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 channels are inactive in unfatigued muscle and become activated during fatigue. It has been postulated that ATP-sensitive potassium channels shorten the action potential duration, increase the potassium efflux and contribute to the decrease in force during fatigue. Although blocking 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 skeletal muscles to recover their tetanic force following fatigue is also observed when ATP-sensitive potassium channels are blocked during fatigue, suggesting that these channels have a myoprotective effect. It is thus 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 fall to affect the rate of fatigue development. Therefore, the results obtained so far do not support the hypothesis that ATP-sensitive potassium channels contribute to the decrease in force during fatigue.
Renaud
J M
JM
Department of Physiology, University of Ottawa, Ontario, Canada.
Gramolini
A
A
Light
P
P
Comtois
A
A
D000255:Adenosine Triphosphate / Q000502:physiology*; D000818:Animals; D006801:Humans; D009119:Muscle Contraction / Q000502:physiology*; D018763:Muscle Fatigue / Q000502:physiology*; D015221:Potassium Channels / Q000502:physiology*; D015222:Sodium Channels / Q000502:physiology
D015221:Potassium Channels; D015222:Sodium Channels; D000255:Adenosine Triphosphate