Int J Sports Med
DOI: 10.1055/a-2296-7604
Review

Cardiomyocyte Adaptation to Exercise: K+ Channels, Contractility and Ischemic Injury

Robert H. Fitts
1   Biological Sciences, Marquette University, Milwaukee, United States
,
Xinrui Wang
2   Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, United States
3   Cardiovascular Center, Medical College of Wisconsin, Milwaukee, United States
,
Wai-Meng Kwok
2   Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, United States
3   Cardiovascular Center, Medical College of Wisconsin, Milwaukee, United States
4   Anesthesiology, Medical College of Wisconsin, Milwaukee, United States
5   Cancer Center, Medical College of Wisconsin, Milwaukee, United States
,
Amadou K. S. Camara
3   Cardiovascular Center, Medical College of Wisconsin, Milwaukee, United States
4   Anesthesiology, Medical College of Wisconsin, Milwaukee, United States
5   Cancer Center, Medical College of Wisconsin, Milwaukee, United States
6   Physiology, Medical College of Wisconsin, Milwaukee, United States
› Institutsangaben

Abstract

Cardiovascular disease is a leading cause of morbidity and mortality, and exercise-training (TRN) is known to reduce risk factors and protect the heart from ischemia and reperfusion injury. Though the cardioprotective effects of exercise are well-documented, underlying mechanisms are not well understood. This review highlights recent findings and focuses on cardiac factors with emphasis on K+ channel control of the action potential duration (APD), β-adrenergic and adenosine regulation of cardiomyocyte function, and mitochondrial Ca2+ regulation. TRN-induced prolongation and shortening of the APD at low and high activation rates, respectively, is discussed in the context of a reduced response of the sarcolemma delayed rectifier potassium channel (IK) and increased content and activation of the sarcolemma KATP channel. A proposed mechanism underlying the latter is presented, including the phosphatidylinositol-3kinase/protein kinase B pathway. TRN induced increases in cardiomyocyte contractility and the response to adrenergic agonists are discussed. The TRN-induced protection from reperfusion injury is highlighted by the increased content and activation of the sarcolemma KATP channel and the increased phosphorylated glycogen synthase kinase-3β, which aid in preventing mitochondrial Ca2+ overload and mitochondria-triggered apoptosis. Finally, a brief section is presented on the increased incidences of atrial fibrillation associated with age and in life-long exercisers.



Publikationsverlauf

Eingereicht: 19. Dezember 2023

Angenommen: 18. März 2024

Artikel online veröffentlicht:
22. April 2024

© 2024. Thieme. All rights reserved.

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Rüdigerstraße 14, 70469 Stuttgart, Germany

 
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