| First Author | Gong B | Year | 2000 |
| Journal | Am J Physiol Cell Physiol | Volume | 279 |
| Issue | 5 | Pages | C1351-8 |
| PubMed ID | 11029282 | Mgi Jnum | J:105244 |
| Mgi Id | MGI:3614377 | Doi | 10.1152/ajpcell.2000.279.5.C1351 |
| Citation | Gong B, et al. (2000) A K(ATP) channel deficiency affects resting tension, not contractile force, during fatigue in skeletal muscle. Am J Physiol Cell Physiol 279(5):C1351-8 |
| abstractText | The objective of this study was to determine how an ATP-sensitive K(+) (K(ATP)) channel deficiency affects the contractile and fatigue characteristics of extensor digitorum longus (EDL) and soleus muscle of 2- to 3-mo-old and 1-yr-old mice. K(ATP) channel-deficient mice were obtained by disrupting the Kir6.2 gene that encodes for the protein forming the pore of the channel. At 2-3 mo of age, the force-frequency curve, the twitch, and the tetanic force of EDL and soleus muscle of K(ATP) channel-deficient mice were not significantly different from those in wild-type mice. However, the tetanic force and maximum rate of force development decreased with aging to a greater extent in EDL and soleus muscle of K(ATP) channel-deficient mice (24-40%) than in muscle of wild-type mice (7-17%). During fatigue, the K(ATP) channel deficiency had no effect on the decrease in tetanic force in EDL and soleus muscle, whereas it caused a significantly greater increase in resting tension when compared with muscle of wild-type mice. The recovery of tetanic force after fatigue was not affected by the deficiency in 2- to 3-mo-old mice, whereas in 1-yr-old mice, force recovery was significantly less in muscle of K(ATP) channel-deficient than wild-type mice. It is suggested that the major function of the K(ATP) channel during fatigue is to reduce the development of a resting tension and not to contribute to the decrease in force. It is also suggested that the K(ATP) channel plays an important role in protecting muscle function in older mice. |
