Cardiovascular System Physiology | Cardiac muscle mechanics & Sarcomere length-tension relationship

Understanding sarcomere length-tension relationship and its major effect on cardiac output. The building blocks of cardiac and skeletal muscles (striated muscles) are muscle fibres. Muscle fibers are composed of myofibrils which in turn are made of sarcomeres linked in series. Each sarcomere contains many parallel, overlapping thin (actin) and thick (myosin) filaments and several other proteins including the highly elastic titin, crucial for force generation (passive tension). The muscle contracts when these filaments slide past each other, resulting in a shortening of the sarcomere and thus the muscle. This is known as the sliding filament theory or the cross-bridge cycle. In the cardiac muscle the giant protein titin plays a crucial role in force generation when preload (venous return) increase, enabling the cardiac muscle to increase contractility (and total force of contraction) thereby increasing stroke volume and cardiac output. Cardiac output increases or decreases in response to changes in heart rate or stroke volume. The intrinsic ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return is called the Frank-Starling mechanism (or Starling's Law of the heart). The Frank-Starling relationship is based on the link between the initial length of myocardial fibers and the force generated by contraction. Keywords: Musculoskeletal system, muscle mechanics, cardiovascular system physiology, cardiac output stroke volume, preload and afterload, titin elasticity, muscle contraction, actin-myosin cross-bridge cycle (sliding filament theory), passive tension, active tension, force generation in the cardiac muscle.