Lecture 10

initial length of muscle (PRINT PAGE IN PPT) PG 24 this is another factor that is going to affect force development

-muscle fibers so when the arm is completely down the sacormere isn't contracted not a lot of power can be generated here when the arm is completely curled and contracted sacromere is completely squeezed together cant contract any further

Satellite cells

-play a role in muscle growth and repair -Increases number of nuclei - undergo nuclear division and then. donates that cellular bulk to new nuclei to the muscle fiber -Myonuclear domain is the *cytoplasm surrounding each nucleus * Each nucleus can support a limited myonucelar domain -More nuclei allow for greater protein synthesis *good if we want muscle growth -Important for adaptation to strength training *Sense we cant make more muscle cells we need to increase strength through hypertrophy

Number of motor units recruited

-this affects force development -requiring more motor units more contraction and more force generated

LOOK AT PPT Over view of the beginning of travel for AP --> to muscle contraction --> no contraction (rest)

1. AP sent down motor neuron 2. causing Ca+2 channels to open influx of Ca+2 into motor end plate 3. Causing release of Ach from synaptic terminal to synaptic cleft 4. Ach going to bind to motor end plate on the sarcolema causing AP to be sent down muscle fiber into the T-tubule 5. As the AP spreads down T-tubules, thats going to cause release of Ca2+ from Sarcoplasmic reticulum 6. Ca2+ then going to bind to troponin & pull tropomyosin out of the way exposing active site on actin 7. myosin head in high energy state is going to bind to active site on actin forming a cross bridge, ADP and Pi are attached to myosin head 8. Once P is released that initiates power stroke, causing pulling of actin filaments closer to m-line of sacormere 9. then going to be in low energy position after power stroke, new ATP attaches to myosin head this weakens the link between actin and myosin and the cross bridge detaches 10. the myosin head is reenergized once ATP is hydrolyzed (splits) into ADP and Pi 12. once reenergized myosin head rebinds to actin and performs power stroke, pulls actin filaments towards M-line release ADP and Pi which is going to be stuck on there until a new ATP binds, break it down to ADP & P to put back to high E eventually signal from motor neuron is going to stop then Ach stopped being released Ach will be broken done by Achesterase breakdown which is going to stop AP being sent to the sarcoplasmic reticulum since that happens Ca2+ is going to be able to be re-uptaked into sarcoplasmic reticulum, this causes tropomyosin ti reblock actins active site stops binding then stops muscle contraction

What are the 3 types of motor units?

1. Fast Fatigable (FF) -Fast glycolytic -Large motor unit - innervates lots of muscle fibers so able to produce lots of force but w/ that is will be easily fatiguable - innervates the most muscle fibers 2. Fast Fatigue Resistant (FR) - Fast oxidative glycolytic -not as easily fatiguable - But still n to a ton of force but produce more force then slow oxidative - using little of both E systems oxidative & glycolytic 3. Slow (S) -slow oxidative - Type 1 (small) slow twitch - not a lot of force - high fatigue resistance but low force - think of how oxidative phosphorylation took so long thats why it doesn't fatigue quickly - ex. calf muscles we can walk a long time allows us to many contraction without quick fatigue -innervates the least muscle fibers

Skeletal Muscle Functions

1. Force generation for locomotion and breathing ex. walking, sprinting, any movement needs force generation 2. Force generation for postural support 3. Heat production ex. Muscles largest metabolic organ in body. as we produce ATP we release heat as a byproduct ex. when shivering and working out 4. Acts as an endocrine organ -Endocrine organ is an organ that releases a hormone and that hormone has an affect some where else on body and travel through the blood stream

How do we develop force 3 things

1. Motor unit -Fast or slow twitch 2. Sarcoplasmic Reticulum -Rate of Ca+ release *more Ca2+ you can release the more active sites you are going to have for myosin to bind to active * dependent ornate of Ca2+ release and rational muscle fiver types 3. Muscle fiber -Myosin ATPase Activity *or the rate that ATP is broken down which is going to put the myosin back in the high E state Myosin head is in low E state until ATP bins and broke down to release E to move it back to high E state, the rate that myosin does this is going to affect their ability to develop force

STEPS for spread of AP

1. START w/ electrical signal AP heading down motor neuron 2. This Allows Ca2+ to rush into the axon terminal (ca2+ voltage gated channels open) as AP reaches gated channels 3. Ca2+ is going t cause the Act vesicles to be released into synaptic cleft 4. Which will then bind to motor end plate 5. Cause the AP to continue in the motor end plate 6. AP continues down muscle fiber

Muscle action- Develop force what are the 3 different muscle actions?

1. isometric contraction *muscle contracts but does not shorten * no movement- holding the weight * this is used for training neuromuscular adaptations 2. Concentric contraction *shorten muscle *movement- bringing weight towards body 3. Eccentric Contraction *cause most muscle damage this is the best way to improve hypertrophy * muscle lengthening * so an increase in muscle damage is going to cause an increase in skeletal muscle protein synthesis and an increase in skeletal muscle protein synthesis is going to allow for greater hypertrophy

Muscle contraction ASK PROFESSOR ON THIS

As AP heads down the axon terminal Ca2+ channels open and Ca2+ rushes into the axon terminal, this pushes Ach vesicles to to the end of the axon terminal and cause Ach vesicles to release Ach into the synaptic cleft. the Ach then goes and binds to the Ach receptors on the motor end plate. & propagate AP down sarcolemma. MUSCLE CONTRACTION: As the AP heads down sarcolemma its going to reach this T-tubule this allows AP to to head down T-tubules this causes the release of Ca2+ from the sarcoplasmic reticulum. This Ca2+ released from the sarcoplasmic reticulum is going to bind to troponin (WHICH IS on the actin filaments) ( before the binding of Ca2+ on troponin, The troponin is blocking the binding of the myosin head to actin meaning myosin is unable to bind to acting and as a result you cant perform skeletal muscle contraction.) So this Ca2+ that is released from the sarcoplasmic reticulum when it binds to troponin it causes a shift in the formation of troponin, which allows myosin heads to connect with actin filaments. Once myosin heads connected to actin filaments its going to create cross bridges (attach, detach) so its going to bind and then pull and then detach, rebind and pull again this allows skeletal muscle contractions. Each time myosin heads connect to actin filaments uses ATP thats going to cause the sarcomere to shorten and muscle to contract. The removal of Ca2+basically allow the troponin to move back and re-block the actin and active sites stops muscle contraction. GOING OVER 2ND TIME: Muscle contraction: AP heads down the Transverse(T) tubules we get a release of Ca2+ from the sarcoplasmic reticulum Ca2+ is then going to bind to troponin & Allow myosin head to interact & form a cross-bridge w/ the actin filaments. once connected perform a power stroke (which is pulling the actin in a certain direction) then after the power stroke actin and myosin will detach use up some ATP reattach and continue to pull unit it performed its contraction then Ca2+ is removed & troponin is going to rpeblock active site of active & detach myosin head. of the myosin head to actin Is a cyclic cycle: 1. Ca2+ has been released minded to troponin and moves troponin out of the way and exposing binding sites on actin 2. Myosin head is up in the energized state holding on to ADP+Pi. Myosin head attaches to the actin filament, forming a cross bridge= formation between actin filaments & myosin head 3. once myosin and actin are attached P is released and this is going to initiate the power stroke. the myosin head pivots and bends as it pulls on actin filament sliding it towards the M line causing ADP to be released. 4. A new ATP is going to come and bind to the myosin head, releasing myosin from actin. detaching the cross bridge. the myosin head is now cocked back in low energy configuration 5. Then as the new ATP (ATP hydrolysis) is spilt into ADP and P the myosin head becomes energized (cocked into the high energy confirmation) the myosin head becomes reenergized due to breaking ATP into ADP and Pi and allowing myosin head to reattach to actin filaments ant then start cycle all over again.

last factor to effect the rate of force development

Fast Fibers= type 2 fibers more force bigger fibers very explosive allows you to produce lots of force ex. sprinting usia n bolt Slow Fibers= long distance -fatigue resistance -long sustain muscle contractions -smaller fibers

Neuromuscular Junction - -What 2 structures make up the Neuromuscular junction. Motor neuron deff. Motor unit deff. Neuromuscular junction deff

Motor neuron- Nerve fiber connected to muscle cell - This is what sends the signal to central & peripheral nervous system to actual muscle Motor unit- motor neuron and all the muscle fibers it innervates Neuromuscular Junction- site where the motor neuron and muscle cell meet -Where the Ach is going to jump across & allow AP to continue from motor neuron to muscle fiber

Skeletal Muscle Development 2 things satellite cells can do

Myoblasts fuse to form a skeletal muscle fiber Satellite cell (muscle stem cell) is going to divide through its nucleus then its going to add its nuclei and cellular bulk to muscle fiber which allows muscle fiber to hypertrophy and muscle gets bigger another thing satellite cells could do is become inactive or senescent & with that they can no longer donate their nucleus which the response would be no hypertrophy or growth in resistance training satellite cell called muscle stem cells with our muscle fibers we don't typically have hyperplasia occurring in these skeletal muscles

Skeletal Muscle Structure

We have the skeletal muscle fiber satellite cells donating nuclei and bulk to muscle fiber. Within the skeletal muscle fiber we have individual myofibril and within the individual myofibril we have a sarcomere which is made up of actin (thin) and myosin (thick) filaments the myosin and actin filaments pull on each other which shortens myofibril, shortening individual skeletal muscle causing contraction of the muscle

Sliding filament theory

When released no myosin head is bound to actin but when you begin to contract you see these myosin heads start to bind and pu;llactin filaments closer other closer towards the m line. as you get more and more contracted get to the point where no more area for myosin heads to bind and pull actin closer together means muscle fully contracted. theory that actin filaments slide toward each other during muscle contraction, while the myosin filaments are still

DISCUSSION- what characteristics of muscle allow for the greatest force generation?

able to do this due to muscle fiber requirement

We have all the skeletal muscle fibers you have at birthrate but can have

hypertrophy muscles can get bigger and this occurs with assistance through satellite cells

WHAT happens when signals for muscle contraction stop? what happens once AP stops coming LOOK AT PPT slides 10-14

if signals for muscle contraction stop and Ach esterase is going to break down Ach on motor end plate thats going to stop AP from heading down T-tubulue into sarcoplasmic reticulum the Ca2+ thats there will head back to the sarcoplasmic reticulum through the effect of SERCA or Ca2+ ATPase cause myosin to move back and troponin and tropomyosin go back to blocking the binding site Once AP stops coming from motor neuron your going to see Ach stopped and broken down which is going to to stop AP from heading down t-tubules which is going to stop the release of Ca2+ and eventually reuptake of Ca2+ ATPase & this is going to stop binding of thick & thin filaments

Hypertrophy-->

is the growth of individual muscle fibers

Hyperplasia-->

is the increase count of skeletal muscle cant undergo this in adulthood

Neuromuscular Junction AP being sent down axon What happens?

motor neuron and a skeletal muscle cell axon transmits signal to the next neuron As AP heads down axon we see these voltage gated Ca2+ channels on the axon terminal are going to open and there is an influx of Ca+2 into axon terminal which is going to push the vesicles of ACH to the edge of the axon terminal and release Act into synaptic cleft. Ach then moves over to Act receptors sites on motor end plate & this causes a depolarization of motor end plate causing AP to spread on motor end plate VIEW THE PICTURE on PPT