Location

Jereld R. Nicholson Library: Grand Avenue

Subject Area

Health, Human Performance and Athletics

Description

Purpose: This study examined whether routine physical activity limits stress-induced tissue remodeling processes that lead to cardiac fibrosis. The study also explored whether the cardiac urocortin 2/corticotropin releasing factor receptor 2β pathway was activated during physical activity and involved in reducing fibrotic processes.

Methods: C67BL/6J male mice were divided into four groups (n=8/group): sedentary/control, voluntary running/control, sedentary/stress and voluntary running/stress. Voluntary running groups were given 24-hour access to a running wheel in the home cage for 9 weeks. During the 9th week, stress groups were exposed to a 5-day resident-intruder stress paradigm that models human post-traumatic stress outcomes. Ventricular cardiac tissue was collected for analysis.

Results: Mice ran an average of 4.75 ± 1 km each night. Interestingly, running behavior essentially ceased following stress. Running distance dropped to 0.31 km following the 1st stress day. Some habituation to stress occurred, as running distance increased to 1.12 km by the 5th day of stress but remained significantly lower than pre-stress running distances and distances recorded in non-stressed mice. Quantitative RT-PCR showed small changes in ventricular urocortin 2 and CRF-R2β expression in the running groups. TGF-β, a signaling molecule known to induce fibrosis, had comparable expression levels across groups over controls.

Conclusion: Further work is planned to fully characterize urocortin 2/ CRF-R2β and fibrotic processes. Our running data lead us in a new direction, as we have stumbled upon a paradigm that will be useful to study underlying mechanisms by which stress exposure impairs physical activity behavior.

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May 5th, 3:00 PM May 5th, 4:30 PM

The Effects of Physical Activity on Stress-induced Cardiac Fibrosis

Jereld R. Nicholson Library: Grand Avenue

Purpose: This study examined whether routine physical activity limits stress-induced tissue remodeling processes that lead to cardiac fibrosis. The study also explored whether the cardiac urocortin 2/corticotropin releasing factor receptor 2β pathway was activated during physical activity and involved in reducing fibrotic processes.

Methods: C67BL/6J male mice were divided into four groups (n=8/group): sedentary/control, voluntary running/control, sedentary/stress and voluntary running/stress. Voluntary running groups were given 24-hour access to a running wheel in the home cage for 9 weeks. During the 9th week, stress groups were exposed to a 5-day resident-intruder stress paradigm that models human post-traumatic stress outcomes. Ventricular cardiac tissue was collected for analysis.

Results: Mice ran an average of 4.75 ± 1 km each night. Interestingly, running behavior essentially ceased following stress. Running distance dropped to 0.31 km following the 1st stress day. Some habituation to stress occurred, as running distance increased to 1.12 km by the 5th day of stress but remained significantly lower than pre-stress running distances and distances recorded in non-stressed mice. Quantitative RT-PCR showed small changes in ventricular urocortin 2 and CRF-R2β expression in the running groups. TGF-β, a signaling molecule known to induce fibrosis, had comparable expression levels across groups over controls.

Conclusion: Further work is planned to fully characterize urocortin 2/ CRF-R2β and fibrotic processes. Our running data lead us in a new direction, as we have stumbled upon a paradigm that will be useful to study underlying mechanisms by which stress exposure impairs physical activity behavior.

 

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