Physical Activity and the Brain

Dr. Tim Noakes, author of Lore of Running and Waterlogged, has long studied the role of the brain as the central governor of performance in endurance activities. In a 2013 paper titled, “Physical activity and the brain: A review of this dynamic, bi-directional relationship,” Noakes and colleagues explain how the brain regulates physical activity and how physical activity impacts the health and function of the brain.

The “central governor” hypothesis states that the brain plays a role in maintaining energy homeostasis and thermoregulation by coordinating input from the body with physical output. For example, physical output will decline if body temperature reaches dangerous levels. However, the central governor model suggests there is a complex interaction between motivation, sensation of pain, and feelings of urgency. In spite of the pain of accumulated fatigue, increased lactic acid, and reduced energy stores in the muscles, runners are able to increase their pace in the final stretch of a race.

The brain also plays a role in regulating physical activity beyond the realm of competitive racing. When injected with various neurotransmitters, mice can increase or decrease exploration of their environment or even shut off spontaneous movement, depending on which part of the brain is injected. Habits such as tapping your foot are regulated by your brain, though they are not consciously initiated. It has been suggested there is subconscious governance of many types of physical activities.

Noakes cites a paper he wrote with H. G. Laurie Rauch and Georg Schönbächler that demonstrates the potentially subconscious role of the brain during physical activity through the story of a man with Parkinson’s disease:

It was discovered that a 65-year-old male patient, who had been unable to run for many years and could only walk about 12 steps before losing his balance, was nevertheless able to run after his wife when a rocket warning siren sounded. Significantly, this patient was unable to elicit more than a shuffle during dozens of other rocket warning sirens before and after this incident. According to the patient, the difference during this particular warning siren was that his wife grabbed his arm while he was slowly getting out of his chair and he then ran following in her exact footsteps.

It is postulated that he was able to run in this extreme scenario because he was able to visualize how to run by observing his wife and following her steps. Coupled with the urgency of the situation, this may have activated a portion of the brain unaffected by Parkinson’s disease.

Noakes’ paper with Rauch and Schönbächler further elucidates the difference between voluntary, vigorous, and urgent motor behaviors during exercise. Voluntary activities are formulated by areas of the brain responsible for executive function and are then carried out by various reflexive actions of the brain and body. These are distinct from involuntary movements, such as twitches or nervous tics, which are random and not goal-directed. Vigorous movement is inwardly driven by motivational factors, such as a desire to set a new PR or win a race. In a competitive scenario, a runner’s pace is determined largely by internal factors. Experienced competitors are better able to self-regulate nervousness and other factors that might distract from an optimal pacing strategy. The burst of speed seen in runners as they approach the finish line is an example of internal motivating factors overriding subjective feelings of pain and fatigue. Urgent behavior is the result of external stimuli, such as the sight of an angry dog or the sound of a gunshot.

In the various ways discussed above, the brain regulates the activity of the body. However, the function and health of the brain are substantially influenced by physical activity, which suggests there is a bi-directional relationship between the brain and exercise. In Spark, author Dr. John Ratey touts the beneficial effects of exercise, particularly with regard to a chemical called brain-derived neurotrophic factor (BDNF):

Early on, researchers found that if they sprinkled BDNF onto neurons in a petri dish, the cells automatically sprouted new branches, producing the same structural growth required for learning — and causing me to think of BDNF as Miracle-Gro for the brain. (p. 43)

When their brains were injected with a molecule that binds to BDNF and scanned, not only did the scans of the running rodents show an increase in BDNF over controls, but the farther each mouse ran, the higher the levels were. (p. 44)

Emerging science related to BDNF and physical activity more generally has affected approaches to various disease treatments. It was once thought physical activity would have little effect or may pose a risk for Parkinson’s patients. However, that is no longer the prevailing attitude. One research study showed tai chi training to be effective for improving postural stability and reducing falls. Another study showed progressive resistance training to improve walking capacity. “Physical activity and the brain” mentions two studies indicating an inverse association between exercise intensity and the development of Parkinson’s disease, meaning more vigorous exercise might have a protective effect. Several recent studies demonstrate high-intensity interval training (HIIT) is more effective for boosting levels of BDNF than moderate-intensity continuous training (1). In addition, another study found HIIT greatly improved cerebral blood flow and metabolism, whereas moderate-intensity cardio did not.

Neurodegenerative disorders such as Parkinson’s disease and late-onset Alzheimer’s disease are both linked to physical inactivity. These conditions correlate with Type 2 diabetes and hyperlipidemia in middle age, which suggests they could be metabolic diseases (2). “Physical activity and the brain” elaborates on the benefits of physical activity as a method of neurodegenerative disease prevention and treatment. Exercise is known to stimulate vascular endothelial growth factor (VEGF), which improves cerebral blood flow and metabolism independent of diet. Exercise also releases reactive oxygen species (ROS), also known as free radicals. This stimulates our body’s natural antioxidant mechanisms.

Furthermore, the body’s neuroendocrine system, related to stress and anxiety, is positively impacted by physical activity. Noakes et al. explain, “Chronic stress can lead to dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis, which has been shown to decrease levels of BDNF, and increase inflammation, oxidative damage, and amyloid-β peptides, and it is well established that physical activity may help to reduce stress levels and depression symptoms.”

Exercise is one of the greatest methods of stress reduction currently known. Physically active people are 45% less likely to report symptoms of depression. This effect has been observed in over 100 population studies. Monoamines in the brain, such as serotonin (the “happiness chemical”), dopamine (the “pleasure and reward molecule”), epinephrine/norepinephrine (the adrenaline hormones), and more are positively affected by exercise. Prescription and recreational drugs manipulate these neurotransmitters but often have side effects. Rarely are diet and exercise used as frontline treatments for anxiety and depression, even though they come with additional benefits rather than risk.

Given the benefits of exercise and low risk of harm, why are so many people inactive? “Physical activity and the brain” posits several reasons. Neurobiological mechanisms regulate physical activity with little day to day variation, in spite of differences in work and leisure time on weekends. Likewise, changes in environment do not provoke changes in activity levels in several animal studies. This suggests neurobiological mechanisms control physical activity as a means to maintain homeostasis. Furthermore, there is a strong hereditary component to exercise participation. One paper cited in this review suggests genetic factors could account for 42% of exercise behavior, though this observation is based on survey data.

Significantly, the effects of some genes can be tempered through physical activity as well. Roughly 40% of the people with late-onset Alzheimer’s disease have a gene called APOE e4. Physical exercise has been shown to reduce the incidence of neurodegeneration among carriers of this gene.

These are just some of the examples supporting Noakes et al.’s claim that the brain regulates the body and is affected by physical activity in a bi-directional manner. They conclude:

Our paper … underscores the importance of promoting safe forms of physical activity across the lifespan. Evidence-based strategies to increase physical activity levels include, for example, teaching individuals how to adopt an active lifestyle approach, and emphasizing the use of key behavioral (e.g., enlisting social support) and cognitive (e.g., understanding the consequences of living an inactive lifestyle) strategies known to help initiate and maintain activity behavior (Loprinzi et al., 2012b). To effectively promote physical activity, it is essential that multidisciplinary research is conducted to further our understanding of the “bio-cultural” aspects that influence physical activity behavior and sport performance, and, ultimately, health.

Notes

1. High-intensity interval training evokes larger serum BDNF levels compared with intense continuous exercise; High-intensity interval training may help stave off dementia
2. Is Alzheimer’s diabetes of the brain?; Is Alzheimer’s disease a Type 3 diabetes? A critical appraisal