ELM 17 Muscles 2

Question 1

Question: What is the difference between a contraction action potential (AP) and a normal AP in skeletal muscle?

Answer 1

Answer: A contraction AP is similar to a normal AP but results in a muscle twitch, which is delayed longer than a normal AP and lasts 20-100 milliseconds due to dependence on calcium concentration.

Question 2

Question: How does increased stimulation frequency affect muscle contraction?

Answer 2

Answer: Increased stimulation frequency leads to summation and unfused tetanus, resulting in a bigger force of contraction. Further increase in stimulation frequency leads to fused tetanus, where the muscle is maximally stimulated.

Question 3

Question: What is Henneman’s Size Principle?

Answer 3

Answer: Henneman’s Size Principle states that the bigger the axon of a neuron, the more muscle fibers it innervates. Motor units are recruited in order of size, with smaller motor units being stimulated first.

Question 4

vQuestion: What are the characteristics of slow-twitch oxidative muscle fibers?

Answer 4

Answer: Slow-twitch oxidative fibers, also known as Type I fibers, have myoglobin as an oxygen store, many mitochondria, and are used for sustained contractions with resistance to fatigue.

Question 5

Question: What are the characteristics of fast-twitch glycolytic muscle fibers?

Answer 5

Answer: Fast-twitch glycolytic fibers, also known as Type IIB fibers, have a fast myosin isoform and fast calcium transient. They allow rapid shortening but have a high energy cost due to quick ATP hydrolysis.

Question 6

Question: What can limit contraction in fast-twitch glycolytic muscle fibers?

Answer 6

Answer: Lactate accumulation and acidosis can limit contraction in fast-twitch glycolytic muscle fibers.

Question 7

Question: What are the characteristics of fast-twitch oxidative muscle fibers?

Answer 7

Answer: Fast-twitch oxidative fibers, also known as Type IIA fibers, have lots of mitochondria, good blood supply, and good glycogen stores. They resist fatigue but have high energy demands.

Question 8

Question: What is Duchenne muscular dystrophy (DMD)?

Answer 8

Answer: DMD is an X-linked disorder caused by a mutation in the dystrophin gene, affecting approximately 1 in 3500 male births.

Question 9

Question: What is the underlying cause of Duchenne muscular dystrophy?

Answer 9

Answer: DMD causes skeletal muscle fibers to not be properly linked to the extracellular matrix, leading to excess calcium entering cells, muscle fiber death, and replacement by fat and connective tissue.

Question 10

Question: What are the symptoms of Duchenne muscular dystrophy?

Answer 10

Answer: DMD results in progressive muscle weakness, and the average life expectancy is 25-30 years.

Question 11

Question: Is there a treatment for Duchenne muscular dystrophy?

Answer 11

Answer: Currently, there is no treatment for DMD, but gene therapy is being explored as a potential candidate for treatment.

Question 12

Question: What is myostatin, and what does it regulate?

Answer 12

Answer: Myostatin regulates muscle growth in the body.

Question 13

Question: Can you provide examples of animals with myostatin deficiencies?

Answer 13

Answer: Animals with mutations in the myostatin gene, such as the Belgium blue cow and the “bully” whippet, often exhibit extra muscle mass and little body fat.

Question 14

Question: Has myostatin deficiency been observed in humans?

Answer 14

Answer: Yes, myostatin deficiencies have been found in humans, such as “super toddler” Liam Hoekstra, who displayed exceptional strength at a young age compared to typical children.

Question 15

Question: How does cardiac muscle differ from skeletal muscle?

Answer 15

Answer: Cardiac muscle forms a branched syncytium, with cells incompletely fused and joined by intercalated discs. Its control mechanisms, action potentials (APs), and excitation-contraction coupling are different from skeletal muscle, and it is found exclusively in the heart.

Question 16

Question: Describe the action potentials in cardiac muscle.

Answer 16

Answer: Cardiac muscle action potentials have an initial rise due to the opening of sodium channels and a broad plateau caused by the opening of calcium channels. These action potentials last around 200 milliseconds.

Question 17

Question: How is excitation-contraction coupling achieved in cardiac muscle?

Answer 17

Answer: In cardiac muscle, excitation-contraction coupling is primarily mediated by calcium, mostly from the sarcoplasmic reticulum (SR). L-type calcium channels trigger the release of calcium from the SR via calcium-induced calcium release (CICR).

Question 18

Question: What initiates contraction in the heart?

Answer 18

Answer: Contraction is initiated by the sinoatrial node (SAN), which generates a pacemaker potential—a slow depolarization of the membrane. When the threshold is reached, the SAN fires an action potential, spreading it through the atria and then to the atrioventricular node (AVN) and ventricles.

Question 19

Question: How is the force of contraction in cardiac muscle regulated?

Answer 19

Answer: The force of contraction is regulated by the degree of stretch of cardiac muscle (Frank-Starling law of the heart) and the concentration of cytoplasmic calcium, which is modulated by the autonomic nervous system (ANS).

Question 20

Question: How is the pacemaker potential regulated by the autonomic nervous system?

Answer 20

Answer: The steeper the pacemaker potential, the quicker it reaches threshold, leading to sympathetic stimulation. Conversely, a slower threshold is associated with parasympathetic division activation.

Question 21

Question: How does cardiac muscle generate energy for continuous beating?

Answer 21

Answer: Cardiac muscle relies on oxidative metabolism due to its continuous beating. It requires a good blood supply, and deprivation of blood supply can lead to conditions such as angina and heart attacks.

Question 22

Question: How does smooth muscle histologically differ from skeletal muscle?

Answer 22

Answer: Smooth muscle lacks striations and t-tubules and consists of small, spindle-shaped cells. It can be electrically coupled by gap junctions, forming a syncytium.

Question 23

Question: Where is smooth muscle found, and what is its function?

Answer 23

Answer: Smooth muscle is found around hollow organs such as blood vessels, the gut, bladder, uterus, and bronchi. Its function is to propel contents and regulate flow within these organs.

Question 24

Question: How does smooth muscle contraction differ from skeletal muscle contraction?

Answer 24

Answer: Smooth muscle contracts slowly, remains contracted for longer periods, and is more energy-efficient than skeletal muscle. It utilizes actin-myosin cross-bridges for contraction.

Question 25

Question: Describe the excitation-contraction coupling mechanism in smooth muscle.

Answer 25

Answer: Excitation-contraction coupling in smooth muscle involves the entry of calcium through L-type calcium channels in the membrane, calcium-induced calcium release (CICR) via ryanodine receptors on the sarcoplasmic reticulum (SR), and release of calcium through IP3 receptors on the SR.

Question 26

Question: What is the role of calcium in smooth muscle contraction?

Answer 26

Answer: Calcium binds to calmodulin, activating myosin light-chain kinase (MLCK), which phosphorylates regulatory light chains on myosin, leading to increased ATPase activity and muscle contraction.

Question 27

Question: How is smooth muscle excitation initiated?

Answer 27

Answer: Smooth muscle excitation can be myogenic, initiated by action potentials triggered by neuron stimulation, or graded responses to depolarization. It can also be modulated by neurotransmitters and hormones.

Question 28

Question: What is a key difference between smooth muscle and cardiac muscle in terms of cell communication?

Answer 28

Answer: Smooth muscle cells communicate via gap junctions, whereas cardiac muscle cells communicate through intercalated discs, which also contain gap junctions.