(1) To evaluate the nervous response needed to cause calcium to be released for muscle to contract.
(2) To discuss the role of calcium in turning muscle “on.”
(3) To show the steps necessary for muscle to relax.
Reading material: Principles of Meat Science (5th Edition), chapter 3, pages 61 to 74.
Below are two different but similar descriptions of muscle contraction that explain the processes involved in notification, contraction, and relaxation.
The following steps are involved in muscle contraction:
(1) The sequence of events leading to contraction is initiated somewhere in the central nervous system, either as voluntary activity from the brain or as reflex activity from the spinal cord.
(2) A motor neuron in the ventral horn of the spinal cord is activated, and an action potential passes outward in a ventral root of the spinal cord.
(3) The axon branches to supply a number of muscle fibers called a motor unit, and the action potential is conveyed to a motor end plate on each muscle fiber.
(4) At the motor end plate, the action potential causes the release of packets or quanta of acetylcholine into the synaptic clefts on the surface of the muscle fiber.
(5) Acetylcholine causes the electrical resting potential under the motor end plate to change, and this then initiates an action potential which passes in both directions along the surface of the muscle fiber.
(6) At the opening of each transverse tubule onto the muscle fiber surface, the action potential spreads inside the muscle fiber.
(7) At each point where a transverse tubule touches part of the sarcoplasmic reticulum, it causes the sarcoplasmic reticulum to release Ca++ ions.
(8) The calcium ions result in movement of troponin and tropomyosin on their thin filaments, and this enables the myosin molecule heads to “grab and swivel” their way along the thin filament. This is the driving force of muscle contraction.
Contraction is turned off by the following sequence of events:
(9) Acetylcholine at the neuromuscular junction is broken down by acetylcholinesterase, and this terminates the stream of action potentials along the muscle fiber surface.
(10) The sarcoplasmic reticulum ceases to release calcium ions, and immediately starts to resequester all the calcium ions that have been released.
(11) In the absence of calcium ions, a change in the configuration of troponin and tropomyosin then blocks the action of the myosin molecule heads, and contraction ceases.
(12) In the living animal, an external stretching force, such as gravity or an antagonistic muscle, pulls the muscle back to its original length.
Muscle contraction flow chart (figure 3.8)
Motor nerve action potential arrives at motor end plate
Acetylcholine released, sarcolemma and membranes depolarized (Na+ flux into fiber)
Action potential transmitted via T-tubules to SR
Ca++ released from SR terminal cisternae into sarcoplasm
Ca++ bound by troponin
Myosin ATPase activated and ATP hydrolyzed
Tropomyosin shift from actin binding site
Actin-myosin crossbridge formation
Repeated formation & breaking of crossbridges resulting in sliding of filaments and sarcomere shortening
Sarcolemma & T-tubules repolarized
SR Ca++ pump activated & Ca++ returned to SR terminal cisternae
Actin-myosin crossbridge formation terminated
Return of tropomyosin to actin binding site
Mg++ complex formed with ATP
Passive sliding of filaments
Sarcomeres return to resting state
Review of Material — What the student should know:
(1) The nervous events that take place in contraction.
(2) The role of calcium in turning the muscle “on.”
(3) The factors related to the actual contraction process.
(4) The events that take place to cause relaxation to occur.
Links to related sites
Beef muscle contraction and relaxation. Beef Quality Research on behalf of The Beef Checkoff, National Cattlemen’s Beef Association. Prepared by Center for Meat Safety and Quality, Department of Animal Sciences, Colorado State University.
Rigor mortis. Beef Quality Research on behalf of The Beef Checkoff, National Cattlemen’s Beef Association. Prepared by Center for Meat Safety and Quality, Department of Animal Sciences, Colorado State University.