O2•‐ production at 37oC plays a critical role in depressing tetanic force of isolated rat skeletal muscle

Abstract

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 O2•− production, O2•− 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 O2•− 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 Ca2+-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 Ca2+-activated force and membrane potential were largely prevented by 1mM Tempol, a membrane permeable O2•− dismutase mimetic. These results show that the increased O2•− 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.