Frank-Starling Law: Skeletal Muscle Application?

The Frank-Starling law describes the relationship between the force of contraction and the initial length of muscle cells. The law states that the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction (the end diastolic volume), when all other factors remain constant. This law applies to striated muscle, including skeletal muscles, arthropod muscle, and cardiac muscle.

The Frank-Starling law is based on the relationship between the initial length of myocardial fibres and the force generated by contraction

The Frank-Starling law is based on the observation that the energy of a contracting muscle is a function of its length and that muscle shortening depends on its load. The law dictates that an increase in fibre length enhances the maximal force-generating capacity and calcium sensitivity of myofibrils, leading to increased force development. The Frank-Starling relationship thus allows the heart to work on a beat-to-beat basis, capable of adjusting the output of both its sides to any alteration affecting venous return, or preload.

The Frank-Starling relationship is the observation that ventricular output increases as preload (end-diastolic pressure) increases. The left ventricular performance (Frank-Starling) curves relate preload, measured as left ventricular end-diastolic volume (EDV) or pressure, to cardiac performance, measured as ventricular stroke volume or cardiac output. On the curve of a normally functioning heart, cardiac performance increases continuously as preload increases.

The Frank-Starling mechanism is an intrinsic cardiac autoregulatory mechanism. It is a fundamental and ancient property of the myocardium; all vertebrate hearts and probably also insect hearts possess this ability. The main underlying mechanism is that with increasing sarcomere length, the sarcomeres become more sensitive to calcium somehow, and the force of their contraction increases as a result.

The Frank-Starling law is also known as the Frank-Starling mechanism or Starling's law

The Frank-Starling law, also known as the Frank-Starling mechanism or Starling's law, describes the relationship between the force of contraction and the initial length of muscle cells. In 1895, German physiologist Otto Frank studied the impact of stretching on the pressure generated by a frog heart. He found that the isovolumetric pressure increased as the heart was stretched by increasing the diastolic volume.

English physiologist Ernest Starling built on Frank's work, using a more physiological preparation of the isolated heart and lung of a dog. Starling's experiments confirmed the relationship between the degree of ventricular distension and the force of contraction, now known as the Frank-Starling law.

The Frank-Starling law specifically states that the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles before contraction. This increase in blood volume stretches the cardiac muscle, resulting in a more forceful contraction. The law is based on the link between the initial length of myocardial fibres and the force generated by contraction.

The Frank-Starling mechanism has important physiological implications, particularly in maintaining ventricular output equality. It allows the cardiac output to be synchronised with venous return, arterial blood supply, and humoral length, without the need for external regulation. Additionally, it helps adapt left ventricular output to right ventricular output, preventing blood accumulation in the pulmonary or systemic circulation.

The Frank-Starling law is not limited to the heart muscle but also applies to skeletal and arthropod muscles. It occurs due to the length-tension relationship observed in striated muscles. As the muscle is stretched, active tension is created by altering the overlap of thick and thin filaments. This results in the greatest isometric active tension when the muscle is at its optimal length.

The law states that the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles

The Frank-Starling law of the heart (also known as Starling's law and the Frank-Starling mechanism) represents the relationship between stroke volume and end-diastolic volume. The law states that the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction (the end diastolic volume), when all other factors remain constant.

The Frank-Starling mechanism allows the cardiac output to be synchronised with the venous return, arterial blood supply and humoral length, without depending upon external regulation to make alterations. The Frank-Starling mechanism occurs as the result of the length-tension relationship observed in striated muscle, including skeletal muscles, arthropod muscle and cardiac (heart) muscle.

The Frank-Starling law dictates that an increase in fibre length enhances the maximal force-generating capacity and calcium sensitivity of myofilaments, leading to increased force development. Although a unifying concept that explains how myofilaments "sense" length alterations is still to be proven, stretch-induced effects rather than changes in filament spacing dominate the literature. Also, changes in calcium activation upon muscle lengthening have to be considered.

Overall, myofilament length-dependent activation is the composite of several synergistically mechanokinetic processes. Length-dependent activation is associated with:

• Increased calcium affinity of cardiac troponin C
• Alterations in interfilament lattice spacing
• Titin-induced stretch and formation of strong-binding cross-bridges
• Cardiac troponin complex changes
• Cooperative mechanisms

The Frank-Starling law applies to striated muscle, including skeletal muscles, arthropod muscle and cardiac muscle

The Frank-Starling law is a result of the length-tension relationship observed in striated muscle. As striated muscle is stretched, active tension is created by altering the overlap of thick and thin filaments. The greatest isometric active tension is developed when a muscle is at its optimal length. In most relaxed skeletal muscle fibres, passive elastic properties maintain the muscle fibres' length near optimal, as determined by the fixed distance between the attachment points of tendons to the bones (or the exoskeleton of arthropods) at either end of the muscle.

In the human heart, maximal force is generated with an initial sarcomere length of 2.2 micrometres, a length which is rarely exceeded in a normal heart. The Frank-Starling mechanism allows the cardiac output to be synchronised with the venous return, arterial blood supply and humoral length, without depending on external regulation to make alterations.

The Frank-Starling law is named after the two physiologists, Otto Frank and Ernest Henry Starling. However, neither Frank nor Starling was the first to describe the relationship between the end-diastolic volume and the regulation of cardiac output. The first formulation of the law was theorised by the Italian physiologist Dario Maestrini, who on 13 December 1914, started the first of 19 experiments that led him to formulate the "legge del cuore".

The Frank-Starling law is named after Otto Frank and Ernest Henry Starling

The Frank-Starling law is named after two physiologists, Otto Frank and Ernest Henry Starling. However, neither Frank nor Starling was the first to describe the relationship between the end-diastolic volume and the regulation of cardiac output. The first formulation of the law was theorised by Italian physiologist Dario Maestrini, who, on December 13, 1914, started the first of 19 experiments that led him to formulate the "legge del cuore".

Otto Frank's contributions are derived from his 1895 experiments on frog hearts. Frank observed changes in diastolic pressure with varying volumes of the frog ventricle to relate the work of the heart to skeletal muscle mechanics. His data was analysed on a pressure-volume diagram, which resulted in his description of peak isovolumic pressure and its effects on ventricular volume.

Ernest Starling experimented on intact mammalian hearts, such as from dogs, to understand why variations in arterial pressure, heart rate, and temperature do not affect the relatively constant cardiac output. More than 30 years before the development of the sliding filament model of muscle contraction and the understanding of the relationship between active tension and sarcomere length, Starling hypothesised in 1914 that "the mechanical energy set free in the passage from the resting to the active state is a function of the length of the fibre". Starling's data and diagrams provided evidence that the length of the muscle fibres, and resulting tension, altered the systolic pressure.

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