Role of KATP Channels in Beneficial Effects of Exercise in Ischemic Heart Failure
Is the exercise-induced improvement in cardiac function in postischemic heart failure (HF) influenced by positive changes in KATP channels?
Cardiomyocytes were isolated and examined from three different rat groups: exercise-trained postischemic HF (CHF Tr), sedentary postischemic HF (CHF Sed), and sham rats. Cardiomyocyte survival postischemia and calcium handling were assessed in the presence of KATP channel inhibition using glibenclamide, and expression of KATP subunits (SUR2A and Kir6.2) was assessed using immunoblotting technique.
Exercise improved cardiac function in the CHF Tr rats. The oxidative stress of ischemia induced less cardiomyocyte damage in CHF Tr and sham rats than in CHF Sed. In addition, exercise improved calcium handling in the cardiomyocytes of CHF Tr rats, and increased KATP channel expression, particularly the SUR2A subtype, compared to that of the CHF sed rats and sham rats.
The current study suggests that chronic exercise induces upregulation of sarolemmal KATP channels on cardiomyocytes, which improves calcium handling and tolerance to oxidative stress. This may account for at least part of the beneficial effect on cardiac function observed with exercise training in postischemic HF.
Cardiac rehabilitation is a mainstay therapy for patients with stable postischemic HF. This study reveals a subcellular mechanism, upregulation of KATP, for improved cardiomyocyte handling of calcium with exercise training.
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