Biomedicine

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Science  04 Mar 2011:
Vol. 331, Issue 6021, pp. 1115
DOI: 10.1126/science.331.6021.1115-a
CREDIT: SAFDAR ET AL., PROC. NATL. ACAD. SCI. U.S.A. 108, 10.1073/PNAS.1019581108 (2011)

Recent work has implicated mutations in mitochondrial DNA (mtDNA) in aging, and in humans, endurance training has been linked to health benefits, including increased life expectancy. Safdar et al. wanted to see if these processes could be linked in a strain of mice prone to mtDNA damage and who also exhibit a reduced life span. In these mice, a regime of endurance training—running for 45 min three times a week over 5 months—induced mitochondrial biogenesis, increased mitochondrial respiratory capacity, and prevented mtDNA damage. Furthermore, the trained mice no longer exhibited premature mortality or other symptoms associated with accelerated aging including fat loss, muscle loss, anemia, and graying fur (compare 30-week-old endurance-trained mouse, left, to 30-week-old control mouse, right). Future work will be required to see if similar regimes can protect and “rejuvenate” human mitochondria and mitigate the effects of normal or pathological forms of premature aging.

Proc. Natl. Acad. Sci. U.S.A. 108, 10.1073/pnas.1019581108 (2011).

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