Muscle contraction is
initiated by nerve impulse arriving at the neuromuscular junction. All the
fibers innervated by a single motor neuron are a motor unit, and contract
simultaneously in response to the action potential fired by the motor neurons.
The sarcolemma of muscle fiber cell penetrates deep into the cell to form a
hollow elongated tube the transverse tubule (T. tubule). Its lumen is
continuous with the extra-cellular fluid. Thousands of T. tubule of each muscle
cells are collectively called T-system.
It extends and
encircles the myofibril at the level of Z line or A and I junction. The
nerve impulse is carried through the T-tubule to the adjacent sarcoplasmic
reticulum (SR). The calcium gates of the SR open releasing calcium into
cytosol, binding of calcium ion to troponin molecules of the filament. The
binding sites are exposed and cross bridges with myosin can form and
contraction occurs.
The actin-myosin
interaction is regulated by Ca++ ions in a process known as
calcium-dependent regulation. In skeletal and cardiac muscle cells, Ca++ ions
are released from the sarcoplasmic reticulum in response to an action
potential. The rise in intracellular Ca++ levels then activates the
interaction between actin and myosin, leading to muscle contraction.
In the absence of Ca++,
the interaction between actin and myosin is weak and the muscle remains
relaxed. When Ca++ ions bind to the regulatory protein troponin,
which is located on the thin filaments of the sarcomere, it causes a
conformational change in the troponin-tropomyosin complex, allowing the myosin
heads to bind to actin.
Once the myosin heads
are bound to actin, ATP hydrolysis occurs, leading to a conformational change
in the myosin heads and a sliding of the thin filaments past the thick
filaments. The amount of Ca++ present in the cytosol determines the
strength of the actin-myosin interaction and the force generated by muscle
contraction.
The importance of Ca++
ions in regulating the actin-myosin interaction can be seen in diseases such as
malignant hyperthermia, in which excessive Ca++ release from the
sarcoplasmic reticulum leads to uncontrolled muscle contractions and dangerous
increases in body temperature. Additionally, drugs such as calcium channel
blockers can be used to regulate the interaction between actin and myosin and
reduce muscle contractility.
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