physiological mechanism of excitation-contraction coupling in skeletal muscle

physiological mechanism of excitation-contraction coupling in skeletal muscle

Question 1

1. a) Explain the physiological mechanism of excitation-contraction coupling in skeletal muscle.

Excitation-contraction coupling in skeletal muscle is a process that involves the production of calcium as a result of the stimulus of electrical signals in the body. When sarcoplasmic reticulum secretes calcium, the contraction of muscles occurs. In essence, this process follows a two-set sequence. Firstly, two types of potential changes occur in the cellular structures.  A potential of synapsis fuels a potential of action on the exterior part of the membrane. Consequently, a signal traverses into the crossways of tubes in the body. These processes cause sarcoplasmic reticulum to exude the calcium.

1. b) Draw links between excitation-contraction coupling, EMG, and dynamometry.

The time required to record the beginning of force produced and the start of EMG relies on the passageway of excitation-contraction processes.   These steps involve the timing of excretion of calcium,  linkage with troponin, and the time spent to form a cross- bridges.

Reference

Whiting, W. C., & Whiting, W. C. (2019). Dynamic human anatomy. Champaign, IL: Human Kinetics.

Question 2

1. a) Does sarin affect the effectors of the somatic nervous system, autonomic nervous system, neither, or both?

Sarin affects both somatic and autonomic nervous systems. These systems of the nerve are interlinked, and once one operation fails, the other is affected as well. Sarin acts as a  nerve agent that alters the functioning of neurotransmitters.  These neurotransmitters are biochemicals that transfer intervenous and intravenous signals. In this case, signal transmission occurs in both types of nervous systems. Sarin attaches itself to the junctions of neuro muscles, hence deactivating the acetylcholine, an enzyme responsible for the transfer of signals in the nervous system. These nerve agents cause excessive fluid production through diarrhea, watery eyes, sweat glands, and muscle paralysis.

1. b) Explain at least one symptom above to illustrate your point.

Sarin interferes with the nervous system and causes uncontrolled muscle stimulation. It belongs to a group of chemicals referred to as nerve agents that inhibit acetylcholinesterase. It is an enzyme that controls neurotransmission. If this enzyme stops functioning,  the muscles become overstimulated, leading to a medical condition known as muscle paralysis.

1. C) Briefly describe the mechanism of action of sarin.

Sarin is a nerve agent that alters enzymatic processes of the central nervous system. The most targeted enzyme is acetylcholinesterase. This enzyme breaks down the acetylcholine that helps neurotransmission in synaptic cleave. In biochemical terms, these processes involve chemical bonding in biological molecules in which the enzyme link with serine residues covalently, and within specific active sites.

1. d) Explain how sarin causes watery eyes

Sarin generally affects the functioning of neurotransmitters. Afferent sensory nerves in the eyes are activated to arouse both sympathetic and parasympathetic nerves, subsequently resulting in secretion of water from the eyes.

Reference

Bajgar, J. (2012). Nerve agents poisoning and its treatment in schematic figures and tables. Amsterdam: Elsevier.

Question 3

Explain how having too few plasma proteins lead to systemic edema.

Generally, edema is a condition that is caused by the movement of excess fluids from vascular systems to interstitial systems. Alternatively, it may result from the decreased withdrawal of water from interstitium through the capillaries. This mechanism,  which largely depends on the kidney’s ability to hold water,  is facilitated through decreased plasma proteins that consequently result in low oncotic pressure of plasma. Organs have to retain enough water to aid in the maintenance of plasma volume.   One major factor that can affect renal sodium retention is the depletion of intravascular content, that further results in the activation of ADH.  This increased retention is the primary cause of systemic edema.

Reference

Scallan, J., Huxley, V. H., & Korthuis, R. J. (2010). Capillary fluid exchange: regulation, functions, and pathology. San Rafael, CA: Morgan & Clypool