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Muscle Contraction – Powerstroke mechanism

All muscle contraction occurs by the binding and allosteric properties of the proteins Actin and Myosin. In skeletal and cardiac muscles, the starting and stopping of muscular contraction is dependent upon the proteins Troponin and Tropomyosin.

Myosin is a protein shaped as a 2 headed golf club. The elongated tail (shaft) binds specifically to other Myosin tails forming the thick filaments. The Myosin heads have the ability to bind to Actin and to ATP molecules. The Actin binds to itself to form the thin filaments.

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Partial Hydrolysis of the ATP connected to the Myosin head will produce ADP and Inorganic Phosphate. This will increase the affinity between the Myosin head and the Actin filament which now connect to each other. The following total Hydrolysis promote and allosteric change in the Myosin which causes the head to move and move the thin filament of Actin with it. When a new ATP molecule binds again to the Myosin head, it reshapes the molecular structure of Myosin which makes it lose its affinity for the Actin. The process then repeats itself for each muscle contracture.

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The Actomyosin system (Sliding Filament Theory) is under control by electrical stimulation from nerves and other electrically active cells. This mechanism is known as the Excitation Contraction Coupling and it is dependent on the intracellular concentration of Calcium ions (Ca2+).

Troponin and Tropomyosin react to the change in Ca2+ concentration which basically determines whether or not the Myosin heads will have access to the Actin filaments. Tropomyosin is a thin protein that binds in the groove of the Actin filaments in such a way that it can be located high or deep in the groove depending whether or not the Actin filaments need to be exposed.

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When the concentration of Ca2+ increases, allosteric changes in Troponin are also transmitted to Tropomyosin which in turn will move deeper in the groove to reveal the Actin filaments for the cross-bridging with the Myosin. Once Ca2+ concentration returns to normal, Troponin turns to its normal shape which will then move Tropomyosin back to its higher position in the groove covering the Actin heads and prohibiting cross-bridging.