Session 6: Muscle tissues

Question 1

Describe the process of skeletal muscle contraction

Answer 1

1. Nerve impulse arrives at the neuromuscular junction
2. Action potential from a motor neuron triggers the release of acetylcholine into the motor end plate
3. The sarcolemma undergoes depolarisation
4. Calcium ions are released from the sarcoplasmic reticulum and bind to troponin, exposes binding site, actin and myosin can form a bridge.
5. Muscle contraction begins
6. ATP, on myosin head, is hydrolysed to ADP and phosphate
7. Myosin and actin fibres separate and their cross bridge is lost. Contraction stroke ends, machinery resets for next contraction

Question 2

Compare the features of red and white skeletal muscle fibres

Answer 2

look at notes

Question 3

Compare the 3 different twitch fibres

Answer 3

look at notes

Question 4

Describe the difference between hypertrophy and atrophy

Answer 4

Hypertrophy: heart is bigger than normal
Atrophy: heart is smaller than normal

Question 5

State the structure and function of Purjinke fibres

Answer 5

Purjinke fibres are large cells with: more glycogen, less myofibrils, more gap junction. They help to conduct action potentials rapidly, allowing ventricles to contract in a synchronous manner. Will appear white in H+E due to presence of glycogen.

Question 6

Differentiate between cardiac and skeletal muscle

Answer 6

Both are striated muscles and have similar contraction mechanisms. But:
1. Nuclei in cardiac muscle are central not peripheral, some cardiac may have 2 nucei per cell
2. Cardiomyocytes communicate through gap junctions in intercalated disk
3. Only has one contractile cell type- cardiomyocyte vs 3 in smooth muscle

Question 7

Is mature muscle repair possible?

Answer 7

Skeletal muscle: cannot divide. Regenerate by mitotic activity of satellite cells, cell development follows muscle injury. Satellite cells can also fuse with existing muscle cells to increase mass- hypertrophy
Cardiac muscle: incapable of regeneration. After damage, fibroblasts invade, divide, and lay down scar tissue
Smooth muscle: retain mitotic activity, form new smooth muscle cells. Good at repairing themselves. Eg: muscle wall in uterus becomes thicker by hypertrophy( cell enlargment)

Question 8

How does smooth muscle contract?

Answer 8

Unlike striated muscle, contraction occurs along microtubules that run between dense bodies. When stimulated to contract, myosin and actin filaments interact like in striated muscles and slide over each other, but instead of pulling the z lines together, different sides of the cell are pulled together by the dense plaques.

Question 9

What is the similarity between cardiac muscle cells and smooth muscle cells?

Answer 9

Like cardiomyocytes, smooth muscle cells are joined at numerous points so that as one cell contracts, the entire tissue can act and contract as one. This occurs through gap junction interaction.

Question 10

What is the difference between hypertrophy and hyperplasia?

Answer 10

Tissues and muscles may increase in size by:
1. Hypertrophy: enlargement of individual cells
2. Hyperplasia: multiplication of their cells

Question 11

Describe the origin and insertion of a muscle and relate to its actions

Answer 11

Muscle: biceps brachii muscle
Origin: proximal bone which has a greater mass and is more stable during contraction than muscle’s insertion
Insertion: the structure the muscle attaches to. Tends to be moved by contraction, usually tendon to bone. Greater motion than origin during contraction.

Question 12

Explain the different roles muscles can play in coordinated movement

Answer 12

Agonists: responsible for a particular movement. eg. Biceps brachii, brachialis
Antagonists: oppose agonists. eg. triceps brachii
Synergists: they cannot perform movement, but will assist with angle with agonists
Neutralisers: prevent unwanted actions of muscle caused by agonists
Fixators: stabilise joint, hold body part immobile whilst another part is moving

Question 13

Describe the process of skeletal muscle remodelling

Answer 13

Destruction>replacement: atrophy, decrease in fibre number and fascicle size
Replacement>destruction: hypertrophy
Untrained muscle to trained muscle: involves fusion of satellite cells and growth

Question 14

What is the mechanism behind hypertrophy?

Answer 14

Overstretching so that A and I bands can no longer re-engage. New muscle fibrils are produced from bone marrow. New sarcomeres are added in the middle of existing sarcomere. New muscle fibres arise, overstretching can lead to cardiac issues like enlarged ventricles

Question 15

What is the mechanism behind atrophy?

Answer 15

1. Disuse: sedentary behaviour, age etc
2. Surgery: denervation of muscle, nerve regeneration will take 3 months
3. Disease: muscular dystrophies
   leads to loss of protein, reduced fibre diameter, loss of muscle power

Question 16

How do muscle cells deal with muscle injury?

Answer 16

Skeletal muscle: connective tissue differentiates into myoblasts that finally fuse to form new muscle fibres. Satellite cells(muscle stem cells) are the main producers of muscle fibres
Smooth muscle: injury causes proliferation and differentiation of smooth muscle into new muscle fibres. eg. uterus during pregnancy
Cardiac muscle: regenerates after injury in childhood not adulthood, injured cardiac muscle tissue is replaced with scar( connective) tissue.

Question 17

What is the difference between deep and superficial fascia?

Answer 17

Superficial: connective tissue that separates skin from underlying muscle tissue
Deep: organised connective tissue, surrounds muscles and binds them together. Contains blood vessels, nerves, fat.

Question 18

Describe the mechanism of innervation and contraction coupling in the motor end plate

Answer 18

look at notes

Question 19

Outline the causes and features of myasthenia gravis

Answer 19

Autoimmune disease, caused by error in transmission of nerve impulses to muscles. Antibodies block acetylcholine receptors at neuromuscular junction, prevents muscle from contracting.
Symptoms: ptosis eye( drooping eyelids), slurred speech etc

Question 20

Outline the mechanisms of the sliding filament model of muscle contraction

Answer 20

The lengths of actin and myosin remain the same. Sarcomeres shorten, z lines come together.

Question 21

State how neuromuscular transmission is disrupted in botulism

Answer 21

Botulism toxin is produced by clostridium botulinum, blocks neurotransmitter release at the motor end plate. Skeletal muscle is unable to contract. This toxin usually used to treat muscle spasms or wrinkles

Question 22

State how neuromuscular transmission is disrupted in organophosphate poisoning

Answer 22

Organophosphate is used as a pesticide. It inhibits the normal function of Ach esterase, unable to travel to muscle cell from pre synaptic neuron. Leads to excess of acetylcholine in body.
Symptoms include:
SLUDGE- salivation, lacrimation(tears), urination, defecation, GI cramping, Emesis (vomiting).

Question 23

Describe the pathophysiology of Duchenne muscular dystrophy

Answer 23

Inherited through X-linked recessive pattern. Mutation of dystrophin gene. Absence of this allows excess calcium to enter muscle cell, Ca taken up by mitochondria with water, mitochondria bursts, muscle cells burst, creatine kinase and myoglobin levels are extremely high in the blood, sodium, uric acid, potassium levels are also high

Question 24

Describe the role of Creatine Kinase

Answer 24

Enzyme used in metabolically active tissues like muscle, released into the blood by damaged skeletal muscle and brain, rhabdomyolysis

Question 25

Describe the pathophysiology of malignant hyperthermia

Answer 25

A severe reaction to anasthetics. Medication releases stored Ca in muscle cells, causes muscle contraction, generates excessive heat and metabolic acidosis. Mortality risk: 5% with treatment, 75% without.

Question 26

What is the role of dystrophin?

Answer 26

Attaches filaments to sarcolemma using other proteins. The membrane bound complex connects to the basal lamina. When muscle fibre contracts, it bursts- this is called rhabdomyolysis( rhabdo-striated)