Passive and active tension in single cardiac myofibrils

Area of Science:

• Muscle physiology
• Biophysics

Background:

• Understanding passive and active forces in cardiac muscle is crucial for diagnosing and treating heart conditions.
• Previous studies on multicellular cardiac preparations provided insights into muscle mechanics, but the specific contribution of individual myofibrils remained unclear.

Purpose of the Study:

• To investigate the mechanical properties of single cardiac myofibrils, focusing on passive tension and active force generation.
• To determine the role of myofibrils in cardiac muscle's passive force and to characterize the mechanical properties of titin.

Main Methods:

• Isolation of single myofibrils from chemically skinned rabbit hearts.
• Measurement of passive length-tension relationships and active isometric force using a specialized apparatus.
• Calculation of myofibrillar cross-sectional area from phase-contrast and electron microscopy images.

Main Results:

• Passive tension up to sarcomere lengths of ~2.2 microns was similar to larger cardiac specimens, indicating myofibrils are the primary source of passive force at physiological lengths.
• Above 2.2 microns, passive tension increased less steeply than in multicellular preparations, suggesting other structures contribute at longer lengths.
• The elastic modulus of titin was calculated to be 3.5 x 10^6 dyn cm^-2.
• Maximum active isometric tension was 145 ± 35 mN/mm², comparable to whole cardiac muscle preparations when accounting for non-myofibrillar space.

Conclusions:

• Myofibrils are the main contributors to passive tension in cardiac muscle at physiological sarcomere lengths.
• Titin, a key sarcomeric protein, exhibits an elastic modulus similar to elastin.
• Single cardiac myofibrils generate active tension comparable to whole muscle, but lower than skeletal myofibrils.