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O2•‐ production at 37oC plays a critical role in depressing tetanic force of isolated rat skeletal muscle
Author(s) -
Edwards Joshua,
Macdonald William,
van der Poel Chris,
Stephenson D George
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.lb100-b
Subject(s) - skeletal muscle , chemistry , intracellular , tetanic stimulation , medicine , endocrinology , incubation , biophysics , biochemistry , biology , long term potentiation , receptor
To determine whether the decline in isolated mammalian skeletal muscle performance associated with the increase in temperature towards physiological levels is related to the increase in O 2 •− production, O 2 •− released extracellularly by isolated intact rat EDL muscles was measured at 22, 32 and 37°C in Krebs‐Ringer solution and tetanic force measured at 22 and 37°C. The rate of O 2 •− production increased marginally when the temperature was increased from 22 to 32°C, but increased fivefold when the temperature was increased from 22 to 37°C. This increase was accompanied by a marked decrease in tetanic force after 30min incubation at 37°C. After muscles were exposed to 37°C for 30min, there was a small, not statistically significant decrease in maximum Ca 2+ ‐activated force measured in mechanically skinned fibers, but the resting membrane and intracellular action potentials were significantly affected. The effects of the temperature treatment on tetanic force, maximum Ca 2+ ‐activated force and membrane potential were largely prevented by 1mM Tempol, a membrane permeable O 2 •− dismutase mimetic. These results show that the increased O 2 •− production at physiological temperatures contributes to the observed depression in tetanic force occurring in isolated mammalian skeletal muscle at 37°C by affecting the contractile apparatus and plasma membrane, and that 1mM Tempol is effective for largely preventing this.