Exercise-induced changes in calcium handling in left ventricular cardiomyocytes.
Regular exercise training results in beneficial adaptation of the heart by improving its contractile capacity. This has important consequences for both healthy individuals and those with depressed myocardial function, e.g. heart failure. Studies combining experimental animal models of exercise training and heart failure with biophysical and biochemical characterization of heart function have extended our understanding of how exercise training improves cardiac contractile function at the cellular level. Exercise training improves the strength of contraction and increases the rates of shortening and relengthening of cardiomyocytes. Myocardial force production and power output in heart cells studied under loaded conditions is also increased. These changes are associated with faster rise and decay of the intracellular calcium transient and improved myofilament sensitivity to calcium. Translated to global cardiac function, these cellular changes explain exercise training-induced improvements in left ventricular systolic and diastolic function. In particular, exercise training is able to restore depressed contractility and calcium cycling associated with heart failure, to a value comparable to healthy individuals.
Kemi
Ole J
OJ
Institute of Biomedical and Life Sciences, University of Glasgow, Glasgow, UK. o.kemi@bio.gla.ac.uk
Ellingsen
Oyvind
O
Smith
Godfrey L
GL
Wisloff
Ulrik
U
D008841:Actin Cytoskeleton / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D015444:Exercise; D006333:Heart Failure / Q000378:metabolism / Q000473:pathology; D006352:Heart Ventricles / Q000378:metabolism*; D006801:Humans; D008954:Models, Biological; D009119:Muscle Contraction; D009206:Myocardium / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000378:metabolism*; D010805:Physical Conditioning, Animal; D051381:Rats
D002118:Calcium