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Articles in PresS, published online ahead of print August 23, 2002
J Appl Physiol, 10.1152/jap.00097.2002
Submitted on February 6, 2002
Accepted on August 16, 2002
1 Department of Regulatory Cell Physiology, Nagoya City University, Graduate School of Medical Sciences, Nagoya, Aichi, Japan
2 Department of Morphological Anatomy, Nagoya City University, Graduate School of Medical Sciences, Nagoya, Aichi, Japan
3 Nursing, Nagoya City University, Nagoya, Aichi, Japan
4 Department of Health Science, Nagoya City University, Institute of Natural Sciences, Nagoya, Aichi, Japan
5 Department of Physical Therapy, Nagoya University, School of Health Sciences, Nagoya, Aichi, Japan
6 Department of Veterinary Biosciences, The Ohio State University, Columbus, Ohio, USA
* To whom correspondence should be addressed. E-mail: tooba{at}med.nagoya-cu.ac.jp.
We studied whether hydrogen peroxide (H2O2) at 10 µM or less activates the ryanodine receptor and decreases releasable Ca2+ content in the sarcoplasmic reticulum after fatiguing stimulation. Exposure of rabbit- or frog-skeletal muscle ryanodine receptors to H2O2 at 
10 µM enhanced significantly channel activity in lipid bilayers, when the redox potential was defined at cis (cytoplasmic)=-220mV and trans (transluminal)=-180mV. Channel activation by 10 µM H2O2 was also observed when cis potential was set at -220mV without defining trans potential, but the effect was less than that under both cis and trans potential control. Reduction of trans redox potential from -180mV to -220mV, while keeping cis potential at -220mV, did not alter channel activity. H2O2 at 
500 µM failed to activate the channel, when the redox potential was not controlled. Electrical stimulation of the frog single skeletal muscle fiber for 2 min at a frequency of 50 Hz on a duty cycle of 200 ms per s, decreased tetanus tension ~50%. After 1 min, tetanus recovered rapidly to ~70% of control and thereafter, slowly approached the control level. Amplitudes of caffeine- and 4-chloro-m-cresol-induced contractures were markedly decreased after a 60-min rest from fatigue. The decrease is enhanced by exposure to 100 µM H2O2, but not by 10 µM. In the presence of H2O2, the tetanic force and its half-duration failed to recover from fatigue even after a 60-min rest. These results suggest that H2O2 has a marked ability to activate the ryanodine receptor under the redox potential control in vitro, but externally applied H2O2 may not play an important role in the post-fatigue recovery process.
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