Muscular System Lecture
(Day 2)
Muscle Structure and Contraction
Various methods for naming muscles:
1)Direction of fibers (obliques=slanted & rectus = straight)
2) Size of muscle (gluteus maximus & gluteus minimus)
3) Location (frontalis=near frontal bone)
4) # of Origins (biceps = 2 origins)
5) Location of attachment (sternocleidomastoid= connects to sternum, clavicle, and
mastoid process of temporal bone)
6) Shape (deltoid = triangular shaped muscle)
7) Action of muscle (flexor & adductor)
Now, let’s look at how muscles contract…
How structure relates to function:
We’ve already discussed that skeletal muscle is striated
(these stripes play an important role in contraction).
One muscle cell is called a muscle fiber. Each fiber is covered
by a plasma membrane called a sarcolemma (“muscle husk”).
Each muscle fiber (cell) is filled with myofibrils.
sarcolemma
myofibril
Each myofibril contains chains of tiny contractile units called
sarcomeres.
The sarcomeres are lined up like boxcars on a train.
But within the sarcomere itself are tiny, thinner protein
fibers, that produce the horizontal banding pattern and which
allow for muscle contraction.
Two Types of Protein Filaments within the myofibril (see pg. 183):
1) Actin (thin filaments)
2) Myosin (thick filaments, along which are “myosin heads”)
actin
myosin
Muscle cells are irritible (meaning able to receive and respond to
stimuli) and contractile (response to stimuli).
Steps Involved in Skeletal Muscle Contraction:
(Sliding Filament Theory)
1) Nerve impulse travels from brain, down motor neuron to target
muscle.
2) At the neuromuscular junction, ACh (Acetylcholine) is released
and binds to receptors on the sarcolemma.
motor
neuron
Muscle fiber
ACh released
sarcolemma
3) This results in Na+ ions rushing in which creates an electrical
current known as an action potential (due to rush of positive ions
into cell which upsets the balance and changes the electrical conditions
inside the cell).
An Action Potential is like an electrical current flowing down cell
4) The action potential triggers Ca++ to be released into muscle cell
(calcium is required for muscle cell contraction to occur).
5) Calcium ions bind to actin, changing its shape and position,
exposing myosin binding sites.
actin
myosin heads
muscle contraction animation
calcium
ions
6) Myosin heads grab onto actin (at the exposed sites) and “pull”,
causing the sarcomere to contract.
actin
myosin head
Note: Muscle cells don’t get shorter, but the sarcomere does
due to the filaments sliding past each other.
(think of sliding glass doors).
sarcomere shortens
sarcomere shortens animation
7) New ATP molecules are then brought to the myosin heads
which allow them to let go of actin, to be ready to pull on next
actin binding site.
8) Contractions continue, with new crossbridges forming, pulling,
and detaching, until action potential ends.
9) Once action potential ends (due to lack of nerve signals),
Ca++ is removed by active transport.
10) With Ca++ gone, active sites on actin get covered up and
muscle fiber relaxes.
Actin binding sites are covered (unavailable)
(All 10 steps occur in a few thousandths of a second!)
When a muscle cell contracts, it does so all the way.
However, a whole muscle can contract partially
depending on the # of cells contracted or the frequency of
muscle stimulation.
What occurs if there is too much stimulation of muscle
cells?
If the sending of nerve impulses continues, the muscles don’t
get a chance to relax and successive contractions are added/
summed. This results in a state called tetanus, when muscles get
“locked into place”. The crossbridges are connected and can’t release
as they’ve run out of ATP. Will need new supplies of ATP to get
“unlocked”.
Without ATP,
crossbridges get stuck!
Let’s experiment…..!
This is what happens with rigor mortis (but when dead,
no new ATP is supplied, thus muscles remain locked.)
The End!