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Antioxidant overexpression reduces diaphragm maximal specific tension but does not alter resistance to fatigue
Author(s) -
DeRuisseau Keith C,
McClung Joseph M,
Kavazis Andreas N,
Whidden Melissa A,
Van Remmen Holly,
Richardson Arlan,
Powers Scott K
Publication year - 2007
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.21.6.a1306-d
Subject(s) - superoxide dismutase , catalase , antioxidant , reactive oxygen species , oxidative stress , medicine , chemistry , contraction (grammar) , endocrinology , dismutase , skeletal muscle , diaphragm muscle , genetically modified mouse , biochemistry , transgene , biology , respiratory system , gene
Skeletal muscle contraction during exercise leads to increased production of reactive oxygen species (ROS). Because oxidative stress is linked to muscle fatigue development, we hypothesized that diaphragms from mice overexpressing antioxidant enzymes would be more resistant to contraction induced fatigue. To test this postulate, diaphragm fiber bundles from transgenic mice overexpressing the specific antioxidant enzymes: catalase (Cat; n=6), manganese superoxide dismutase (MnSOD; n=6), and copper‐zinc superoxide dismutase (CuZnSOD; n=9) were examined to determine maximal specific tension, endurance, and recovery from fatigue. Wild‐type littermates (WT; n=8) served as controls. Diaphragms from antioxidant overexpressing animals demonstrated lower (p<0.05) submaximal and maximal specific tension values compared to WT controls; with diaphragms from MnSOD overexpressing animals exhibiting the greatest decrement. However, no differences in diaphragm endurance or recovery from fatigue were observed between groups (p>0.05). Moreover, protein carbonyl levels of the stimulated fiber bundles did not differ between groups (p>0.05). Collectively, these results suggest that cellular ROS are critical to normal diaphragm contractile function and chronic overexpression of antioxidant enzymes is not sufficient to alleviate the development of fatigue. Funded by 1R01HL072789 (SKP)

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