MODULATION OF MUSCLE CONTRACTILITY DURING FATIGUE AND RECOVERY BY ATP-SENSITIVE POTASSIUM CHANNEL

The activity of ATP-sensitive potassium channels of skeletal muscle is controlled by changes in the bioenergetic state of the cell. These ch annels are inactive in unfatigued muscle and become activated during f atigue. It has been postulated that ATP-sensitive potassium channels s horten the action potential duration, increase the potassium efflux an d contribute to the decrease in force during fatigue. Although blockin g ATP-sensitive potassium channels during fatigue prolongs the action potential duration and decreases the potassium efflux as expected. it does not affect the rate of fatigue development. as observed from the decrease in tetanic force. Even though such results are not consistent with the hypothesis that ATP-sensitive potassium channels contribute to the decrease in force during fatigue. a reduced capacity of skeleta l muscles to recover their tetanic force following fatigue is also obs erved when ATP-sensitive potassium channels are blocked during fatigue . suggesting that these channels have a myoprotective effect. It is th us possible that removing this myoprotection during fatigue results in deleterious effects which counteract the expected slower decrease in force. However. ATP-sensitive potassium channel openers also fail to a ffect the rate of fatigue development. Therefore. the results obtained so far do not support the hypothesis that ATP-sensitive potassium cha nnels contribute to the decrease in force during fatigue.