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”) Muscle cells are irritible (meaning able to receive and respond to stimuli) and contractile (response to stimuli). actinmyosin

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. muscle contraction animation myosin heads actin calcium ions

6) Myosin heads grab onto actin (at the exposed sites) and “pull”, causing the sarcomere to contract. myosin head actin

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!