They had two groups of mice, the active ones and the "loungers", which shared the same environment and routine. The active mice would run on the treadmill everyday for 30 minutes for eight weeks.
After the eight weeks, researchers noticed that the active mice were able to last on the treadmills for 126 minutes but the "loungers" only lasted 74 minutes ... which is not surprising at all. The main point was to see if their brain cells have changed. The brains activity was different all over but the brain cells had developed new mitochondria. This finding was very important because it's a lead on implying that exercise can lead to mitochondrial biogenesis in the brain.
Dr. Davis, a professor at the Arnold School of Public Health at the University of South Carolina, quoted that "that mitochondrial deficits in the brain may play a role in the development of neurodegenerative diseases". If working out increases the mitochondria, it is possible that a large amount of mitochondria in your brain cells could prevent neurological diseases like Alzheimer's and Parkinson's disease. A re-energized brain after a few workouts also help with being less or not at all fatigue and sharpens your thinking.
As of now, this experiment hasn't been tested on humans but since mitochondrial biogenesis has been proved in human and animal muscles, its possible that it could happen in human brains as well.
http://well.blogs.nytimes.com/2011/09/28/how-exercise-can-strengthen-the-brain/
This is a very interesting approach to disease prevention; however, I am curious as to whether the level of mitochondrial biogenesis varies in different parts of the brain. Such comparison would definitely be an important consideration when evaluating the effectiveness of potential applications of these findings. Another possible factor to further investigate would be whether different types of exercise promote mitochondrial biogenesis at different rates.
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ReplyDeleteAlzheimer's disease and Parkingson's disease are associated with defects in the cellular autophagy machinery. In cells that are autophagy-incompetent, reactive oxygen species (produced mainly in the cell's mitochondria) further contribute to oxidative stress. It is interesting that in this situation, exercise can potentially increase a cell's ability to maintain homeostasis and health. The increase in the quantity of mitochondria in neuron's must exert its effect via a different mechanism. It would be interesting to see if further studies could be conducted to determine the biochemical pathway(s) affected by a greater mitochondrial population.
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