muscle physio 1

Question 1

Describe the communication at the NMJ -

Answer 1

1. Action potential arrives at terminal bouton
2. Voltage-gated calcium channels open
3. Calcium enters cell triggering release of ACh
4. ACh diffuses across cleft and binds to nicotinic receptors on
   motor end plate
5. ACh triggers opening of channels for small cations sodium
   and potassium
6. Net movement of positive charge
   in → depolarization
   • End plate potential = EPP
   • EPP > EPSP
7. EPP causes action potential in muscle cell
8. Action potential spreads through muscle causing
   contraction

Question 2

Myasthenia Gravis

Answer 2

-Autoimmune damage of
nicotinic cholinergic receptor
-Weakness improves after a period of
rest or after administration of
acetylcholinesterase inhibitors
-Tensilon Test

Question 3

Lambert–Eaton Myasthenic Syndrome (LEMS)

Answer 3

-Muscle weakness is caused by
an autoimmune attack against
Ca2+ channels in the nerve
endings at the NMJ.
-decrease in Ca and decrease in Ach released

Question 4

Lambert–Eaton Myasthenic Syndrome (LEMS) results in

Answer 4

Proximal muscles of the lower
extremities are primarily
affected, producing a waddling
gait and difficulty raising the
arms.

Question 5

Latrotoxin

Answer 5

The venom of the black widow
spider, it opens presynaptic Ca2+ channels
resulting in excess Ach release →profound
muscle contraction → muscle spasms,
muscle pain, and abdominal rigidity

Question 6

Botulinum toxin/ Botulism/Botox

Answer 6

-Protease that prevents release of ACh
vesicles from the NMJ
-Symptoms include weakness of muscles
innervated by cranial nerves, blurred
vision, flaccid Paralysis

Question 7

Tubocurarine

Answer 7

-NMJ blockers / Muscle Relaxants
-Nm receptors
antagonist
-

Question 8

Curareis

Answer 8

plant-derived alkaloid,
used as arrows/blow dart poison. It is
a competitive inhibitor of Nm

Question 9

Sarcoplasmic Reticulum (SR)-Resting muscle

Answer 9

Intracellular [Ca2+] very low (<10-9M or nM).
• Majority Ca2+stored in sarcoplasmic reticulum
(SR).
• Ca2+ bound to SR proteins e.g., calsequestrin.

Question 10

Sarcoplasmic Reticulum (SR)-Contracting muscle

Answer 10

Muscle depolarization → Ca2+ release from SR.
• SR ONLY source of Ca2+ for contraction (skeletal
muscles)
• Intracellular [Ca2+] increased (>10-6M or μM)

Question 11

Excitation-Contraction Coupling

Answer 11

-Depolarization of the muscle fiber membrane creates an end-plate potential (EPP)
• A muscle twitch is a single contraction-relaxation cycle
• A latent period is the short delay between the muscle action potential and beginning of muscle tension development
– Time required for calcium release and binding to tropoin

Question 12

Malignant hyperthermia

Answer 12

-Mutations or dysregulation of Ca2+release channels in muscle
- high environmental heat
or strenuous exercise can trigger an abnormal release of Ca2+from the sarcoplasmic
reticulum in the muscle cell, resulting in sustained muscle contraction and heat
production.

Question 13

Malignant hyperthermia-Treatment:

Answer 13

Dantrolene directly interferes with muscle contraction by binding
RyRreceptors.

Question 14

Muscle Contraction-Muscle tension:

Answer 14

: Force created by

muscle

Question 15

Muscle Contraction-Load

Answer 15

Weight or force opposing

contraction

Question 16

Muscle Contraction-Contraction:

Answer 16

Creation of tension in

muscle

Question 17

Muscle Contraction-Relaxation:

Answer 17

Release of tension

Question 18

Muscle Contraction- Relaxed state

Answer 18

Myosin head cocked
• Tropomyosin partially blocks
• binding site on actin
• Myosin is weakly bound to actin

Question 19

Rigor Mortis

Answer 19

• This cycle is dependent on ATP supply and
activation via Ca2+.
• After death cellular energy stores are depleted,
detachment can’t occur because of the lack of
ATP, and the cycle stops in an attached state

Question 20

Length-Tension Relationship

Answer 20

Too much or too little overlap of thick and thin filaments in resting muscle
= Decreased tension