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Effect of mouse strain on mitochondrial biogenesis and exercise
Author(s) -
Davis Greggory Ryan,
Wang Pingyun,
Hwang Paul M
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.806.17
Subject(s) - treadmill , mitochondrial biogenesis , strain (injury) , exercise intolerance , medicine , mitochondrial dna , aerobic capacity , physiology , endocrinology , biology , mitochondrion , gene , genetics , heart failure
Sponsor: Jacqueline M. Stephens Purpose Improvement in exercise capacity and change in mitochondrial DNA (mtDNA) were examined in B6 mice compared to wild‐type p53 and heterozygous FVB mice. Methods FVB and B6 mice performed a high‐intensity five‐week treadmill exercise protocol. Maximal exercise testing was performed on all groups and time was recorded at the point of exhaustion. All groups were rested for 72 hours prior to dissection to minimize any acute effects of exercise. Body fat percentage was determined and the gastrocnemius and soleus muscles were harvested and analyzed. Results The FVB strain nearly doubled work capacity and had a significantly lower body fat percentage compared to the B6 strain. mtDNA copy number did not change significantly in either strain and it actually decreased in the trained FVB p53 +/+ and p53 +/− groups. Conclusions FVB mice demonstrated both a greater intrinsic exercise capacity as well as a greater response to exercise training while variation in the genotype of the FVB mice did not significantly affect response to exercise. The greater exercise capacity seen in the FVB mice may be due to a number of other factors including cardiovascular, biomechanical, and psychological aspects. It is also possible that exercise capacity may have increased due to genes mediated by nuclear DNA, making change in mtDNA more difficult to detect. National Heart, Lung, and Blood Institute. National Institutes of Health, Bethesda, MD 20892