Exercise is both healthy and free, so why don’t most people do it?

Alexxai Kravitz

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Physical activity is one of the best things people can do for their health, lowering the risk of cardiovascular disease, type 2 diabetes, and certain forms of cancer. Physical activity has been shown in studies to help as much as medication for many conditions, and a common activity like taking a walk is low-cost and doesn’t require special skills or equipment.

Yet despite its benefits, less than half of Americans achieve the federally recommended guidelines for aerobic activity—at least 150 minutes of moderate intensity exercise per week.  And only one fifth of Americans achieve the federally recommended guidelines for both aerobic activity and strength training.

This disconnect is puzzling—why do so many people not do something that is both healthy and often free? Commonly, efforts to increase activity levels tend to promote education about how or where to exercise and encourage people to exercise more, but while these are laudable goals, they have not resulted in activity levels anywhere near the federal guidelines. The lack of effective methods for increasing activity is reflected in our limited understanding of the cellular and molecular underpinnings of physical activity. Basic questions remain, such as—why are some people so much more active than others? Why do some people gain pleasure from exercise, while others are averse to it? Why do some people stick with a new exercise program, while others fall off?

We think about these questions a lot in my lab, where we use mice to understand physical activity in obesity. On average, obese mice run around about half as much as mice of normal weight, and use their running wheels sparingly. So we asked a question that sounded simple enough—why are obese mice inactive? Surprisingly, no one knows the answer to this. Excess body weight makes movement more difficult, and this is often assumed to be the main reason people with obesity have low levels of movement. But certain clues made us doubt that this was the full explanation.

In normal-weight mice (all of whom weigh roughly the same amount), activity levels vary widely. Some mice run on their wheels for more than 5 miles per day, while others barely touch their wheels. A similar phenomenon occurs in people: even among people of similar weight, some are much more active than others. Clearly body weight doesn’t explain these differences.

Further, we have observed that when we track the activity levels of mice over time, the average activity of the group drops as they become obese, but some mice buck this trend. Like the rare people with obesity who remain highly active, these mice keep moving despite their weight gain. If excess body fat makes mice too heavy to move, why are some mice still moving?

Lastly, researchers have tracked the activity levels of people across periods of weight loss. Even in people who lose 50 pounds or more following bariatric surgery, activity levels do not increase. If body weight were the main cause of inactivity, shouldn’t people move more after they lose weight? It is puzzling, but the data seem clear: body weight does not fully explain inactivity in obesity.

To help answer this question, about three years ago, we began investigating an alternative explanation. Many researchers have reported differences in brain function in people with obesity. A large number of these studies reported impairments of the dopamine system, a brain system that is well known for controlling positive feelings. In addition to its role in feelings of reward, dopamine is critical for motor function. For example, the loss of neurons that produce dopamine causes Parkinson’s disease, a debilitating movement disorder.

Based on the critical role of dopamine for movement, we hypothesized that changes in the dopamine system may underlie inactivity in obesity. To test this idea, we studied multiple parts of this circuitry in obese mice and identified a dysfunction in a specific dopamine receptor—the D2 receptor. When we reduced this receptor in lean mice, these mice also became inactive. The D2 dopamine receptor has been implicated in movement for decades, so we were not too surprised that it popped up in our studies of inactivity in obese mice. However, when we restored signaling of this receptor in the brains of obese mice, they started moving around just as much as their lean counterparts. This was exciting, and suggested that there were switches in the brain that can be used to increase activity of obese animals, despite their body weight.

While mouse studies are difficult to translate into information people can directly act on, I believe our results indicate that if we want to change behavior, we need to understand the brain circuits that control that behavior. For instance, many research groups beyond our own have linked obesity in rodents to alterations in D2 receptors, but it remains unclear if this receptor is linked to inactivity in human obesity.

When I think about the low levels of physical activity in our country, and of the many efforts to alter this, I am reminded of a statement written by Susan Sontag in 1978: Theories that diseases are caused by mental states and can be cured by willpower, are always an index of how much is not understood about the physical terrain of a disease. Rather than invoking willpower as a solution for getting people to exercise, we need to learn more about the biology of physical activity. Understanding this biology may lead us to more effective strategies for increasing physical activity levels in people, as well as increasing our understanding of why it is so difficult for people to alter their activity levels through will power alone.


This has been an excerpt from The Neuropsychotherapist. To download the full article, and more excellent material for the psychotherapist, please subscribe to our monthly magazine.


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