Muscle Contraction

Contraction of skeletal muscle tissue occurs due to the sliding of actin and myosin
myofilaments past one another, causing the sarcomeres to shorten. The sarcomeres are
joined to each other to form myofibrils. As the sarcomeres shorten, this causes the
myofibrils to shorten as well, and this makes the whole muscle shorten.

When actin myofilaments and myosin myofilaments slide past one another during
contraction, it is called the sliding filament model of muscle contraction. During
contraction, neither the actin nor the myosin fibers shorten. It is actually the H zones
and I bands that shorten during contraction, but the A bands do not change in length
(figure 7.7).

On the other hand, during muscle relaxation, the sarcomeres lengthen. This lengthening
requires another force, such as that the contraction of other muscles or gravity.

When a stimulus causes a skeletal muscle to contract, action potentials produced in

skeletal muscle fibers at the neuromuscular junction pass through the sarcolemma and
then the T tubule membranes (see figure 7.6). After the T tubule membranes, these
action potentials cause the sarcoplasmic reticulum to accept Ca2+. The Ca2+ binds to
troponin molecules attached to the actin myofilaments. This binding causes
tropomyosin molecules to move along the actin molecule and expose the myosin
attachment sites on the actin myofilament. The exposed attachment sites on the actin
myofilament bind with the myosin myofilaments and they both form cross-bridges.

The energy used for muscle contraction is in the form of adenosine triphosphate or ATP,
which comes from the energy released during the metabolism of food. The energy is
released as ATP is broken down to adenosine diphosphate (ADP) and phosphate (P).
During muscle contraction, the energy released from ATP is temporarily stored in the
myosin head. This energy is used to move the heads of the myosin myofilaments toward
the center of the sarcomere, which makes the actin myofilaments slide past the myosin
myofilaments. As they slide against one another, ADP and P are released from the
myosin heads.

When a new ATP molecule attaches to the head of the myosin molecule, the cross-
bridge is released and the ATP breaks down to ADP and P, with both molecules still
bound to the myosin head), and then the myosin head returns to its original position, so
it can attach to the next site. As long as there are Ca2+ attaching to troponin there is
ATP available, the cycle repeats.

Muscle relaxation occurs as Ca2+ travels back into the sarcoplasmic reticulum and this
process requires ATP. As this happens, the attachment sites on the actin molecules are
covered again by tropomyosin so that cross-bridges cannot reform.

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A new ATP must bind to myosin before the cross-bridge can be released. After a person
dies, ATP is not available, and the cross- bridges that have formed are not released,
causing the muscles to become rigid. This condition is called rigor mortis (riger m rtis;
stiffness + death).

Part of the energy from ATP involved in muscle contraction is required for the formation
and movement of the cross-bridges, and part is released as heat. The heat released
during muscle contraction increases body temperature, which explains why a person
becomes warmer during exercise. Shivering, a type of generalized muscle contraction, is
one of the bodys mechanisms for dealing with cold. The muscle movement involved in
shivering produces heat, which raises the body temperature.

In summary, the cycle of muscular contraction happens in 4 steps:

1. the breaking down of ATP into ADP and P to reorient the myosin head
2. the attachment of myosin to actin to form cross-bridges
3. the sliding of the thin filament past the thick filament toward the M line
4. the detachment of myosin from actin