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

Autor: Fitts RH; Biological Sciences, Marquette University, Milwaukee, United States., Wang X; Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, United States.; Cardiovascular Center, Medical College of Wisconsin, Milwaukee, United States., Kwok WM; Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, United States.; Cardiovascular Center, Medical College of Wisconsin, Milwaukee, United States.; Anesthesiology, Medical College of Wisconsin, Milwaukee, United States.; Cancer Center, Medical College of Wisconsin, Milwaukee, United States., Camara AKS; Cardiovascular Center, Medical College of Wisconsin, Milwaukee, United States.; Anesthesiology, Medical College of Wisconsin, Milwaukee, United States.; Cancer Center, Medical College of Wisconsin, Milwaukee, United States.; Physiology, Medical College of Wisconsin, Milwaukee, United States.
Jazyk: angličtina
Zdroj: International journal of sports medicine [Int J Sports Med] 2024 Oct; Vol. 45 (11), pp. 791-803. Date of Electronic Publication: 2024 Apr 22.
DOI: 10.1055/a-2296-7604
Abstrakt: 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 Ca 2+ 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 K ATP 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 K ATP channel and the increased phosphorylated glycogen synthase kinase-3β, which aid in preventing mitochondrial Ca 2+ 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.
Competing Interests: The authors declare that they have no conflict of interest.
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Databáze: MEDLINE
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