Exam 2 is October 25

You should be reviewing Lectures 8-13 by now!

Memorize your student ID number correctly and fill in the bubbles completely.
This time add two zeroes to the end of the ID number (returning students)!
Exam 2 review session: October 18, 5-7pm, 159 Mulford

MCB 32 Lecture 14: Skeletal muscle contraction

Review neuromuscular junction
Skeletal muscle structure
Myofibrils and sarcomere structure
Sliding filament model
Excitation-contraction coupling
Muscle metabolism
Force generation
- Summation (temporal)
- Recruitment (spatial)
Fiber length vs tension

Review question

Which of the following does NOT have nicotinic cholinergic

receptors?
A) skeletal muscle cells
B) parasympathetic postganglionic neuron dendrites
C) sympathetic postganglionic neuron dendrites
D) effector organs for the parasympathetic nervous system
E) chromaffin cells

Clicker question
Remember that myasthenia gravis is an autoimmune
disorder, which causes the body to destroy nicotinic AChRs.
The disease is progressive (more and more nAChRs are
destroyed).
What would be the best treatment for myasthenia gravis,
especially in the early stages of the disease?
A)
B)
C)
D)
E)

Nicotinic AChR antagonist

Muscarinic AChR agonist
Acetylcholine esterase inhibitor
Beta blocker (beta adrenergic antagonist)
Albuterol (beta adrenergic agonist)

Neuromuscular junction

Three types
of muscle
tissue

A) Cardiac muscle

B) Skeletal muscle C) Smooth muscle

5
4

Three types
of muscle
tissue

Fig 12.33

Anatomy of skeletal muscle

Fig 12.1

Fig 12.2

Myofibril

Fig 12.3

Myosin and Actin

In vitro experiment to
show how myosin can
make actin move

Sarcomere is made of myosin and actin

Fig 12.5

Clicker question
During a muscle contraction
A) The actin filaments get shorter
B) The myosin filaments get shorter
C)The sarcomere gets shorter
D)The motor neuron gets shorter
E) The sarcoplasmic reticulum gets shorter

Sarcomere during muscle contraction

Fig 12.6

Crossbridge cycle

Myosin hydrolyzes ATP

Head moves back

Needs ATP
to unbind

Myosin head
pivots forward
Fig 12.7

Rigor mortis
Rigor mortis sets in a couple of hours after death. It is characterized
by very stiff limbs and lasts for several hours before the body goes
limp.
Think about what will happen to muscles after death and explain what
causes rigor mortis.
Hint: think ATP and the cross-bridge cycle

Clicker question
Which of the following statements about end-plate potentials (the
potential change in the muscle) is FALSE?
A) They are graded potentials.
B) They are always depolarizations.
C) They are almost always of sufficient magnitude to generate an
action potential.
D) They are a result of acetylcholine binding to muscarinic
cholinergic receptors.
E) They are terminated by removal of acetylcholine from the synaptic
cleft.

Excitation-contraction coupling

Ca+2 in cytoplasm is necessary for crossbridge formation

Fig 12.9

Clicker Question

What role does Ca+2 play in muscle contraction?

A) Activates myosin ATPase activity (hydrolyzes ATP)
B) Release of acetylcholine from motor neuron
C) Exposes myosin binding sites on actin
D) Causes graded potential
E) Binds myosin head during power stroke

Clicker question
The role(s) of ATP in muscle contraction include:
A) ATP hydrolysis is necessary for myosin to form a crossbridge
with actin
B) Binding to the troponin complex to expose myosin-binding
sites
C) Binding to myosin to break an actin-myosin crossbridge
D) The energy from ATP is used to pump Ca+2 into the
sarcoplasmic reticulum
E) Binding to receptors on the muscle fiber to depolarize the
membrane and trigger an action potential

Aerobic respiration
-

Requires O2
Makes lots of ATP
CO2 is byproduct
Both sugars and fats are broken down
in this process
- Occurs in mitochondria
Anaerobic respiration
-

Independent of O2
Makes just a little bit of ATP
Lactate is byproduct
Can only breakdown sugars (not fats)
Occurs in cytoplasm only

Fig 12.22

Energy sources for muscle

Creatine supplements
Taking extra creatine does increase creatine levels in the muscle,
but the body stops synthesizing as much as before
Allowed in professional sports and in the Olympics
Which athletes would benefit the most from creatine supplements?

Clicker question
What is the physiological explanation for tetanus?
A) Action potentials are at such a fast frequency that they
summate
B) Myosin power stroke is more forceful
C)Next stimulus occurs before Ca+2 is pumped back into
sarcoplasmic reticulum, so more Ca+2 in the cytoplasm
D)More crossbridges are forming

Summation of tension in a single muscle fiber

Muscle doesnt get a chance to relax before the next stimulus (release
of ACh)
Ca+2 concentration keeps on increasing in cytoplasm. The Ca+2 pump
cant put it back into the SR fast enough.

Fig 12.16

Recruitment of multiple motor units

Smaller motor
units recruited
first

Fig 12.18

Smaller motor units are recruited first

Fig 12.19

Fiber length vs tension produced

Leg bent
completely

Leg straight

Fig 12.17

Practice Questions
1) Which of the following does NOT influence the force generated by an
individual muscle fiber?
A) frequency of stimulation
B) fiber diameter
C) fiber length
D) recruitment
E) summation
2) Which one of the following steps of muscle contraction does NOT directly
require ATP?
A) Pumping Ca+2 into the sarcoplasmic reticulum
B) Maintaining the appropriate Na+ and K+ ion gradients
C) Myosin head releases actin
D) Moving tropomyosin off the myosin binding sites
3) During skeletal muscle contraction
A) the thick and thin filaments get shorter
B) the Z lines in the sarcomere get closer together
C) Ca+2 binds myosin
D) the graded potential causes voltage-gated Ca+2 channels to open on the
membrane
E) myosin forms crossbridges with tropomyosin