Download Why do muscles shorten? 112ch11

Why do muscles shorten?
• What is the sliding filament theory of contraction?
• How are myofibers organized?
• What is the structure and function of actin, myosin and
troponin?
• Why do we “see” striations when we look through a light
microscope?
• What limits the degree of shortening in a sarcomere?
• What is a muscle “twitch”?
• How does a muscle create “All or None” and “Graded”
responses?
• What are the phases of muscle contraction?
• Compare and Contrast smooth, skeletal and cardiac muscle
The “Sliding Filament Theory” describes how two
proteins called actin and myosin interact to shorten
sarcomeres and the muscle to generate force.
• THE BASICS:
• Myosin tails and the Myosin Head• Thick filaments-
• Thin Actin and troponin• Function of Calcium and troponin• The function of ATP• Ratchet Action and shortening:
• What happens during rigormortis?
Microscopic view of skeletal muscle
How do these parts
create a contraction?
A single myosin filament has a tail
that is fixed and a head that flexes.
Many myosin filaments fit together to
make the thick filaments
Myosin heads bind actin fimaments, only if TROPONIN does
not cover actin. Normally very little calcium is present and
troponin is attached to actin (myosin blocked). Calcium binds
troponin causing tropomyosin to move away from actin. Actin
is now exposed and the myosin heads can bind to actin and a
contraction begins if ATP is available (energy) to flex the
myosin heads.
Many actins bind with many myosin heads on the thick filaments
during a contraction.
One Sarcomere=Z-line to Z-line with actin/mysin/actin in between.
Sarcomeres consist of all the actin and myosin found between
two Z-lines. Sarcomeres shorten during a contraction.
Striations look like this at really high magnification.
“Myofibrils” are organized groups of actin/myosin
filaments inside a myofiber.
During contraction the
opposing Z-lines are
drawn closer together by
the ratcheting action of
the myosin heads along
the actin filaments.
TITAN-myosin to Z-line
Ratcheting of myosin heads across actin shortens the myofiber!
As the sarcomeres shorten, the z-lines (discs) get
closer, eventually crunching into myosin. This
crunch prevents further shortening and limits the
maximum contraction (muscle shortening)!
Cardiac Muscle functions in a manner similar to that of
skeletal muscle with a few exceptions.
Cardiac cells depolarize for long periods and do not have the quick
twitches that are characteristic of skeletal muscle
Cardiac cells are linked by Gap Junctions so when Na+ enters a cell it
can cross into and depolarize the next cell and so-on.
While each skeletal myofiber requires a depolarization from a synapse,
cardiac cells can depolarize (heart beats) independently of the
nervous system. (Take it out and watch it beat autorhythmically)
• CARDIAC Muscle cannot undergo tetany ! 
Cardiac myocytes have a pacemaker
potential and autorhythmicity!
Their membranes become leaky to Na+ and K+ such that it
causes “pacemaker” cells to depolarize. We call this
pacemaker activity autorhythmicity.
The depolarization is passed on to all neighbors via gap
junctions and so on to all the cells of the heart.
The autonomic nervous system serves simply to modify the
function of the pacemaker cells (heart rate) and the amount of
Ca++ that enters during contraction (force of contraction).
Cardiac cells work 24/7 so they need more ATP and have
more mitochondria than the typical skeletal muscle cell.
Smooth Muscle cells contain actin and myosin, but are
quite different from skeletal and cardiac myocytes.
1) Where do we find smooth muscle under involuntary control?
2) Smooth Muscle usually comes in flat sheets or tubes with cells that
may or may not be connected by gap junctions.
3) The gut and artery have both circular and longitudinally arranged
sheets of smooth muscle to complement each others function.
Function of circular fibers
Function of longitudinal fibers
4) In smooth muscle cells the actin and myosin are not organized into
sarcomeres, but more loosely attached to the plasma membrane and
sarcoplasm (no striations)
5) Smooth Muscle can generate force that is sustained for a longer
time and uses less ATP (its cells typically have fewer mitochondria
and rely more on glycolysis)
6) Smooth muscle is stimulated by the autonomic NS at a classic
synapse (Multi-unit) or via a series of varicosities from a single
axon (Single-Unit) where gap junctions carry depolarization to
neighboring cells.
Smooth muscle cells are found in blood vessels, glands, guts,and
other places. SMCs contract using calcium entry/calmodulin
binding as a signal to activate myosin light chain kinase (MLCK).
MLCK phosphorylates myosin letting it bind actin and contract.
Once the myosin in smooth muscle is phosphorylated it
binds actin and the cell contracts, contraction ends when
Ca++ leaves the cell and MLC-phosphatase removes the
phosphate from MYOSIN…leading to SMC relaxation
Smooth Muscle Applications:
Asthma: excess constriction of airways
Solution: promote dilation (reduce SMC contraction)
High Blood Pressure: Excess contraction of blood vessel
Solution: vasodilator drugs
Low Blood Pressure: Not enough SMC tone in blood vessels.
Solution: vasoconstrict blood vessels to push blood back to
heart
Peristaltic Waves in intestine: propel chyme, often the
contractions are not strong enough (constipation)…what is
the solution?
Hypermotile Intestine (Diarrhea): Solution is to reduce
intestinal SCM contractile force
Hyperactive Bladder: improve receptive relaxation