DFF lecture 26: muscles

skeletal muscle

- attached to bones of skeleton - voluntary movement - fatigues quickly - multinucleated - series of bundles - muscle fibers are long and thin - unit of contraction: sarcomere

physiological mechanism behind a skeletal muscle contraction

1. An action potential travels down a motor neuron and arrives at the axon terminal 2. Neurotransmitters (usually ACh) are released and bind to a receptor on the membrane of the muscle cell. This receptor allows both Na+ and K+ to flow, but allows more Na+ to come in than K+ to leave, causing a depolarization of the membrane. 3. The postsynaptic membrane generates an action potential that spreads down T Tubules (invaginations of cell membrane) 4. This causes a change in the conformation of the DHP and ryanodine receptors, releasing Ca+ stored in the sarcoplasmic reticulum 5. Released Ca+ diffuses in the sarcoplasm, stimulating muscle contraction 6. Ca+ is taken up by the sarcoplasmic reticulum w/ ATP pumps, terminating muscle contraction

How do troponin and tropomyosin work together to regulate muscle activity?

Troponin and tropomyosin are bound to each other. When troponin binds calcium, it changes the structure of tropomyosin, moving tropomyosin on the actin (thin) filament and the little sites are revealed, and those little sites are where the myosin interacts with the actin

sympathetic neurons release _________________, while parasympathetic neurons release ___________________

acetylcholine; norepinephrine

how do muscle contractions differ from action potentials?

action potentials are a LOT faster than muscle contractions, and muscle contractions happen BECAUSE of action potentials. In action potentials, there is an "all or none" response- no matter how much stimulus you have, you'll have about the same amplitude every time. However, in muscle contraction, multiple action potentials can add up to make bigger contractions (a single action potential would cause only a small twitch in the muscle, but multiple action potentials close together can cause a bigger, fuller contraction, so the amplitude CAN vary greatly in muscles)

flexor and extensor muscles work ________________ to operate the joint

antagonistically

Ligaments attach _____ to _____

bone; bone

what must be present in order for the actin and myosin filaments to interact? What is the mechanism

calcium must be present in the sarcoplasm on the actin filament, there are 2 proteins bound to each other: troponin and tropomyosin. Troponin binds the calcium, which changes the structure of tropomyosin and reveals little sites on the actin with which the myosin can interact

which types of muscle are uninucleated and involuntary?

cardiac and smooth

how is the calcium flow different in cardiac and skeletal muscle? (and smooth muscle)

in both, action potentials travel down T-tubules or similar structures. But in skeletal muscle, the Ca+ is released only from the sarcoplasmic reticulum because of the unbinding of DHP and ryanodine, while in cardiac muscle, calcium enters the cell from an external environment, and then that calcium binds to a calcium-gated ion channel on the sarcoplasmic reticulum, which causes even more calcium to be released into the cytoplasm the major difference is that cardiac muscle *initially* gets its calcium from outside the cell, while skeletal muscle always gets its calcium from stores in the sarcoplasmic reticulum in smooth muscle, calcium also flows in from outside the cell like cardiac muscle

how does ATP have different effects on cardiac/skeletal and smooth muscle? relate this to calcium's effect

in cardiac/skeletal muscle, the ATP is needed to release contraction, while in smooth muscle, the ATP is needed to break down into ADP and Pi so that the Pi can bind to the myosin and allow it to bind to the actin filament/cause contraction and this kinda stems from calcium's different effects- in smooth muscle calcium triggers phosphorylation of myosin so that it can bind to actin and contract, while in skeletal/cardiac muscle the calcium binds to troponin, changing conformation of tropomyosin and opening up a binding site for the myosin head so that the muscle can contract

In a smooth muscle cell, an AP results in an inflow of calcium. What is calcium's effect?

it triggers the phosphorylation of myosin so that it can bind actin and cause a contraction

what would happen if the phosphate couldn't be released in the sliding filament model?

it would be stuck in stage 3- the myosin head wouldn't change conformation and the power stroke wouldn't fully happen

what would happen if the ADP couldn't be released from the myosin filament?

it would get stuck in the power stroke

what does the myosin phosphatase do in smooth muscle? What is the effect?

it's always active, removing the phosphates, which results in the inability of actin to bind myosin and thus stopping muscle contractions

in smooth muscle, the phosphate bound to the myosin is a covalent bond. What is the significance of this?

it's slower to change- can't be immediately released, it requires more energy and effort

what factors contribute to muscle fatigue?

loss of ATP, buildup of molecules associated with ATP production, leaking of Ca out of cell, etc.

true or false: smooth muscle has a really short action potential

mmm it can be fast but not as fast as skeletal muscle- somewhere between skeletal and cardiac so medium length AP

smooth muscle

muscle tissue in which the contractile fibrils are not highly ordered, occurring in the gut and other internal organs and not under voluntary control.

how do summation and tetanus relate?

muscle twitches close together have a summation effect, where they can create a greater muscle contraction. Continuous summed twitches can bring the muscle fiber to maximum contraction in which it's sustained in contraction, and this is called tetanus

tendons attach __________ to _________

muscle; bone

what 2 things must happen for actin to interact with myosin?

myosin has to have ADP bound + P AND calcium must be present

What action is directly triggered by the binding of ATP to myosin? How does this relate to rigor mortis (stiff state of muscles after death)?

myosin unbinds from actin. If there's no ATP present to unbind the myosin head from the actin, they can't be released and the muscles are stiff

what controls smooth muscle contraction? How?

neurotransmitters- by altering resting membrane potentials or the rate at which AP are fired

do all muscles have sarcomeres?

no, just striated muscles (skeletal and cardiac)

what initiates a heartbeat? How? How is this different from a regular action potential?

pacemaker cells in the sinoatrial node 1. A slow influx of Na+, then Ca+, causes a gradual depolarization of pacemaker cells. 2. once threshold is reached, a major influx of Ca+ generates an action potential 3. opening of K+ channels allows K+ to exit and the cell repolarizes different because calcium drives the action potential instead of sodium, and also prolongs the action potential

what happens right after actin and myosin bind?

phosphate is released, triggering the power stroke

which aspect of the muscle actually contracts? How does this happen?

sarcomere- the filament lengths do NOT change, but they overlap to make the sarcomere shorter in length

how does skeletal muscle differ from cardiac in the direction of contraction?

skeletal muscle moves almost exclusively in one direction, while cardiac muscle contracts in 3 dimensions

why is there a longer depolarization in cardiac cells than other types of cells?

this prevents the heart from having a sustained contraction- if action potentials were shorter like skeletal muscle, you could have summation and eventually get a sustained muscle contraction, which would make the heart contract and go into tetanus and you would die. And even if you don't approach tetanus, having too fast of heartbeats would not give the blood enough time to fill the chamber so you're not efficiently transporting blood

what are joints made of?

typically have connective tissue and cartilage that allow for different types of movements

what might cause muscles to relax?

when stimulation stops OR fatigue

failure of ATP hydrolysis and release of phosphate would cause one thing, while failure of ATP binding would cause another thing. What are they?

ATP hydrolysis and release of phosphate: muscle can't contract ATP binding: muscle won't stop contracting

how is skeletal muscle organized?

The basic contractile unit of skeletal muscle is a sarcomere. Sarcomeres line up into tandem arrays/bundle together to make up the myofibril. Myofibrils bundle together to make the muscle fiber. There is a series of bundling, which allows the contraction to occur almost exclusively in one direction

composition of a myosin (thick) filament

has lots of long polypeptide chains with globular heads sticking out

What is rigor mortis and what causes it?

A fixed muscular contraction after death happens when you run out of ATP so the myosin can't unbind from the actin and muscles get stuck in this conformation

how do smooth muscles contract and relax?

ACh stimulates the firing of smooth muscle cell AP's, causing contraction norepinephrine has the effect of hyperpolarizing the smooth muscle cell membranes, resulting in relaxation note: the typical state of smooth muscle isn't fully relaxed and isn't fully contracted

what are the 8 steps of the sliding filament model?

1. Ca+ is released from sarcoplasmic reticulum 2. Ca+ in the cytoplasm binds troponin and and exposes myosin-binding sites on actin filaments 3. Myosin heads bind to actin, starting the power stroke 4. Phosphate is released and in the power stroke, the myosin head changes conformation, bending so that the actin and myosin filaments are forced to slide past each other 5. The ADP is released, and ATP binds to the myosin head, causing myosin to unbind from actin 6. ATP is hydrolyzed (from ATP to ADP + Pi), releasing energy which is stored in the myosin molecule, readying it for another power stroke 7. If Ca+ is still available in the cytoplasm, the entire cycle repeats, adding to the force of the contraction 8. If Ca+ has left the cytoplasm, tropomyosin is no longer pulled away to expose the myosin-binding sites on actin, so the myosin heads can't bind to actin and the contraction stops

how are action potentials in skeletal and cardiac cells different?

1. duration of action potential- cardiac AP's are WAY longer 2. role of Ca ions in depolarization- in skeletal and non-pacemaker cardiac cells, depolarization occurs quickly by the fast opening of Na+ channels, but in pacemaker cells, the calcium influx prolongs the duration of the action potential, making a plateau phase

what are the 3 roles of ATP in the sliding filament model?

1. its binding causes myosin to unbind from actin 2. its hydrolysis releases energy which is stored in the myosin molecule, readying it for another power stroke 3. the release of phosphate triggers the power stroke>>actin and myosin filaments slide past each other

composition of actin (thin) filament

2 threads of actin bound around each other, and there are 2 additional proteins: troponin and tropomyosin, which are bound together.

composition of a sarcomere

Composed of an actin filament (thin) and a myosin filament (thick), with a Z line on the edge between the sarcomeres and a M line in the middle of the sarcomere. The myosin and actin filaments are the same size.

what are DHP and ryanodine receptors? What function do they have in muscle contractions?

DHP and ryanodine receptors are proteins that bridge the gap between the T tubule and sarcoplasmic reticulum in a muscle cell. The DHP receptor is associated with the T tubule membrane, and the ryanodine receptor is associated with the sarcoplasmic reticulum membrane and acts as a channel for calcium. DHP blocks the calcium channel but once the membrane is depolarized, the conformation of DHP changes, causing it to unbind from ryanodine and allowing calcium to flood out of the sarcoplasmic reticulum through ryanodine, allowing actin and myosin to join see slide 6 for good visual

cardiac muscle

Involuntary muscle tissue found only in the heart - uninucleated - connected via gap junctions - myogenic - Calcium release from SR is through a different channel mechanism: Ca++ ion gated Ca++ channels

what action is directly triggered by the hydrolysis of ATP?

energy is released and stored in the myosin molecule, readying it for another power stroke

compare the channel activity in pacemaker cells vs regular heart muscle cells vs regular neurons, and how it affects their action potentials.

sodium: - in neurons and regular heart cells, there is a rapid opening of voltage-gated channels to spike the action potential, while in pacemaker cells there are NOT any voltage-gated sodium channels (although there are a few leak ones) potassium: - both regular heart cells and pacemaker cells have potassium that's high before and after the action potential and then dips during the action potential, while in neurons that potassium level would be highest during the action potential (rise toward end) calcium: - in pacemaker cells, calcium (thru calcium channels) is actually the ion that drives the action potential, while in other cells it's the sodium. Calcium plays a role in regular heart cells by prolonging the action potential (into plateau phase) but isn't the driving force.

what is required for the power stroke to become "un-stuck"? Does this always happen?

the ADP must be exchanged for ATP. In a healthy cell, there is usually a lot more ATP than ADP so this is usually the case, but it's possible for ADP to bind again

the way the muscle attaches to the bone determines what?

the function of that joint- whether it's used for speed, force, etc. (relating to lever systems)

which part of the myosin (thick) filament interacts with the actin?

the globular head

crossbridge cycle

the mechanism that drives muscle contraction

What action is directly triggered by the dissociation of the inorganic phosphate?

the myosin head changes conformation and the actin and myosin filaments slide past each other

generally, what causes the muscle contraction?

the release of calcium

what is the power stroke triggered by?

the release of phosphate (ADP + Pi >> ADP)

what do all muscles have in common?

they all utilize actin and myosin filaments for contraction