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Antioxidant enzyme protein content in lean and obese women prior to and following a 12‐week endurance training protocol
Author(s) -
Devries Michaela C,
Hamadeh Mazen J,
Glover Sandy,
McCready Colin,
Raha Sandeep,
Tarnopolsky Mark A
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.21.5.a668-c
Subject(s) - catalase , superoxide dismutase , antioxidant , enzyme , medicine , endurance training , endocrinology , oxidative stress , enzyme assay , chemistry , western blot , biochemistry , gene
We investigated the interactive influence of obesity and endurance exercise training on the anti‐oxidant enzyme capacity in 24 (12 obese) women. Muscle biopsies were taken prior to and following a 12‐week progressive endurance exercise training protocol. CuZnSOD, MnSOD and catalase protein content were determined using Western blot analysis. CS and COX enzyme activities were determined using spectrophotometry. Prior to training, MnSOD, CuZnSOD and catalase protein content were similar for both groups. Training decreased CuZnSOD in obese women (P = 0.04). Correlational analyses revealed that the change in % body fat (BF) was negatively correlated with the change in CuZnSOD (r = −0.44, P = 0.04), and positively correlated with the change in MnSOD (r = 0.45, P = 0.04). In obese women, %BF was positively correlated with catalase at baseline (r = 0.73, P = 0.02), whereas in lean women baseline % BF was positively correlated with the change in catalase (r = 0.63, P = 0.03). CS and COX enzyme activity were similar in both groups prior to training, and training increased CS and COX (P < 0.001) enzyme activity in both groups. There was no correlation between CS or COX and the antioxidant enzymes. The primary cellular superoxide dismutases respond differently to a change in % BF induced by endurance exercise and may be indicative of the source of oxidative stress. The lack of correlation between mitochondrial function and antioxidant defense enzymes indirectly implies that mitochondrial sources of radical production may not contribute significantly to obesity related pathologies. (Supported by CIHR, Canada).