Ventricular Action Potential Adaptation to Regular Exercise: Role of {beta}-Adrenergic and KATP Channel Function

Regular exercise-training is known to affect the action potential duration (APD) and improve heart function, but the involvement by β-adrenergic receptor (β-AR) subtypes and/or K_ATP channel is unknown. To address this, female and male Sprague-Dawley rats were randomly assigned to voluntary wheel running or control groups and after 6-8 weeks training anesthetized and myocytes isolated. Exercise-training significantly increased APD of apex and base myocytes at 1Hz, while decreasing the APD at 10Hz. Ca²⁺ transient durations reflected the changes observed in APD, while Ca²⁺ transient amplitudes were unaffected by wheel running. The non-selective β agonist Isoproterenol (ISO) shortened the myocyte APD an effect reduced by wheel running. The ISO-induced shortening of the APD was largely reversed by selective β₁-AR blocker Atenolol, but not the β₂-AR blocker ICI 118,551 providing evidence that wheel running reduced the sensitivity of the β₁-AR. At 10Hz, the KATP channel inhibitor glibenclamide prolonged the myocyte APD more in exercise-trained compared to controls implicating a role for this channel in the exercise-induced APD shortening at 10Hz. A novelty of this work is the demonstration of the duel importance of altered β₁-AR responsiveness and K_ATP channel function in the training-induced regulation of the APD. Of physiological importance to the beating heart, the reduced response to adrenergic agonists would enhance cardiac contractility at resting rates where sympathetic drive is low by prolonging the APD and Ca²⁺ influx, while during exercise an increased K_ATP channel activity would shorten APD thus protecting the heart against Ca²⁺ overload or inadequate filling.

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