Muscle and Muscular Dystrophy II Flashcards
What is the difference between fascicles and myofilaments?
A fascicle is a bundle of muscle cells. A myofibril is a bundle of myofilaments (actin and myosin)
What are the three layers of connective tissue that surround muscle tissue, and what do they do?
Epimycium surrounds the entire muscle. Perimycium surrounds fascicles. Endomycium surrounds each muscle cell. These layers of connective tissue have different signaling molecules for the individual layers of muscle tissue they contact.
What is the length-tension relationship in sarcomeres?
The force generated in a sarcomere increases with increasing overlap between the actin and myosin filaments up to the point where the opposing actin filaments collide. This results from increases in the number of myosin heads that can contact the actin filament at one time. This is more important in cardiac and smooth muscle.
Why do muscles tighten after death, resulting in rigor mortis?
The cell runs out of ATP to reset the myosin cross bridge and release the myosin from the actin filament. The myosin head is an ATPase that hydrolyses ATP to “re-cock” the head, extending it to bind to actin again.
How frequently does one myosin head reset in a contraction?
In fast twitch muscle, the myosin heads are reset about 20x per second. In slow twitch they are reset about 4-5x per second. This occurs because the slow and fast twitch muscle myosins are from different genes, and the fast twitch gene can hydrolyse the ATP faster.
When do the specific steps of binding and unbinding actin occur in relation to ATP hydrolysis by myosin?
Myosin remains bound to actin without ATP. ATP binds to myosin and myosin releases actin. Myosin hydrolyses ATP -> ADP + Pi, extends head, and reattaches to actin. Release of ADP + Pi leads to “power stroke” head movement.
What is a significant difference between the signaling of striated muscle and smooth muscle, and how is smooth muscle contracted?
Smooth muscle has no troponin, but contraction is still signaled by Ca2+. A light chain on the myosin head can be phosphorylated, and the myosin head can bind actin. Calcium-calmodulin activated kinase phosphorylates the myosin head. A phosphatase must be present to remove the phosphate and relax the muscle. Both of these are slow processes compared to striated muscle.
How does a nerve synaspe trigger muscle conraction?
The nerve releases AChE which opens Na+ channels on the muscle, depolarizing just the small section of muscle it connects to. That depol triggers a fast AP that spreads throughout the whole muscle fiber. Each muscle fiber gets 1 axon terminal.
How does Ca2+ trigger all of the sarcomeres of the muscle to contract simultaneously?
If the VGCa2+ channels were just in the cell membrane, the sarcomeres nearest the membrane would begin to contract before those on the interior had recieved the message. The cell creates Transverse Tubules, tubes that run between the myofibrils and transverse to the length of the cell and serve to propagate the AP into the middle of the cell.
How is the SR arranged inside a muscle cell and how far does Ca2+ need to travel from the SR to active the myofibrils?
Each myofibril is surrounded by the sarcoplasmic reticulum, storing Ca2+ for muscle contraction. This means that no actin/myosin compounds are more than 1/2 a micron away from a high source of Ca2+. Myofibrils are arranged akin to a package of dry spaghetti.
What channels do Ca2+ flow through out of the SR?
This calcium is released via DHPR and RyR Ca2+ channels. DHPR is the Dihydropuradine Receptor located in the TT and RyR is the Ryanodine Receptor located on the SR. DHPR is voltage sensitive and is in physical contact with RyR channels. The AP propgates into the transverse tubule where the DHPR receptor is located, triggering confromation shift in DHPR which opens the RyR channels. DHPR allows Ca2+ influx from extracellular env, but this is unnecessary.
What is the difference between the DHPR/RyR system in cardiac cells vs skeletal muscle?
They are made from different genes. Skeletal DHPR does not need EC Ca2+ to trigger contraction. Cardiac DHPR must allow influx of extracellular Ca2+, and a lack of it results in no contractions. This is because the cardiac DHPR and RyR do not have physical contact, and Ca2+ must be present to signal RyR.
How does contraction stop?
Ca2+ is pulled back from cytosol into SR by Ca2+ pumps/Ca-ATPase. These are ALWAYS working to pull Ca2+ into the SR. Lack of Ca2+ leads to troponin/tropomyosin covering the binding sites on actin.
How is contraction signaling in smooth muscle different from that in striated muscle?
The smooth muscle cells are only 5 microns across and all signaling can be done from the surface. They do not need SR or transverse tubules, but some still have them. Also, acetyl choline may be excitatory on some smooth muscle and inhibitory on others. Very complex.
What is myostatin and what does it do?
Myostatin (Myo - muscle, statin - stop/slow) slows muscle growth. Mature muscle cells do not divide, but their size can increase through increasing length (myoblasts) and girth (added sarcomeres). Myostatin production may be modulated by age or by exercise. May also be increased by disease (HIV)
