Despite decades of effort in fitness tracking, gyms, and public health promotion, about 80% of adolescents are physically inactive. In his presentation to our seminar, Dr. Trevor Buhr presented evidence that we may be addressing the wrong issue. Lack of activity may actually be more related to motivation than capacity. Psychological stress can damage motivation to be active.
In one set of experiments, rats were given the ability to voluntarily run on a treadmill and receive a rewarding signal for running. Rats exposed to a single session of 50 or 100 uncontrollable tail shocks ran 2-4 times less than stress-free rats. Additionally, the amount of running deficit correlated with the amount of shocks. The deficit persisted for all nine weeks of the experiment and did not show signs of recovery. Importantly, the stressor induced anxiety- and depression-like behaviors that resolve within about 72 hours. Perhaps most interesting to me was the running data. Stress reduced running in rats despite limited habituation to the task. Furthermore, when the task was made less mandatory and less difficult, stressed rats were 31% more likely to stop running earlier. They were capable of running yet did not. Running in unstressed rats increased dopamine turnover in the hippocampus and prefrontal cortex. However, prior stress reduced this effect of running. Additionally, stressed rats had a mild deficit of dopamine in the striatum (a brain region involved in both movement and reward).
In another experiment (published in Nature in December 2022 and summarized by the NIH), Dr. Christoph Thaiss and colleagues at the University of Pennsylvania sought to determine why some mice run more than others. They found that the mouse gut microbiome was the best predictor of running activity, rather than metabolism or genetics. When gut bacteria was ablated in mice via antibiotics, mice showed a reduction in wheel running and ran for a shorter duration on a treadmill. Exercise increased dopamine in the striatum of mice with intact gut microbiomes but not in mice with ablated gut bacteria. Furthermore, blocking dopamine in mice replicated the effects of ablated gut microbiota while stimulating dopamine reversed the deficit in running. A class of compounds made by gut bacteria and acting on sensory neurons in the gut appeared to be the link. Supplementing these compounds to the diet reversed the deficit in running observed in mice with ablated gut microbiota.
Both of these experiments highlight the complex nature of motivation to run as a biological state that can be influenced by multiple factors and that similar dopamine signaling can be reduced by very different insults (both stress and disrupted gut microbiota). Importantly, no injury was present in either set of experiments. Rather, the motivation to run was simply reduced.
Interestingly, while there is much overlap between these experiments, there also exists a difference that is useful to highlight. In the experiment by Dr. Thaiss et al., the deficit in motivation to run was reversible upon restoration of the missing signal. In contrast, the deficit seen by Dr. Buhr was not reversible within the time frame of the experiment (nine weeks). I believe it is important to explore whether stress-induced deficits in motivation to run are reversible and at what point intervention may be effective. Additionally, this question is not limited to rodents. A 2026 longitudinal study of 667 college students found that adverse childhood experiences predicted lower intrinsic motivation to run six months later.
I believe this has important implications for the current popular sentiment of “run more.” I hope to work in emergency or military medicine. In these settings, patients tend to have more trauma than in other fields. If trauma has long lasting effects on the motivation to run, then a patient who does not comply with an exercise prescription may not be noncompliant. Rather, they may be anhedonic for effort itself and additional persuasion will not suffice in this case.
I do wish to add some caution. These are rodent studies and only male rats were used by Dr. Buhr. Furthermore, Dr. Buhr’s team also observed oxidative stress in the muscle of stressed rats which cannot be taken as evidence that capacity is not involved. However, the concept is important and should be explored. Perhaps in order to increase activity we must also address motivation to be active.
References
Buhr, T. J., Reed, C. H., Wee, O. M., Lee, J. H., Yuan, L.-L., Fleshner, M., Valentine, R. J., & Clark, P. J. (2023). The persistence of stress-induced physical inactivity in rats: An investigation of central monoamine neurotransmitters and skeletal muscle oxidative stress. Frontiers in Behavioral Neuroscience, 17, Article 1169151. https://doi.org/10.3389/fnbeh.2023.1169151
Doctrow, B. (2023, January 10). Gut microbes may affect motivation to exercise. NIH Research Matters. https://www.nih.gov/news-events/nih-research-matters/gut-microbes-may-affect-motivation-exercise
Dohnalová, L., Lundgren, P., Carty, J. R. E., Goldstein, N., Wenski, S. L., Nanudorn, P., … Thaiss, C. A. (2022). A microbiome-dependent gut–brain pathway regulates motivation for exercise. Nature, 612(7941), 739–747. https://doi.org/10.1038/s41586-022-05525-z
The longitudinal impact of adverse childhood experiences on college students’ intrinsic motivation for physical exercise: The chain mediating effect of meaning in life and psychological resilience. (2026). Frontiers in Psychology. https://doi.org/10.3389/fpsyg.2026.1875230
No comments:
Post a Comment