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Muscle Contraction: Regulation

  1. John M Squire

Published Online: 18 OCT 2010

DOI: 10.1002/9780470015902.a0000674.pub2



How to Cite

Squire, J. M. 2010. Muscle Contraction: Regulation. eLS. .

Author Information

  1. University of Bristol, Bristol, UK

Publication History

  1. Published Online: 18 OCT 2010


Remarkably we can tell our arms or legs to move and they do it. We can directly control or regulate the activity of our skeletal muscles. Striated muscle movement, produced by the interaction of filaments containing the proteins myosin and actin, is regulated by the proteins tropomyosin and troponin on the actin filaments. When an electrical signal passes down the motor nerve to a muscle it triggers a depolarisation of the muscle membrane (sarcolemma). In turn this triggers the sarcoplasmic reticulum to release calcium ions into the muscle interior where they bind to troponin, thus causing tropomyosin to shift from the face of the actin filament to which myosin heads need to bind to produce contraction. During relaxation calcium is pumped back into the sarcoplasmic reticulum, troponin loses its calcium and tropomyosin reverts to its off position. This is the steric blocking mechanism of muscle regulation.

Key Concepts:

  • Striated muscles contain repeating sarcomeres of overlapping arrays of long, thin actin and thicker myosin filaments.

  • Myosin filaments carry projections, the myosin heads, which are enzymes that can bind to actin and can split and make use of the energy from ATP.

  • During muscle contraction myosin heads bind to actin, change their configuration on actin along with releasing the products of ATP hydrolysis and cause relative sliding of the actin and myosin filaments.

  • Vertebrate striated muscle contraction is controlled (regulated) by the action of the proteins troponin and tropomyosin on the actin filaments.

  • Nervous stimulation causes a depolarisation of the muscle membrane (sarcolemma) which triggers the release of calcium ions from the sarcoplasmic reticulum.

  • Calcium ions bind to troponin and thus cause or allow the tropomyosin strands on the actin filament to move so that the part of the actin surface where myosin heads need to bind is uncovered.

  • Contraction (force generation) then occurs and only stops when the sarcoplasmic reticulum pumps calcium out of the muscle interior, troponin loses its bound calcium and tropomyosin shifts back to its off position.


  • myosin;
  • actin;
  • crossbridge cycle;
  • tropomyosin;
  • troponin;
  • ryanodine receptor;
  • steric blocking model