Key result
Swim training reduces cardiac passive stiffness in rats by increasing the N2BA/N2B titin ratio.
Why the study?
There was very limited knowledge about titin's role in cardiac adaptation and passive stiffness during long-term exercise.
Does 12-week-long swim-based training alter the N2BA/N2B ratio and titin phosphorylation in a rat model of athlete's heart?
Does 12-week-long swim-based training alter the N2BA/N2B ratio and titin phosphorylation in a rat model of athlete's heart?
Long-term exercise in a rat model induces a shift towards the more compliant N2BA titin isoform and hypophosphorylation of the PEVK domain, reducing passive cardiac stiffness.
Hypothesis-generating for titin-mediated stiffness reduction with exercise; leaves open human translation and requires prospective validation.
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.
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Kellermayer et al. (2021) studied Athlete's heart. 12-week-long swim-based training was evaluated on N2BA/N2B ratio, post-translational phosphorylation of titin, and sarcomeric transverse elastic modulus. A 12-week swim-based training in a rat model significantly increased the N2BA/N2B titin ratio and reduced the sarcomeric transverse elastic modulus, leading to reduced cardiac passive stiffness.
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