Muscle physiology

Question 1

Contrast the roles of dihydropyridine receptors and ryandodine receptors in excitation-contraction coupling.

Answer 1

DHP receptors ( L-type Ca2+ channel) are located in the membrane of the transverse tubules (T-tubules) and are stimulated by the depolarization of the membrane during excitation contraction coupling. They are mechanically coupled to the calcium release channel of the SR via a Ryanodine receptor; which is activated following DHP depolarization, which (unpluggs the cork) releases Ca2+ onto the sacromers of the myofibrils.

Question 2

Describe how the crossbridge arrangement explains the length-tension curve.

Answer 2

The length-tension curve (bell curve for active movement) is related to the degree of cross bridging (myosin binding actin). The peak represents the point at which the maximum number of myosin heads are binding actin. On either side of the bell curve the tension is low because of max contraction or stretch of the muscle leading to fewer cross bridging points due to actin being too crowded, or too far from the myosin heads.

Question 3

Describe how the crossbridge cycling explains the relationship between initial velocity of shortening and afterload.

Answer 3

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Question 4

Contrast a muscle twitch with muscle tetanus.

Answer 4

A single action potential through the muscle will yield a given amount of Ca2+ release and will cause a contraction or a twitch.
A subsequent action potential will do the same thing, but the removal and relaxation of the muscle after each twitch takes time.
If the action potentials are at a high enough rate (Hz), the twitches will start to fuse.
Fused tetanus is the state where the muscle does not have a chance to relax.

Question 5

Contrast fast twitch and slow twitch muscle fibers.

Answer 5

Fast twitch (white, type II), extensive sarcoplasmic reticulum, more active enzymes that promote rapid release of energy.

Slow twitch (red, type I), more oxidative metabolism, myoglobin (iron containing substance similar to hemoglobin, combines with oxygen and stores it, this speeds oxygen delivery to mitochondria)

Question 6

Troponin consists of three subunits; name them

Answer 6

Troponin I (strong affinity for actin)
Troponin T (strong affinity for tropomyosin)
Troponin C (strong affinity for Ca2+)

Question 7

What are the steps of cross bridge cycling?

Answer 7

ATP bound to myosin head causes release of myosin from actin

Hydrolysis of ATP into ADP and Pi relaxes myosin head into cocked position

Myosin binds actin (cross bridge)

Pi is released leading to the power stroke

Movement released ADP and allows new ATP to be bound

Question 8

How is Ca2+ removed from the sarcomere?

Answer 8

2 pumps move Ca2+ out of the cell (Ca-H+, Ca-Na)
SERCA (sarcoplasmic,endoplasmic, reticulum, calcium ATPase) pumps Ca2+ into SR increasing concentration 10,000 fold.
2 binding proteins inside SR hold Ca2+- Calreticulin, and Calsequestrin

Question 9

What’s the difference between an isotonic and isometric contraction?

Answer 9

Isometric-no movement (no change in muscle length), increased load; holding an object in front of you

Isotonic- same load, changing muscle length. Bicept curl at stead rate

Question 10

What’s the main protein responsible for resisting a passive stretch? What is not responsible?

Answer 10

Titin

connective tissue is not responsible

Question 11

Contrast concentric and eccentric contractions

Answer 11

Concentric (muscle actively shortening) muscle shortens as force is applied.

Eccentric (muscle actively lengthening) muscle lengthens as force is applied

Question 12

List some ways that the NMJ can be disrupted.

Answer 12

Mimicking ACh- methacholine, carbachol, nicotine (drugs aren’t broken down by AChE)

Block choline uptake- Hemicholinium

Stopping ACh Release

Inactivating ACh esterase-increase ACh

Blocking ACh receptor- drugs succinylcholine, or Myasthenia Gravis (blocks or destroys self ACh receptors)

Question 13

What is ALS?

Answer 13

Initially an upper motor neuron disease. Loss of neurons projecting to the spinal cord.

Progresses to a lower motor neuron disease. Loss of spinal motorneurons.

Maybe noticed with muscle weakness.

Question 14

What is taxol-induced peripheral neuropathy?

Answer 14

Disruption of the microtubles that transport synaptic vesicles from neural cell bodies to the axon terminal. Long axons most affected, but onset delayed due to neurotransmitter recycling at the synapse.

Question 15

Describe botulinum toxin from a physiologic standpoint

Answer 15

Failure to dock synaptic vesicles presynaptically at the NMJ because of the loss of one or more SNAP proteins.

Question 16

Describe myasthenia gravis from a physiologic standpoint

Answer 16

Autoimmune disease where self Ab block or destroy self ACh receptors which reduces their number. Although turnover is normal the process is accelerated, treat with AChE inhibitors to keep more ACh in the synapse and help with the overall decrease in receptor numbers.

Question 17

What is Ca2+ role in synaptic transmission?

Answer 17

mobilize and dock synaptic vesicles.

Question 18

Differentiate between botulism and tetanus

Answer 18

Both botulism and tetanus inhibit synaptic transmission and prevent normal muscle activation.
The botulinum toxin works on the neuromuscular junction. It prevents the release of ACh into the neuromusclular junction. The muscle cannot be activated.
Tetanus also prevents synaptic transmission but does is at the inhibitory interneurons. Without the inhibition, the motorneurons become overactive. The muscles are overstimulated and become tetanic. Rigidity produced.

Question 19

How does caffine affect your muscle?

Answer 19

Effects the movement of Ca2+ from the SR the release is easier to activate and lasts longer. Good in low dose, less effective in high dose.

Question 20

What is Duchenne Muscular Dystrophy?

Answer 20

Dystrophin proteins anchor the cytoskeleton of muscles cells to the ECM. Abnormalities of the protein lead to weakness and dysfunction despite functional actin and myosin. (no supporting structure)