Exercise training improves cardiac function
Cardiovascular disease is a leading cause of shortened life expectancy globally, with a 50% mortality rate five years after receiving the diagnosis of heart failure. Heart failure is commonly the endpoint of cardiovascular disease and the majority of patients perish from irregular heartbeat or pump failure. In both cases impaired calcium homeostasis and altered cellular electrophysiology are key underlying mechanisms.
Exercise training is included in the guidelines for prevention, treatment and rehabilitation of a broad spectrum of the most prevalent cardiovascular conditions. Not only can exercise training be a treatment in itself, but the cellular mechanisms underlying the benefit has also been used as a means to reveal new molecular targets in the search for novel treatments for heart failure.
Exercise training following development of heart failure shifted the cardiac phenotype back towards normal in an exercise intensity-dependent manner based on key parameters ranging from whole body exercise capacity, systolic and diastolic cardiac function as well as susceptibility for cardiac ventricular fibrillation, to underpinning mechanisms at the cellular level with restoration of cardiomyocyte function, calcium handling and electrophysiological properties.
This study showed that a magnitude of improvements in calcium handling and electrophysiological properties are exercise intensity dependent, indicating that high intensity exercise is superior to moderate intensity on reducing disposition for irregular heartbeats.
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Exercise training reveals micro-RNAs associated with improved cardiac function and electrophysiology in rats with heart failure after myocardial infarction - PubMed (nih.gov)
J Mol Cell Cardiol. 2020 Nov;148:106-119.
Tomas O Stølen, Morten A Høydal, Muhammad Shakil Ahmed, Kari Jørgensen, Karin Garten, Maria P Hortigon-Vinagre, Victor Zamora, Nathan R Scrimgeour, Anne Marie Ormbostad Berre, Bjarne M Nes, Eirik Skogvoll, Anne Berit Johnsen, Jose B N Moreira, Julie R McMullen, Håvard Attramadal, Godfrey L Smith, Øyvind Ellingsen, Ulrik Wisløff
PMID: 32918915
DOI: 10.1016/j.yjmcc.2020.08.015
Short excerpts from the article shared under Elsevier license number 5515400146093