Muscle Contraction Explained

This assignment delves into the intricate mechanism of muscle contraction. It begins by outlining the role of motor neurons in transmitting signals to muscle fibers, leading to depolarization and sodium influx. The subsequent release of acetylcholine and calcium ions triggers a cascade of events involving actin and myosin filaments. The interaction between these proteins, fueled by ATP hydrolysis, results in the power stroke and shortening of sarcomeres, ultimately causing muscle contraction.

Running head: ANATOMY
Muscle contraction
Name of the Student
Name of the University
Author Note

1ANATOMY
Muscles are composed of a number of muscle fibers that are under the control of motor
neurons. The transmission of a nerve impulse down the motor neuron leads to contraction of the
muscle fibers. The somatic motor neuron transmits a signal to the muscle fiber that initiates a
sequence of events, which lead to muscle contraction.
These signals lead to depolarization of the sarcolemma that opens the voltage-gated
sodium channels and sodium influx occurs. The inactivation of these channels lead to
repolarisation. The action potential reaches the neuromuscular junction by salutatory conduction
along the axon and causes an influx of Ca2+ by opening the voltage-gated calcium channels
(Beckendorf). This influx leads to release of acetylcholine from the synaptic vesicles into the
synaptic cleft between the neuromuscular junction and the motor end plate. It binds to and
activates the nicotinic acetylcholine receptors present on the junction which leads to reversal of
polarity due to opening of the sodium/potassium channels (Eto, Masumi and Kitazawa). The
calcium released from the sarcoplasmic reticulum binds to troponin, which shift tropomyosin
that blocked an active site on actin. Myosin heads attach to actin by breaking ATP to ADP and
phosphate through Myosin-ATPase (Katz).
Cross-bridges are formed on the active sites of actin filament that slides over myosin
(power stroke). ADP release completes the cross-bridge and ATP gets attached to myosin,
thereby breaking the cross-bridge. This leads to shortening of sarcomere and the rigor state
continues until myosin binds to another ATP. This brings about muscle contraction and the
person pulls up the leg from the track.

2ANATOMY
References
Beckendorf, Lisa, Wolfgang A. Linke, and G. J. M. Stienen. "When skeletal muscles are
stretched during activation in the absence of myosin-actin interactions, the force increases
significantly. The force remains elevated throughout the activation period. The mechanism
behind this non-crossbridge force, referred to as static tension, is unknown and generates debate
in the literature. It has been suggested that the static tension is caused..." Journal of Muscle
Research and Cell Motility 36.1 (2015): 71-143.
Eto, Masumi, and Toshio Kitazawa. "Diversity and plasticity in signaling pathways that regulate
smooth muscle responsiveness: Paradigms and paradoxes for the myosin phosphatase, the master
regulator of smooth muscle contraction." Journal of Smooth Muscle Research 53 (2017): 1-19.
Katz, ARNOLD M. "Contractile proteins of the heart." Physiological Reviews 50.1 (2017): 63-
158.