Nakamura Human Physiology Lecture 6 Flashcards
(18 cards)
Skeletal muscle
-Composed of individual muscle fibers. (Cells)
•Contract when stimulated by motor neuron. (Somatic)
•Motor neuron innervates several muscle fibers. (Bouton attaches to muscle fiber at motor end plate of muscle fiber)
-called neuromuscular junction
•Activation of varying numbers of muscle fibers causes gradations of strength of contraction.
Structure and actions
Skeletal muscle attached to bone on each end by tendons.
•Tension on tendons by muscles cause movement of the bones.
•Insertion:
–More movable attachment.
•Origin:
–Less movable attachment.
Motor unit
-Each motor neuron and all of the muscle fibers it innervates
•Each muscle fiber receives a single axon terminal from a motor neuron.
•Each axon has collateral (a side branch) branches to innervate several fibers.
-ventral horn and ventral roots
-When somatic neuron activated, all the muscle fibers it innervates contract with all or none contractions.
Innervation ratio
.motor neuron/muscle fibers):
–Small motor units are involved in finely controlled movements
Recruitment
Activation (spatial recruitment) of larger motor units increases the contraction strength.
Mechanisms of contraction characteristics
-neuromuscular junction, this occurs in muscle (receptor)
•Na+ diffuses into and K+ out of the membrane (Ach-Nicotinic receptors: Na+ > K+ causes EPSP).
•End-plate potential occurs (depolarization).
•+ ions are attracted to negative membrane.
•If depolarization sufficient, threshold occurs, producing AP.
Structure of skeletal muscle
-Epimysium:
–Fibrous sheath.
-layer of connective tissue (dense irregular)
-covers entire muscle
-continuous with fascia and endomysium and perimysium
•Fascicles:
–Columns of muscle fibers (bundle of skeletal muscle fibers)
-fascia is thickened connective tissue that envelops a group of muscles
-all the sheaths fuse together to become the tendon
-entire muscle is organ
-endomysium is connective tissue, surrounds the sarcolemma (cell membrane)
•Contain same organelles as other cells.
Single muscle fiber
- nucleus located peripherally (sides)
- cell membrane: sarcolemma
- cytoplasm: sarcoplasm
- within cells myofibrils
- within myofibrils are filaments(actin and myosin)
Myofibrils
.Each myofibril contains myofilaments.
•Thick filaments:
–primarily composed of myosin
•Thin filaments:
–primarily composed of actin
–Center of each I band is Z line.
–Sarcomere: functional unit of striated muscle:
•Z line to Z line (z disk)
-h band: only thick
-A band: thick and thin
-I band: only thinSliding filament theory
-Sliding of filaments is produced by the actions of cross bridges.
•Cross bridges are part of the myosin proteins that form arms that terminate in heads.
•Each myosin head contains an ATP-binding site (ATP-adenosine 5’-triphosphate).
•The myosin head functions as a myosin ATPase.
-thick filaments pulls thin closer together
-z disks get closer, thick filaments don’t move
Mechanisms of contraction steps
-AP travels down the motor neuron to presynaptic terminal
•VG Ca2+ channels open, Ca2+ diffuses into the terminal
•Ca2+ causes vesicles of NT to fuse with presynaptic membrane
•ACh released into neuromuscular junction
•ACh binds to nicotinic ACh receptor
•Chemical gated channel for Na+ and K+ open (end plate potential, EPP)
EEP (mechanisms of contraction continued)
,EPP in muscle fiber always reaches threshold and evokes a muscle fiber action potential
•1 action potential in motor neuron evokes 1 muscle fiber action potential
•AP on muscle fiber membrane (sarcolemma) travels into transverse tubules (T-tubules)
•Depolarization of T-tubules activates Ca2+ release channels in sarcoplasmic reticulae (where calcium is stored in muscles)
Role of calcium in muscle contraction
-Stimulated:
•Ca++ is released from SR.
•Ca++ attaches to troponin
•Tropomyosin-troponin configuration change (Ca++ causes troponin/tropomyosin complex to move
•Myosin heads bind to actin filament and undergo a powerstroke (energy released): sliding filaments
Steps in mechanism contraction
-AP travels down the somatic motor neuron to bouton.
•VG Ca++ channels open, Ca++ diffuses into the bouton.
•Ca++ binds to vesicles of NT.
•ACh released into neuromuscular junction.
•2 ACh binds onto receptor in sarcolemma .
•Chemical gated channel for Na+ and K+open (depolarizes)
-end plate potential produced
-EEP conducted along transverse tubule (t tubule)
-opens voltage gated calcium channels
-calcium is released from Sarcoplasmic reticulum
-calcium diffuses out into sarcoplasm
-in the myofibrils, calcium binds to troponin, stimulating contraction
Contraction (crossbridge cycle overview)
-Myosin binding site splits ATP to ADP and Pi.
•ADP and Pi remain bound to myosin until myosin heads attach to actin.
•Pi is released, causing the power stroke to occur.
Power stroke pulls actin toward the center of the A band.
•ADP is released, when myosin binds to a fresh ATP at the end of the power stroke.
•Release of ADP upon binding to another ATP, causes the cross bridge bond to break.
•Cross bridges detach, ready to bind again.
Regulation of contraction
.Regulation of cross-bridge attachment to actin due to:
–Tropomyosin.
–Troponin.
What leads to muscle fiber relaxation?
-ACh-esterase degrades ACh
•Ca2+ pumped back into SR
•Decrease in Ca2+ concentration causes toponin/tropomyosin complex to block the myosin binding site on actin
•No cross bridge formation; No contraction
Cross bridge cycle causing sliding filaments and muscle contraction
- Resting fiber: crossbridge is not attached to actin. ADP and Pi in myosin head,
- Cross bridge binds to actin
- Pi is released, causing conformational change in myosin
- Powerstroke causes filaments to slide
- ADP is released, a new ATP binds to myosin head, allowing it to release from actin
- ATP is hydrolyzed, causing cross bridge to return to original orientation
