The objective of this study was to determine how an ATP-sensitive K+ (KATP) 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. KATP 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 KATPchannel-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 KATP channel-deficient mice (24–40%) than in muscle of wild-type mice (7–17%). During fatigue, the KATP 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 KATP channel-deficient than wild-type mice. It is suggested that the major function of the KATP 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 KATP channel plays an important role in protecting muscle function in older mice.
Muscle contractile dysfunction and oxidative injury are observed in the soleus muscle of metallothionein deficient mice following acute spinal cord injury
