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, ONEric 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:

Metabolism. 2015 Jul 6. pii: S0026-0495(15)00182-1. doi: 10.1016/j.metabol.2015.07.002. [Epub ahead of print]

Chronic treadmill running does not enhance mitochondrial oxidative capacity in the cortex or striatum.

Herbst EA1, Roussakis C2, Matravadia S2, Holloway GP3.

 

 

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Eric A.F. Herbst MSc Ph.D. student (2015). Exercise Did Not Improve Mitochondrial Content in Healthy Brains 

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