Exercise Motivation

By Amanda Kauffman and Aaron Goldman

Whether it’s a New Year’s resolution to be more healthy, or the imminence of summer and the desire to get that beach body, the motivation to work out and eat clean is often at its highest during these times. However, no matter how inspired you may feel, for many, the act of actually bringing yourself to exercise and change your eating habits can be daunting, and most people end up getting off track with their fitness plans after just two weeks! Beyond the lack of immediate physical change, the inability to follow through with one’s fitness goals can lead to significant levels of frustration, self-loathing and can even impact our mental health. Although one can take control of their exercise to some extent, certain genes also play a role in affecting an individual’s ability to successfully carry out a fitness plan – some people get more pleasure following exercise and perceive exercise as requiring less effort. In this brief column, we’ll describe two genes that influence this natural inclination to want to exercise.

Exercise motivation is influenced by two genes that coordinate the interplay between the central nervous system and musculature, and ultimately, the difficulty, enjoyability and effectiveness of a workout. Variants in these genes may lead to increased difficulty and subsequently decreased enjoyability of workouts and less-visible results, thereby decreasing motivation further.

The BDNF gene encodes a protein called Brain-Derived Neurotrophic Factor. BDNF works in the brain to support the growth and survival of neurons, and is partly responsible for exercise-induced neurogenesis (the creation of new neurons in the brain). About 20% of the overall population and almost 50% of East Asian populations carry a version of the BDNF gene that results in lower expression levels of the gene, which in turn was shown to be associated with a more positive mood response to moderately intense exercise, and increased intrinsic motivation during exercise. Individuals that carry that version of the BDNF gene were also more likely to continue to exercise when given the option to stop.

The LEPR gene also influences our natural inclination to exercise. This gene encodes the leptin receptor and is involved in the regulation of body weight and energy balance. About half of the population carry a version of this gene that results in an impairment of leptin signalling. Interestingly, leptin normally plays a role in our sympathetic nervous system (SNS), which controls our stress response by increasing our heart rate, and increasing blood flow to our muscles. This variant in the LEPR gene has been shown to be associated with lower energy expenditure and lower physical activity levels, which is consistent with the observation that SNS activity is associated with spontaneous physical activity in humans. The LEPR gene variant was also shown to be associated with higher subcutaneous abdominal adipocyte size (SAAS), which is a fancy way of saying bigger fat cells. Large fat cells are associated with excessive fat storage, and interestingly, the same effect was observed in mice – mice lacking the LEPR gene had fat cells that were 5 times larger than fat cells from normal mice.

So what can we do about it? To overcome a genetic tendency of potential decreased motivation for exercise, individuals can increase their personal accountability and use strategies to proactively ensure they are able to stay on track with their fitness goals. These can be as simple as working out with a friend to make sure you show up, using a calendar to schedule daily workouts, or signing up (and paying for) a group fitness class ahead of time or working out with a personal trainer. While most adults know from experience whether they’re more likely to run a marathon or watch one on TV, sometimes understanding the genetic basis of your behaviour can be an effective reminder to maintain accountability.

De Moor et al., 2009. Genome-wide Association Study of Exercise Behavior in Dutch and American Adults. Med Sci Sports Exerc; 41(10): 1887–1895.

Caldwell Hooper et al., (2014). What keeps a body moving? The brain-derived neurotrophic factor val66met polymorphism and intrinsic motivation to exercise in humans. J Behav Med; 37, 1180–1192.

Stefan et al., (2002). The Gln223Arg polymorphism of the leptin receptor in Pima Indians:

Influence on energy expenditure, physical activity and lipid metabolism. International Journal of Obesity; 26, 1629–1632

Johnson and Hirsch, (1972). Cellularity of adipose depots in six strains of genetically obese mice. J Lipid Res; 13(1): 2 – 11.

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