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1 Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, Ontario, Canada
2 Department of Molecular Medicine, Chiba University Graduate School of Medicine, Chiba, Japan
* To whom correspondence should be addressed. E-mail: jmrenaud{at}uottawa.ca.
Although it has been suggested that the KATP channel protects muscle against function impairment, most studies have so far given little evidence for significant perturbation in the integrity and function of skeletal muscle fibers from inactive mice that lack KATP channel activity in their cell membrane. The objective was therefore to test the hypothesis that KATP channel deficient skeletal muscle fibers become damaged when mice are subjected to stress. Wild type and KATP channel deficient mice (Kir6.2-/- mice) were subjected to 4-5 weeks of treadmill running at either 20 m/min with 0° inclination or at 24 m/min with 20° uphill inclination. Muscles of all wild type mice and of non-exercised Kir6.2-/- mice had very few fibers with internal nuclei. After 4-5 weeks of treadmill running, there was little evidence for connective tissues and mononucleated cells in Kir6.2-/- hindlimb muscles, whereas the number of fibers with internal nuclei, which appear when damaged fibers are regenerated by satellite cells, was significantly higher in Kir6.2-/- than wild type mice. Between 5% and 25% of the total number of fibers in Kir6.2-/- EDL, plantaris and tibialis muscles had internal nuclei, and most of such fibers were type IIB fibers. Contrary to hindlimb muscles, diaphragm of Kir6.2-/- mice that had run at 24 m/min had few fibers with internal nuclei, but mild to severe fiber damage was observed. In conclusion, the study provides for the first time evidence i) that the KATP channels of skeletal muscle are essential to prevent fiber damage, and thus muscle dysfunction and ii) that the extent of fiber damage is greater while the capacity of fiber regeneration is less in Kir6.2-/- diaphragm muscles compared to hindlimb muscles.
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