Post-Grant Reports


The Effects of Physical Activity on Stress-Induced Cardiac Fibrosis

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Cardiovascular System | Exercise Physiology


The aim of this project was to examine whether routine physical activity limits stress-induced tissue remodeling processes that lead to cardiac fibrosis. A secondary aim was to take the first steps to explore a potential and novel underlying mechanism, wherein a cardiac urocortin 2/corticotropin releasing factor receptor 2β pathway may be activated during physical activity and involved in reducing fibrotic processes. C67BL/6J male mice were divided into four groups (n=8/group); sedentary control, voluntary running control, sedentary/stress and voluntary running/stress. Mice in the voluntary running groups were given 24-hour unlimited access to a running wheel in the home cage for 9 weeks with wheel running activity recorded continuously. During the 9th week of running, mice in the stress groups were exposed to a 5 day resident-intruder social stress paradigm that is considered to model human post traumatic stress outcomes and has been shown to induce cardiovascular fibrosis. Ventricular cardiac tissue was collected for analysis at the end of the experiment.

We found that mice in the voluntary running groups ran an average of 4.75 ± 1 km each day with the majority of running bouts occurring within the first 6 hours of the dark cycle. Interestingly, running behavior essentially ceased in mice exposed to stress. Running distance dropped to 0.31 km following the first day of stress. Some habituation to stress occurred, as running distance increased to 1.12 km by the 5th day of stress but was still significantly lower then pre-stress running distances and distances recorded in non-stressed mice. Quantitative RT-PCR showed a 2-fold increase in ventricular urocortin 2 gene expression in the sedentary/stress group, while levels were slightly lower in the voluntary running/stress group with a 1.78-fold increase over controls. CRF-R2β expression was not significantly altered. TGF-β, a signaling molecule known to induce fibrosis, showed slight elevation in expression in the stress group. Total protein was isolated from heart ventricles and we are in the process of performing Western blots to assess levels of specific proteins that are indicative of fibrosis. Complete findings will be presented at the Linfield College Student Symposium this spring.


This research was conducted as part of a Linfield College Student-Faculty Collaborative Research Grant in 2016, funded by the Office of Academic Affairs.

The student collaborator was Erin Kinney.

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