Cardiomyocyte Adaptation to Exercise: K+ Channels, Contractility and Ischemic Injury. Int J Sports Med 2024 Oct;45(11):791-803
Date
04/23/2024Pubmed ID
38648799DOI
10.1055/a-2296-7604Scopus ID
2-s2.0-85191888061 (requires institutional sign-in at Scopus site)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.
Author List
Fitts RH, Wang X, Kwok WM, Camara AKSAuthor
Amadou K. Camara PhD Professor in the Anesthesiology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
Action PotentialsAdaptation, Physiological
Adenosine
Animals
Apoptosis
Atrial Fibrillation
Calcium
Exercise
Humans
KATP Channels
Myocardial Contraction
Myocardial Reperfusion Injury
Myocytes, Cardiac
Potassium Channels
Sarcolemma