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Muscle Contraction_notes

Muscle contraction involves two key variables: length and tension, with tension being produced without muscle shortening. There are three types of muscles in mammals: skeletal, cardiac, and smooth, each with distinct structures and control mechanisms. Striated muscles, including skeletal and cardiac, utilize a complex process of excitation-contraction coupling, while smooth muscles have a different mechanism for contraction involving calmodulin and myosin light chain kinase.

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Muscle Contraction_notes

Muscle contraction involves two key variables: length and tension, with tension being produced without muscle shortening. There are three types of muscles in mammals: skeletal, cardiac, and smooth, each with distinct structures and control mechanisms. Striated muscles, including skeletal and cardiac, utilize a complex process of excitation-contraction coupling, while smooth muscles have a different mechanism for contraction involving calmodulin and myosin light chain kinase.

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perfectninjagaming
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© © All Rights Reserved
Available Formats
Download as TXT, PDF, TXT or read online on Scribd
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The physiological concept of muscle contraction is based on two variables: length

and tension. In physiology, muscle shortening and muscle contraction are not
synonymous. Tension within the muscle can be produced without changes in the length
of the muscle, as when holding a dumbbell in the same position or holding a
sleeping child in your arms. Upon termination of muscle contraction, muscle
relaxation occurs, which is the return of muscle fibers to a low-tension state.

Mammals have three types of muscles: skeletal, cardiac, and smooth. Skeletal
muscles are attached to bones and give the body structure and strength. Cardiac
muscle comprises the walls of the heart, allowing blood to be pumped through the
vasculature. Smooth muscle is found throughout the blood vessels, gastrointestinal
(GI) tract, bronchioles, uterus, and bladder.[1]

Muscle contraction throughout the human body can be broken down based on muscle
subtype specialization.[2] In general, muscle fibers are classified into two large
categories: striated muscle fibers and smooth muscle fibers.

Striated muscle fibers contain actin and myosin filaments that power contraction
and are organized into repeating arrays, called sarcomeres, with a striated
microscopic appearance.[1] Cardiac muscle tissue is a striated muscle fiber under
involuntary control by the body's autonomic nervous system (ANS).[3] Skeletal
muscle tissue is a striated muscle fiber under voluntary control.

Smooth muscle fibers do not contain sarcomeres but use actin and myosin contraction
to constrict blood vessels and move the contents of hollow organs in the body.
These fibers are under involuntary control by reflexes and the body's ANS.[4]

Go to:
Cellular Level
Striated Muscle

To understand the mechanism of striated muscle contraction, it is first essential


to understand its structure. The striated muscles in our body comprise many
individual muscle fibers. Inside these muscle fibers are smaller units called
myofibrils made of parallel thin and thick filaments. These filaments are arranged
longitudinally in small units known as sarcomeres, which give the muscle a striated
appearance under microscopy.[5]

The thick filaments are made from the protein myosin, which has one pair of heavy
chains and two pairs of light chains; these heavy and light chains differ from the
thin and thick filaments of myofibrils. At the tail of the thick filament, the two
heavy chains are intertwined in a helical formation. At the other end of the thick
filament, each heavy chain is paired with two light chains, giving rise to two
heads. The myosin heads have an actin-binding site that helps them attach to the
thin filaments.[6]

The thin filaments are composed of actin, tropomyosin, and troponin. Actin is a
globular protein that combines with other actin globules to form two intertwined
strands with positive and negative ends. The double-stranded actin filaments are
covered by tropomyosin, which blocks the interaction between myosin and actin when
the muscle is inactive. The troponin group comprises troponins I, T, and C and is
located along the actin filaments next to tropomyosin.[7]

The complex process leading to muscle contraction, called excitation-contraction


coupling, begins when an action potential causes depolarization in the myocyte
membrane. The depolarization is spread via the transverse (T) tubules,
invaginations of the muscle cell membrane, that help spread depolarization signals
to the entire muscle fiber. Depolarization of the T tubules causes a conformational
change in the dihydropyridine receptors, which causes the opening of nearby
ryanodine receptors on the sarcoplasmic reticulum (SR), the storage site for
calcium within muscle cells. When calcium is released from the SR, it binds to
troponin C. This causes a conformation change, which shifts tropomyosin, allowing
the myosin heads to attach to the actin filaments, creating what is known as a
cross-bridge.

Cross-bridge cycling begins when ATP binds to an ATP-binding domain on the myosin
head. Myosin dissociates from the actin, breaking the cross-bridge. ATP is then
hydrolyzed into ADP and P, which causes the myosin heads to change conformation and
move toward the positive end of the actin, cocking the myosin head. The phosphate
is released, and the ADP-bound myosin binds to a new location on the actin
filament. ADP is then released, which causes the myosin to return to its original
position, pulling on the actin filament and causing the sarcomere (and, therefore,
the muscle fiber) to contract. These cycles continue until calcium levels in the
myocyte fall, causing tropomyosin to cover the actin filaments' myosin-binding
sites.[8]

Smooth Muscle

The same thin and thick filaments discussed in striated muscles are present in
smooth muscles. However, in smooth muscle tissue, these filaments are not organized
into sarcomeres. As a result, smooth muscle does not contain the troponin complex
required for skeletal muscle contraction and, thus, has a different mechanism for
controlling contraction. This difference is characterized by how calcium (Ca)
enters the cell, with three mechanisms increasing intracellular concentration:

Voltage-gated Ca channels are activated by membrane depolarization, allowing Ca to


enter the cell.
Hormones or neurotransmitters can open ligand-gated channels on the cell membrane.
Hormones and neurotransmitters such as norepinephrine and angiotensin II can, via
the phospholipase-C (PLC) pathway, cause an increase in intracellular inositol
triphosphate (IP3).
IP3 can bind to receptors on the SR and cause Ca to be released. Once Ca is
released, it binds to a calmodulin protein instead of troponin C, as it does in
striated muscle. Calmodulin then activates myosin light chain kinase (MLCK), which,
as the name suggests, phosphorylates the myosin light chain. The phosphorylated
myosin light chain has ATPase activity, which hydrolyzes ATP, increasing its
affinity to actin. The myosin can then readily bind to actin. From this point,
cross-bridge cycling is the same as in striated muscle. The smooth muscle will
remain contracted as long as Ca is bound to calmodulin and the MLCK is
phosphorylated. This allows for prolonged periods of vasoconstriction in blood
vessels.[4]

A step-by-step outline of each type of muscle contraction is discussed in a later


section.

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