University Anatomy Assignment: Muscle Contraction Mechanism

This assignment delves into the intricate process of muscle contraction, beginning with the role of motor neurons in initiating the process. The assignment explains how the nerve impulse leads to the release of acetylcholine at the neuromuscular junction, which triggers a cascade of events. It describes the influx of calcium ions and the subsequent binding to troponin, which allows myosin heads to bind to actin filaments. The assignment outlines the process of cross-bridge formation, power stroke, and the release of ADP, leading to the shortening of the sarcomere and ultimately, muscle contraction. References to relevant research articles are provided to support the explanation of the mechanism.

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.