07 Sep Exercise Did Not Improve Mitochondrial Content in Healthy Brains
MedicalResearch.com Interview with:
Eric A.F. Herbst MSc Ph.D. student
Human Health and Nutritional Sciences
University of Guelph
Guelph, ON
Medical Research: What is the background for this study? What are the main findings?
Response: Many neurological diseases result in declines in mitochondrial content and function in the brain. Therefore, the purpose for this study was to determine if mitochondrial content could be enhanced in the brain through exercise, as previously demonstrated in skeletal muscle, and also to determine if similar exercise-signaling pathways are activated between the two tissues in the process.
This study found that despite reproducing similar findings in skeletal muscle, acute and chronic exercise did not activate traditional signaling mechanisms (AMPK, ERK1/2, CAMKII, P38) in either the cortex or striatum of the brain, nor did it result in sustained increases in mitochondrial respiration, DNA copy number, or protein content.
Medical Research: What should clinicians and patients take away from your report?
Response: Where it would be ideal to employ exercise to preventatively augment mitochondrial content and respiratory efficiency prior to the onset of a given debilitating neurodegenerative disorder to potentially slow disease progression, the present findings suggest that exercise cannot be used to increase mitochondrial content in the healthy brain beyond a given set point.
Medical Research: What recommendations do you have for future research as a result of this study?
Response: Despite the inability to increase mitochondrial content in the brain above control levels with exercise, the next question to answer is whether or not exercise can be used to prevent loss of mitochondrial function and content associated with neurological disease. Interestingly, in work recently published in Neurology (Herbst & Holloway 2015), we demonstrated beneficial effects of exercise in a transgenic mouse model of Huntington’s disease, where we could delay, but not completely prevent, the effects of Huntington’s within the mitochondrial environment. Therefore, exercise may possess clinical implications to delaying the metabolic impact of neurodegenerative diseases on the brain.
Citation:
Herbst EA1, Roussakis C2, Matravadia S2, Holloway GP3.
MedicalResearch.com is not a forum for the exchange of personal medical information, advice or the promotion of self-destructive behavior (e.g., eating disorders, suicide). While you may freely discuss your troubles, you should not look to the Website for information or advice on such topics. Instead, we recommend that you talk in person with a trusted medical professional.
The information on MedicalResearch.com is provided for educational purposes only, and is in no way intended to diagnose, cure, or treat any medical or other condition. Always seek the advice of your physician or other qualified health and ask your doctor any questions you may have regarding a medical condition. In addition to all other limitations and disclaimers in this agreement, service provider and its third party providers disclaim any liability or loss in connection with the content provided on this website.
Eric A.F. Herbst MSc Ph.D. student (2015). Exercise Did Not Improve Mitochondrial Content in Healthy Brains
Last Updated on September 7, 2015 by Marie Benz MD FAAD