The Muscular System
actin and myosin protein filaments from interact-ing.
However, when calcium ions are released by the
sarcoplasmic reticulum, the action of these inhibitor
substances is negated. It is the release of the calcium ions
that brings about the contractile process at the molecular
level in the myofilaments. When the action potential ceases
to stimulate the release of the calcium ions from the
reticulum, these ions begin to return and recombine with
the sarcoplasmic reticulum. What causes this to happen is
the sodium-potassium pump of the muscle cell membrane.
As the sodium ions rushed into the cell and potassium
rushed out to try to restore the original resting potential but
could not do so, the sodium-potassium pump began
operating to restore the ionic distribution to its normal
resting potential. Contraction occurs in a few thousandths
of a second and once the sodium-potassium pump re-stores
ionic distribution, contraction ceases because the action
potential is now stopped and all the calcium ions are once
again bound to the reticulum. A contin-ued series of action
potentials is necessary to provide enough calcium ions to
maintain a continued contrac-tion. Now let’s discuss the
chemical interactions and those calcium ions.
Chemical Interactions
In 1868, a German scientist named Kuhne extracted a
protein, which he called myosin, from muscle using a
strong salt solution. In 1934, myosin was shown to gel in
the form of threads. Shortly thereafter, it was dis-covered
that the threads of myosin became extensible when placed
near adenosine triphosphate (ATP). It was not until 1942
that scientists discovered that this myo-sin was not
homogeneous, and that in fact there was another protein in
the muscle distinct from myosin and it was called actin. In
actuality, the actin unites with the myosin to form
actomyosin during the contraction process.
The release of the calcium ions from the sarcoplas-mic
reticulum inhibits the activity of the troponin and the
tropomyosin, which have kept the actin and myosin
myofilaments apart. The calcium ions attach to the tro-
ponin and now cause the myosin to become activated
myosin. The myosin filaments have large heads that
contain ATP molecules. The activated myosin releases the
energy from the ATP at the actin active site when the
myosin links up and forms actomyosin. The head link-age
makes a cross-bridge that pulls the actin filaments inward
among the myosin filaments and breaks down
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the ATP into adenosine diphosphate (ADP) and PO 4 and
the release of energy, which causes contraction. Refer to
Figure 9-4. The shortening of the contractile elements in
the muscle is brought about by the pulling of the actin
filaments over the myosin filaments. The width of the A
bands remains constant while the Z lines move closer
together during contraction (see Figure 9-1). When the
sodium-potassium pump (Figure 9-5) has restored the
resting potential of the cell and sodium ions are back
outside and potassium ions are back inside the cell, the
action potential ceases and calcium ions get reabsorbed by
the sarcoplasmic reticulum. Now contraction ceases and the
actin filaments get released from the myosin and the Z lines
move further apart. This whole complex process occurs in
1/40 of a second. Keep in mind that we discussed only one
small part of a muscle cell’s fila-ments. There are
thousands of myofilaments in a single muscle cell, and a
muscle like your biceps contains hun-dreds of thousands of
muscle cells, all interacting and coordinating together at the
molecular level to bring about contraction.Energy Sources
Muscle cells convert chemical energy (ATP) into me-
chanical energy (contraction). This source of energy is ATP
molecules (review Chapter 4). Actin 1 myosin 1 ATP →
actomyosin 1 ADP 1 PO 4 1 energy (causing contraction).
The energy given off by the breakdown of ATP is used
when the actin and myosin filaments inter-mesh. ATP is
synthesized by glycolysis, the Krebs citric acid cycle,
electron transport, and in muscle cells, by the breakdown of
phosphocreatine.
In glycolysis, you will recall from Chapter 4, glucose
present in the blood enters cells where it is broken down
through a series of chemical reactions to pyruvic acid. A
small amount of energy is released from the glucose
molecule with a net gain of two molecules of ATP.
In the Krebs citric acid cycle and electron transport, if
oxygen is present, the pyruvic acid is further broken down
into CO 2 and H 2 O and 36 more ATP molecules. If oxygen
is not available to the muscle cell, the pyruvic acid changes
to lactic acid and builds up in the muscle cell with only two
ATP produced until oxygen again be-comes available.Muscle cells have two additional sources of ATP.
Phosphocreatine (fos-foh-KREE-ah-tin) is found only
in muscle tissue and provides a rapid source of high-energy
ATP for muscle contraction. When muscles are at rest,
excess ATP is not needed for contraction, so phosphate