Physical activity is recommended as part of every healthy lifestyle in order to maintain appropriate body weight and composition and to prevent a myriad of diseases. Now, researchers suggest that genetics plays a role in how much voluntary physical activity one is likely to engage in. Predispositions to active, athletic lifestyles are passed on from generation to generation, as are predispositions to be sedentary.

The current study, published in the Proceedings of the Royal Society B, analyzes house mice that have been selectively bred for high-activity lifestyles. The mice have been bred for 43 generations to include 4 lines of high runners (HR) and 4 corresponding control lines. Overall, at this generation, the HR mice ran almost 3 times as many revolutions per day on exercise wheels than the control mice. The increased number of revolutions was due to increased speed in the HR mice more than increased time spent running, compared to the control mice.

Through several similar studies on previous generations of mice, the same researchers have proved that activity levels can be enhanced by selective breeding. That is, offspring of mice who enjoy high levels of activity also enjoy high levels of activity. In addition to voluntarily engaging in wheel running, the HR mice have evolved over dozens of generations to have increased running economy, spending less energy per distance run compared to control mice. Over time, HR mice also showed lower body mass and less body fat, despite consuming more food, as well as increased oxygen consumption, higher muscle aerobic capacity, and lower anaerobic muscle capacity than the more sedentary control mice.

The authors assert that this research has implications for human health, and that, in the future, activity-related genes could be targeted with drug therapy to increase a person’s enjoyment in engaging in physical activity. With obesity levels skyrocketing, such an intervention might be useful. Other research suggests that the dopamine system of motivation and reward regulates physical activity levels in humans. This regulatory system has been proposed as another target of pharmacological therapy to prevent inactivity-related diseases in the future.

Researchers have also shown that, while many traits in humans may be genetically predisposed, it is possible to override one’s genetics. People who are susceptible to being obese, based on genetic makeup, can reduce their risk of obesity by choosing to live an active lifestyle. As with almost all human traits, reducing the epidemic of overweight and inactivity to a simple genetic problem is likely too simplistic. Human behaviors and diseases are a result of a combination of biological and environmental factors in most cases. And with physical activity and exercise, current health status, physical limitations, and the role of childhood experiences affect the inclination to be a couch potato or a competitive athlete.

While the research surrounding voluntary physical activity could shed some light on why some people prefer watching television while others enjoy running marathons, the results should not allow people to blame their genes for all their ills. People, more than the mice in the study, make choices about their lifestyle and activity levels. True, it may be harder for some to overcome environmental or genetic susceptibilities to a sedentary lifestyle, but not impossible. Refuse to be defined by genetics and run fast and run far in the rat race of life.

References

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