Download Muscles may shorten up to @ 70% of their resting length!

Muscle Physiology
Muscle Tissues differ in structure, but
share common function
pg. 407
What do all
muscle tissues
have in common
in terms of their
structure and
function?
Figure 12-1: Three types of muscles
Smooth muscle cells may function
independently, or as a unit
p. 433
What is moving between cells,
indicated by the arrows?
See also p. 392
Smooth muscle is effective at decreasing the
diameter of the lumen in a hollow organ
p. 435
Ca+2 binds to calmodulin in the
cytosol (not thin filaments). This
activates a kinase associated with
the myosin filaments, and then
myosin ATPase.
Note the globular heads along the
entire length of the thick filament.
Muscle cells and connective tissue arranged
to produce movement at a joint
pg. 410
What changes (in structure and function) would occur in this muscle
with anaerobic training? Can you explain why?
See also the concept map on pg. 400
Figure 12-3a-1: ANATOMY SUMMARY: Skeletal Muscle
The architecture of skeletal muscle fibers is
complex because of their size
Pg. 411
Figure 12-3b: ANATOMY SUMMARY: Skeletal Muscle
Myofibrils: Site of Contraction
Pg. 414
What are the
functions of
Troponin and
Tropomyosin?
What/where is
myosin ATPase?
Figure 12-3c-f: ANATOMY SUMMARY: Skeletal Muscle
The interaction of voltage and mechanical
events allows myofilaments to interact
p. 418
Is the DHP receptor
sensitive to voltage,
mechanical change,
or a ligand?
Figure 12-11a: Excitation-contraction coupling
Troponin pulls Tropomyosin away from
binding sites when Ca+2 is present
These figures are also included in your packet, on page 113.
Figure 12-11b: Excitation-contraction coupling
ATP must be present on myosin, before
myosin can bind to actin
Pg. 416
1 This stage is very short-lived.
See also pp. 111-112 in your packet.
Figure 12-9 (steps 1 & 2): The molecular basis of contraction
2 In other words, a molecule of
ATP must bind to the myosin
head in order for it to be
“locked and loaded”; ready to
interact with actin.
Myosin uses an ATPase to split ATP, but
hangs onto ADP and Pi for a short time
Of all the energy consumed during
muscle contraction, only @ 25% is
realized as external work (i.e. 75% is lost
as heat!).
4 Hydrolysis of ATP results in the
binding of the myosin head to the actin
filament, but no movement has
occurred yet.
Figure 12-9 (steps 3 & 4): The molecular basis of contraction
Release of Pi causes a conformational change
in the myosin head, now attached to actin
6
Almost
done…
A single power stroke of myosin cross bridges
shortens the muscle cell by only @ 1%.
Why isn’t muscle contraction “jerky”?
Muscles may shorten up to @ 70% of their
resting length!
5 The release of the phosphate group
causes a conformational change in
myosin, pulling the actin toward the
center of the sarcomere.
Actin
Figure 12-9 (steps 5 & 6): The molecular basis of contraction
What is the role of the Na-K pump?
Myosin releases ADP, but is still bound to
actin until a new ATP arrives…
7
8
What happens if there
is no ATP available?
Timing of Electrical & Mechanical Events
p. 419
What ions are moving (and
through what kind of ion
channel) during the depolarizing
phase of the motor neuron?
How quickly does contraction
begin after the sarcolemma
depolarizes?
Myogram of Single Muscle Twitch
ATP can be produced via 3 methods
Pg. 420
• Aerobic Respiration
•
•
•
•
Oxygen
Glucose
Fatty acids
30-32 ATPs
• Anaerobic Respiration
• Fast = power (…but)
• 2 ATP/glucose
What is oxygen debt?
How does a cell repay its
oxygen debt?
• Phosphocreatine (CrP) ATP
ATP can be produced rapidly by the action
of Creatine Kinase
Pg. 420
This process is referred to
as the “phosphagen
system”. Explain why.
What does a “kinase” do?
How does it apply in this
case?
Figure 12-13: Phosphocreatine
Cellular Energy Stores in Human Muscle
R.W. McGilvery, Biochemistry, a Functional Approach, W. B. Saunders, Philadelphia 1970
How is it possible that you get more power (ATP/time) with fermentation,
when a cell produces only 2 ATP per molecule of glucose by this metabolic
pathway? Why aren’t proteins/amino acids listed?
Substrate usage as a function of
exercise duration
Explain the
differences in
muscle vs. plasma
sources of
substrates.
Could there be
hormones
involved?
Substrate usage as a function of exercise
duration
Plasma fatty
acids
Plasma glucose
Relationship between Oxygen Consumption
and Work
O2 consumption
increases 23X!
Explain the changes (or lack
there of) in these organs.
CONTROLLING SKELETAL
MUSCLES
The “final common pathway” in voluntary
muscle movement receives 3 kinds of info.
Describe the three “levels” of
direct control over motor
neurons that innervate
skeletal muscles:
1. Spinal reflexes
2. Cortical (pyramidal)
pathways
3. Subcortical
(extrapyramidal
pathways)
Relate this information to the
GPSP at these motor
neurons.
a.k.a. “pyramidal pathway”
p. 461
Muscle Proprioceptors
See also pg. 114 in your packet
Proprioceptors detect change in length and
tension
What part of the
CNS do these
receptors send
information to,
regarding position
or a change in
position?
Pg. 450
Figure 13-3: Sensory receptors in muscle
Tonic Activity of the Muscle Spindle
(producing muscle tone in a muscle at rest)
The sensitivity of the muscle spindle depends on…?
p. 452
List some other
inputs to the alpha
motor neuron.
Muscle Spindle sends more frequent APs
in the Stretch Reflex
Pg. 452
Does this reflex
change the length
of the muscle?
Explain.
Do these receptors
adapt?
Co-activation of
Alpha and Gamma Motor Neurons
p. 453
What would happen to the
firing rate of the primary
afferent neuron if the gamma
motor neuron was not
functioning?
Coactivation of pyramidal and
extrapyramidal tracts maintains sensitivity
Golgi Tendon Reflex prevents injury
What neurotransmitter is released
by the interneuron, and how does it
inhibit the alpha motor neuron?
Pg. 454