A K(ATP) channel deficiency affects resting tension, not contractile force, during fatigue in skeletal muscle.
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.
Gong
B
B
Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, Ontario, Canada K1H 8M5.
Miki
T
T
Seino
S
S
Renaud
J M
JM
D000818:Animals; D005260:Female; D007700:Kinetics; D008297:Male; D051379:Mice; D018345:Mice, Knockout / Q000235:genetics; D009119:Muscle Contraction / Q000502:physiology*; D018763:Muscle Fatigue / Q000502:physiology*; D018482:Muscle, Skeletal / Q000378:metabolism / Q000502:physiology*; D015221:Potassium Channels / Q000172:deficiency* / Q000235:genetics; D024661:Potassium Channels, Inwardly Rectifying
D015221:Potassium Channels; D024661:Potassium Channels, Inwardly Rectifying