., Alzheimer’s), an overall lack of brain use, or the effect of depression or medications, the key biological risk factors associated with these declines include:
- Oxidative stress – our brain utilises approximately 20% of the body’s oxygen supply and over time, the accumulation of free radicals may result in damage to DNA and essential lipids within the brain that triggers neuronal death.
- Inflammatory agents accumulate in the brain. Generally, they are filtered out by our blood brain barrier (BBB), a fine capillary network separating cerebral blood flow from systemic circulation. With aging, we experience less filtration of many inflammatory agents (e.g., cytokines like interleukin-1 beta) which can destroy neurons and inhibit neurogenesis (the growth of new neurons).
- Elevated levels of homocysteine, a naturally occurring amino acids found in plasma promotes atherosclerosis within vessels, thereby reducing cerebral blood flow, memory and overall brain volume.
- Hormonal imbalances and hormonal losses within the body – key steroid hormones like estrogen, testosterone and dehydroepiandrosterone (DHEA) collectively help preserve cognitive ability but decrease with aging.
- Declining cerebrovascular health – healthy blood vessels and elevated HDL-cholesterol levels facilitate blood flow into the regions of the brain like the gray matter.
- Hypertension – small capillaries within the brain are susceptible to damage caused by chronically-elevated blood pressure.
- Diabetes and insulin-resistance – hyperglycemia and the inability to utilise glucose has been linked with lower levels of neuronal growth factors, decreased brain volume, and higher incidence of dementia.
- Stress and anxiety trigger greater sustained levels of cortisol which can damage brain tissue (discussed later in this article).
Many of these triggers to cognitive decline are inevitable, but can we slow down, stop or even reverse these age-related decreases? The answer is yes, and an ever-growing list of compounds continues to be discovered that collectively lead to improved brain health and function. Interestingly, these compounds appear to be more important in some regions of the brain versus others. For example, the hippocampus, a region of the brain involved in converting short-term information into long-term knowledge, losses its mass and capacity as we age, but is significantly impacted by increased levels of some of these compounds (2, 8-10).
- Brain-derived Neurotropic Factor (BDNF) is perhaps the most important as it stimulates neurogenesis and increases dendrite (nerve ending) length, thickness and density which improves nerve connectivity, especially in the hippocampus. BDNF strengthens and cleans synapses (junctions between two nerves), enhances synaptic efficiency, and increases synaptic mapping (connectivity between neurons and new circuits to offset lost circuits).
- Vascular Endothelial Growth Factor (VEGF) helps build new capillaries within the brain, improving oxygen and glucose delivery to the various regions of our brain.
- Fibroblast Growth Factor-2 (FGF-2) stimulates brain tissue growth by improving synaptic efficiency and the affinity neurons may share for each other to facilitate learning and retention.
- Insulin-like Growth Factor-1 (IGF-1), manufactured within muscle cells, it is pushed into the brain and helps increase glucose uptake into cells, thereby providing the fuel needed by BDNF.
So how do we spark increases of these compounds? A good majority of research has focused upon the effects of exercise on increasing levels of these compounds (10). Low-to-moderate intensities of cardio stimulate increases BDNF, but little increases in IGF-1. By comparison, moderate-to-vigorous intensities of cardio (> 65% of VO2max) increases levels of BDNF, VEGF, FGF-2, IGF-1, and even human growth hormone (HGH) which contributes to building brain mass. Resistance training performed two times a week also demonstrates increases in BDNF, VEGF, FGF-2, IGF-1 and HGH. Exercising daily versus on alternate days results in greater increase in BDNF (150% v. 124%), but levels become equal after about four weeks of training (10). Exercise also improves the efficiency of our BBB and promotes greater balance between many of our brain’s neurotransmitters like serotonin, dopamine, norepinephrine, glutamate and GABA, which will positively affect moods and cognition.
Although much research points towards 30-minutes of exercise, two to three times a week, John Ratey, author of Spark and A User’s Guide to the Brain (3, 11), cites that just eight to twelve minutes a day of exercise that evokes a sweat and labored-breathing (i.e., approximately 60% of maximum heart rate or higher) is adequate to demonstrate increase in many of these compounds like BDNF. Furthermore, the inclusion of cross lateral patterns (XLP) (i.e., movement crossing over the body or involving contralateral limbs) helps strengthen the corpus callosum, which is essentially the glue that connects the left and right cerebral hemispheres and facilitates interhemispheric communication.
To expand the versatility of any brain-boosting programs you may seek to implement, consider incorporating mental exercises into your programs (they might also offer a welcomed break from physical fatigue):
- Mental exercises, regardless of whether they are performed using a mobile brain function application (e.g., Luminosity) or manually, can also stimulate increases in some brain-building compounds. The idea is to (a) challenge your brain to complete tasks in non-conventional manners or (b) complete tasks by incorporating multiple regions of the brain simultaneously:
- Backward Digit Span – counting numbers backwards in set intervals (e.g., intervals of 7 from 100) as quickly as possible.
- Backwards Word Spell – spell words backwards and out loud (no writing), and progressively increase the length and challenge of the words (e.g., world, hospital, responsibility).
- Sequenced Information Games – where a sequence of names (e.g., Fred, Stacy, Richard, Stanley, Ida, Edward) are written down after which the individual is challenged to complete various tasks from memory:
- Recite backwards
- Arrange alphabetically
- Arrange by word length
- Tasking Challenges – completing a sequence of tasks and continuing to perform each task until it has to be replaced by another task. (Note, multiple verbal or physical tasks can be performed simultaneously.) Upon completing all tasks, individuals are asked to recall a specific task (e.g., what was the 3rd task?). This question can be asked immediately or at some later stage in the session.
- Count backwards from 10
- Wave hands above your head
- March in place
- Snap your fingers
- Recite the alphabet backwards
- Stomp your feet
Stress and Cortisol: Unfortunately, many of us live a life where chronic psychological stress and sustained, elevated levels of cortisol are considered the norm. These sustained levels of cortisol impair cells within the hippocampus involved with short-term learning and long-term memory. Ultimately, this can damage and shrink the hippocampus due to free radical attacks that destroy and shorten dendrites, decrease levels of BDNF, reduce neurogenesis, and increase neural atrophy. In this case, the amygdala, a region overseeing much of our emotions may begin to exert more control over learning and over the hippocampus, which increases our emotional stress levels, furthering increasing cortisol, and so goes this vicious cycle.
Furthermore, elevated levels of cortisol may also impede our transition to stage 4 sleep (delta or deep sleep) at night, an important phase of sleep where the brain usually converts short-term learning into long-term memory, and where HGH levels help build and repair tissue (e.g., brain mass). Cortisol can also directly inhibit HGH release from the pituitary gland by stimulating the release of somatostatin, a growth hormone inhibiting hormone, from the hypothalamus. It appears, therefore, that any brain-boosting attempts, either through mental and physical exercise, or even both, may be almost futile without some effective stress coping modalities.
Brain Food: Do foods exist that can boost our brainpower? Although researchers cannot make that claim unequivocally, certain foods do appear to promote some potential benefits:
- Antioxidants, like polyphenols found in green tea and anthocyanins (red, purple, or blue pigments found in flowers, fruits, leaves, stems, and roots like dark berries, red cabbage and eggplant), may prove effective in fighting free radicals.
- Fish oils (1,200 mg eicosapentaenoic acid, 200 mg docosahexaenoic acid) seem to reduce rates of cognitive decline and the risks of developing dementia.
- Folic acid (800 mg), and vitamin B6 and B12 (to a lesser degree) can reduce levels of homocysteine in our blood.
- Moderate intakes of caffeine can help preserve our BBB and perhaps also reduce levels of plasma amyloid-beta, a protein structure associated with Alzheimer’s disease.
- Healthy sources and dosages of glucose, which provides fuel to the brain though the insulin response must also be considered. Because insulin is responsible for nutrient uptake (including amino acids) into cells and considering the fact that muscle cells don’t care much for tryptophan, insulin surges can result in increased tryptophan entering the brain. This in turn can increase serotonin production. However, the inclusion of branched-chain amino acids throughout the day is believed to compete with tryptophan and reduce the amount passing through the BBB – essentially reducing the fatigue-inducing effect of tryptophan and helping to keep the brain focused and alert (12).
In closing, although we are well aware of the mind-body connection of exercise, research supporting exercise’s brain-boosting benefits continues to expand as we discover new compounds that improve overall brain structure and function. Why not consider expanding your services and programs to address, or perhaps even emphasize (for some), the critical psycho-emotional domains that are often neglected with traditional programming. Remember however, that an effective mind-body program may only be as good as the stress-coping mechanisms included, so don’t just train hard, train smart.
Pascual-Leone A, Amedi A, Fregni F, and Merabet LB, (2005). The plastic human brain cortex. Annual Review of Neuroscience, 28:377 – 401.
Shaw C, and McEachern J (editors), (2001). Toward a Theory of Neuroplasticity. London, England: Psychology Press.
Ratey JJ, and Hagerman E, (2008). The Revolutionary New Science of Exercise and Brain. New York, NY. Little, Brown and Company.
Bramble1 DM, and Lieberman DE, (2004). Endurance running and the evolution of Homo. Nature, 432: 345 – 352.
Sparking Life. Power Your Brain Through Exercise. www.sparkinglife.org. Retrieved Sep, 2014.
Lieberman DE, (2011). The Evolution of the Human Head. Cambridge, MA: Harvard University Press.
Centers for Disease Control and Prevention (2011). Cognitive Impairment. http://www.cdc.gov/aging/pdf/cognitive_impairment/cogImp_poilicy_final.pdf. Retrieved Sep, 2014.
Huang EJ, and Reichardt LF, (2001). Neurotrophins: roles in neuronal development and function. Annual Review of Neuroscience, 24:677 – 736.
Cotman CW, and Berchtold NC, (2002). Exercise: a behavioral intervention to enhance brain health and plasticity. Trends in Neuroscience, 25(6):295 – 301.
Erickson KI, Voss MW, Prakash RS, Basak C, Szabo A, Chaddock L, Kim JS, Heo S, Alves H, White SM, Wojcicki TR, Mailey E, Vieira VJ, Martin SA, Pence BD, Woods JA, McAuley E, and Kramer AF, (2011). Exercise training increases size of hippocampus and improves memory. Proceedings of the National Academy of the Sciences of the United States of America, 108(7): 3017 – 3022.
Ratey, JJ (2001). A User’s Guide to the Brain. New York, NY, Random House, Inc.
Davis JM, (1995). Carbohydrates, branched-chain amino acids, and endurance: the central fatigue hypothesis. International Journal of Sports Nutrition, 5:S29 – 38.