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What are sarcoplasmic reticulum (SR)? where can you find them?
- Modified version of endoplasmic reticulum that wraps around myofibrils.
- It consist of Ca2+ which are released from longitudinal tubules
Why is Ca2+ important in muscle?
- They aid in the contraction of muscles
What are the contractile proteins in myofibril?
- Myosin – ability to create movement
- Actin – makes up the thin filaments of muscle fiber
Where would you find myosin and what is its shape/ form?
- Long tail and round head connected by hinge (allows for a swivel mov’t)
- When 250 myosin come together they form a swiveling staircase
What are sarcomeres and where would you find it?
- Sarcomeres are pattern segment in myofibril.
- Starts and ends with z disk (thin filiments/ I band ) --> A band (mainly thick filaments but over laps with thin filiments (actin) H zone --> z disk
What are t-tubules and where are they located?
- T-tubules are lumen in the muscle fiber (myofibrils) that allow for action potential to reach the center at a faster rate
What would happen if we didn’t have t-tubules?
- Action potential would run at a slower rate b/c it would rely on diffusion of + ions from cytosol --> delaying myofibrils response
What are the regulatory proteins of myofibrils?
- Tropomyosin – protein polymer that wraps actin to prevent binding of myosin to actin (* cock blocker) (when muscle isn’t contracting)
- Troponin – turn on/off contraction à b/c its a Ca binding complex of 3 proteins, which positions tropomyosin
What are the giant accessory proteins in myofibrils?
- Titin – huge elastic protein (largest, 25,000 AA)
*returns muscle to rest place*
- Nebulin – inelastic huge protient hat attaches to z disk from thin filaments (helps align actin)
What is muscle tension?
- The force created by contracting muscles
What is the weight or force that opposes contraction of muscle?
What does cross-bridging movement of actin and myosin result in?
- Overlapping of actin and myosin slide pass each other (energy dependent) during contraction resulting in the sliding filament theory of contraction
How can you stop muscle from contraction?
- Decrease the level of Ca in cytosol
- Ca2+ ATPase pumps Ca2+ back in to the sarcoplasmic reticulumà stops Ca2+ from binding to troponin
What happens when sarcomere contracts during contractions?
- The sarcomere gets shorter b/c myosin binds to actin forming a power strike (overlapping in H zone)
What is the power strike?
- - Occurs during contraction, in which Ca binds to troponin -->
- allows tropomyosin to shift -->
- creates myosin binding site to open-->
- myosin hydrolyses ATP (releases Pi ) -->
- crossbridge tilting of 45 degrees from 90
What happens when ATP is hydrolyzed in the myosin?
- ATP releases Pi leaving ADP
- The myosin head moves from 90 degrees to 45 (cock blocker is removed)
- Head swivels and swings toward M line
What is excited-contraction coupling?
- Process in which muscle Ψ initiates ca signals at neuromuscular junction
- --> turns on contraction – Relaxation cycle (muscle twitched)
The 4 major components of excited contraction coupling?
- Release of Ach by a somatic motor neuron
- Ψ of myofibrils
- Increase in Ca2+ from sarcoplasmic reticulum
- Ca binds to troponin
What is a muscle twitched?
- Single muscle contraction-relaxation cycle
What is the neurotransmitter of neuromuscular junction?
What are the two unique things about skeletal muscle?
- Cant initiate there own contraction
- Are not control directly by hormones
What does acetylcholine bind to in neuromuscular junction?
- Motor end plate (receptors)
- These receptors allows influx of Na --> Ψ b/c more Na in cell due to ∆ membrane
What is the calcium channels involved in the t-tubules?
- Dihydropyridine channels (DHP) (voltaged gated)
- DHP is mechanically linked to ryanodine recptors channels on SR
What are the main proteins involved in restoring the system back to normal (contraction)?
- Myosin ATPase – crossbridge mov’t and relase
- Ca ATPase – collect excess ca in cytosol and pumps back to SR
- Na – K ATPase – restores the amount of Na in cytosol to initial state (in order for another contraction to occur)
What are the factors that causes muscle fatigue?
- Physical – muscle cant generate power input
- - Psychological – (central fatigue) long day at work
- --> tired --> party --> you rally
What are the proposed mechanisms of fatique that occur in neuromuscular junction and Ec - coupling?
- Decrease in Neurotransmitter release (dosnt occur w/normal excesice)
*Ach not synthesized fast enough in axon to keep up with firing rate
*threshold at motor end plate not reachedà no Ψ in t-tubule (due to in activity of Na – K ATPase)
What are the proposed mechanisms of fatique that occur in Ca2+?
- depletion of glycogen stored in muscle --> leak of Ca2+ from SR
- increase in Pi from phosphocreatine in muscle fiber b/c Ca2+ binds to it to form Ca2+ phosphate (major in fatigue)
What are the difference between red muscle (oxidative fibers) differ from white muscles (glycotic
- White muscles have less myoglobin, O2 larger diameter few BV --> run out of O2 --> rely on aerobic glycolysis --> faster fatigue
- Red muscle have more myoglobin --> red color --> 02 binding pigment à more oxygen diffusion due to smaller diameter --> rely on glucose
*Better oxidative phosporylation for ATP production*
What happens when the sarcomere length is shorter the optimal resting length?
- The actin and myosin will overlap before the initial contraction begins
- Preventing crossbridge formation (mov’t of actin by myosin ATPase)
what is the difference between summation of incomplete (unfused) and complete tetanus?
- Incomplete has action potential that are close together w/ a slight point and reaches maximum tension
- Complete tetanus also reaches maximum tension, but the Ψ does not relax between stimulus --> steady tension
( fatigue causes lost of tension even when continuous stimulus)
How can we increase the tension that developed?
- We can change the rate of the Ψ in muscle fiber
How can muscles create graded contraction of varying forced and duration?
- Muscles are composed of multiple MU of different type (diversity)
§ Changing the type of MU that are active
§ Changing the number of MU that are responding
What happens during isotonic contraction?
- Creates force and moves load (bicep curls)
§ Primary muscles shortens
What happens during eccentric contraction?
- Resisting the weight from pulling down completely
§ Muscles have a delayed muscle sorness
What are isometric contraction?
- - Contraction that
- create force w/o moving load (front/lateral raises)
§ Muscles doesn’t shortens b/c load is not being moved
§ Not enough force is created to move load
Why does the muscle shorten during isotonic contraction?
- b/c the sarcomere shortens more after the elastic components are stretched
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