Acute exercise modifies titin phosphorylation and increases cardiac myofilament stiffness

Area of Science:

• Muscle Physiology
• Molecular Biology
• Exercise Science

Background:

• Titin's elastic I-band regions, N2-Bus and PEVK, modulate myofilament passive stiffness through phosphorylation.
• Understanding how acute exercise affects titin phosphorylation and stiffness is crucial for muscle adaptation.

Purpose of the Study:

• To investigate the hypothesis that acute exercise modifies titin phosphorylation and myofilament stiffness.
• To examine changes in titin phosphorylation at specific sites (Ser4099, Ser4010, Ser11878, Ser12022) in response to exercise.
• To compare the effects of exercise on titin phosphorylation and stiffness in cardiac versus skeletal muscle.

Main Methods:

• Adult rats underwent a 15-minute treadmill exercise session; controls were untrained.
• Titin phosphorylation was analyzed using Western blot with phosphospecific antibodies.
• Passive tension in skinned cardiomyocytes was measured across varying sarcomere lengths.

Main Results:

• Exercise significantly increased passive tension in cardiac muscle.
• Cardiac N2-Bus phosphorylation (Ser4099) decreased, while PEVK phosphorylation (Ser11878) increased.
• Skeletal muscle showed decreased PEVK phosphorylation (Ser11878) and increased Ser12022 phosphorylation, with unchanged PKCα activity.

Conclusions:

• A single 15-minute exercise bout alters titin domain phosphorylation and myocyte stiffness.
• Exercise elicits divergent effects on titin phosphorylation and stiffness in cardiac and skeletal muscles.
• These titin modifications may play a key role in adapting muscle properties to physical activity.