Abstract
Long-term exercise induces physiological cardiac adaptation, a condition referred to as athlete’s heart. Exercise tolerance is known to be associated with decreased cardiac passive stiffness. Passive stiffness of the heart muscle is determined by the giant elastic protein titin. The adult cardiac muscle contains two titin isoforms: the more compliant N2BA and the stiffer N2B. Titin-based passive stiffness may be controlled by altering the expression of the different isoforms or via post-translational modifications such as phosphorylation. Currently, there is very limited knowledge about titin’s role in cardiac adaptation during long-term exercise. Our aim was to determine the N2BA/N2B ratio and post-translational phosphorylation of titin in the left ventricle and to correlate the changes with the structure and transverse stiffness of cardiac sarcomeres in a rat model of an athlete’s heart. The athlete’s heart was induced by a 12-week-long swim-based training. In the exercised myocardium the N2BA/N2B ratio was significantly increased, Ser11878 of the PEVK domain was hypophosphorlyated, and the sarcomeric transverse elastic modulus was reduced. Thus, the reduced passive stiffness in the athlete’s heart is likely caused by a shift towards the expression of the longer cardiac titin isoform and a phosphorylation-induced softening of the PEVK domain which is manifested in a mechanical rearrangement locally, within the cardiac sarcomere.
Highlights
It is widely accepted that regular exercise has a beneficial role in cardiovascular health [1,2]
We explore the titin-based molecular and sub-cellular mechanisms of stiffness changes associated with long-term physical exercise in a rat experimental model
We investigated titin alterations under physiological conditions that mimic the circumstances of highly trained professional athletes
Summary
It is widely accepted that regular exercise has a beneficial role in cardiovascular health [1,2]. The consequential cardiac remodeling is an important adaptation to exercise, which includes biventricular myocardial hypertrophy and an improved functional and mechanoenergetic status. Previous studies have focused on the cellular mechanisms of the enhanced myocardial function triggered by exercise [5,6,7]. Athlete’s heart was shown to be associated with enhanced left ventricular (LV) diastolic function and cardiac compliance [1,8,9]. These favorable adaptive features contribute to high cardiac output during endurance training and may prevent age-related adverse cardiac deconditioning [10]
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