Lecture 2 Flashcards
(21 cards)
Three types of muscle tissue
- Skeletal: voluntary skeleton
- planned executed movements
- moving muscles (and skeleton) - Smooth: involuntary hollow organs
- stomach, intestine, arterial blood vessels - Cardiac: involuntary heart
- heart muscles
Anatomy of Skeletal Muscles
Attach to tendons —> muscles —> fascicle —> bundles of muscle fibres
Skeletal muscles consists of 75% water (aqueous space), 20% protein, and the remainder is salts, enzymes, pigments, fats and carbohydrates
A myofibril is an individual unit that creates a big muscle fibre, which then multi bundles of muscle fibres create fascicles, which then create big muscles
Myofibrils and sarcomeres
Sarcomere - repeating units between Z lines; structural entity that makes of the functional unit of a muscle fibre
An individual myofibril is made up of millions of sarcomeres
Thin (actin) filaments
Thick (myosin) filaments
Make up the sarcomere
Myofilaments
The parts involved in muscle contraction…
- actin (thin filaments)
- binding of calcium
- troponin complex
- tropomyosin
- G actin - myosin (thick filaments)
- myosin tails point towards the centre of the sarcomere, and the heads (cross bridge) point towards the sides of the myofilaments band
The the m-line is in the middle and z-lines are on the ends
An average muscle fibre contains 4500 sarcomeres; 16 billion myosin and 64 million actin filaments
Skeletal muscle levels of organization
A - muscle
B - single myofibril
C - sarcomere unit
D - actin and myosin filaments
E - The different bands and lines in the sarcomere
F - the different patterns that appear when looking closely at a sarcomere
Other important structures
Mitochondria
Sarcoplasm or cytosol or cytoplasm
- store fat and carbohydrates in cytoplasm
Sarcolemma
Basa lamina
Sarcoplasmic reticulum
- netting that goes around myofilaments is SR
T-tubule system
- tube that allow things on the outside to bind with things on the inside
Neuronal systems that regulate movement
Brain to the spinal cord then to the nerves then to the t-tubules
Major divisions of the nervous system
Central nervous system: brain and spinal cord
Peripheral nervous system: cranial and spinal nerves
Sensory (afferent) nerves: somatic and visceral neurons (conduct impulses from receptors to CNS)
- sensors like heat
Effector (efferent) nerves: motor neurons (conduct impulses from CNS to effectors
- muscles
Autonomic: involuntary (conduct impulses from CNS to cardiac/smooth muscle and glands)
- heart, blood vessels
Somatic: voluntary (conduct impulses from CNS to skeletal muscle
Sympathetic: “fight or flight”
- stress response
Parasympathetic: “rest and digest”
- rest response
The motor neuron
Each muscle fibre generally receives input from only one neuron, yet a motor may innervated many muscle fibres because the terminal end of an axon forms numerous branches
Muscle fibre can receive only 1 motor neuron input at a time, but 1 motor neuron can give many muscle fibres
Axon of motor neurons extend from the spinal cord to the muscle. There each axon divides into a number of axon terminals that form neuromuscular junctions with muscle fibres scattered throughout the muscle.
The neuromuscular junction
One muscle fibre
A nerve impulse goes down a myelinated axon of motor neuron
Then to the axon terminal of neuromuscular junction
The muscle is wrapped underneath the sarcolemma of the muscle fibres and inside are the myofibrils
Neuromuscular transmission
acetylcholine (ACh) - triggers an electrical potential on the sarcolemma
- excites muscle membrane (sarcolemma) - creates voltage in sarcolemma
- changes permeability of membrane to sodium and potassium
- creates transmembrane voltage (changes membrane potential) - depolarization
- if electrical excitation threshold is reached an AP is triggered
- Sac-like vesicles within terminal axon release ACh, which diffuses across the synaptic cleft and attaches to specialized ACh receptors on the sarcolemma
- Muscle action potential depolarizes transverse tubules at the sarcomere’s A-I junction
- T-tubule system depolarization causes Ca2+ release from sarcoplasmic reticulum lateral sacs
Muscle fibre contraction
Muscle fibres shorten because myosin and actin interact in a manner that generates tensions and allows sliding of the filaments past each other without myofilaments changing length
Energy from ATP hydrolysis serves as the molecular motor to drive fibre shortening - ATP drives the myofilaments interaction
How muscles create movement …
-relaxed state (4.0um)
- no actin-myosin interaction occurs at binding site
- myofilaments overlap a little
- contracted state (2.7um)
- myosin head pulls actin toward sarcomere center (power stroke).
- filaments slide past each other
- sarcomeres, myofibrils, muscle fibre all shorten
Muscle contraction process
Muscle shortens or lengthens because protein filaments slide past each other without altering their length
- In the ready state, the myosin cross-bridge is tightly bound at a 45 degree angle to the actin filament
- ATP binds to myosin, allowing it to release from the actin filament
- ATPase on the myosin hydrolyzes the ATP to access energy, and the myosin head moves away from the actin filament. ADP and Pi remain bound to myosin
- The myosin head moves to 90 degrees and binds to a n actin molecule
- The myosin head releases Pi, which initiates the power stroke, where it tilts back to 45 degrees, pulling the thin filament toward the center of the sarcomere
- After the power stroke, the myosin head releases ADP and returns to the ready state. This process continues until the ends of the myosin filaments reach the z-disks, or until Ca+ is pumped back into the SR
A continuation/summary of the muscle contraction process
Happening at any given time to any given muscle
- Sac-like vesicles within terminal axon release ACh, which diffuses across the synaptic cleft and attaches to specialized ACh receptors on the sarcolemma
- Muscle action potential depolarizes transverse tubules at the sarcomere’s A-I junction
- T-tubule system depolarization causes Ca2+ release from sarcoplasmic reticulum lateral sacs
- Ca2+ binds to troponin-tropomyosin in actin filaments, which releases inhibition of actin combining with myosin
- Actin joins myosin ATPase to split ATP with energy release during muscle action. Tension from energy release produces myosin cross-bridge movement
- A muscle shortening occurs after ATP binds to the myosin cross-bridge, which breaks the. Actin-myosin bond and allows cross-bridge dissociation from actin and sliding of thick and thin filaments
- Cross-bridge activation continues when Ca2+ concentration remains high (from me,brand depolarization) to inhibit troponin-tropomyosin action
- When muscle stimulation ceases, Ca2+ moves back into the sarcoplasmic reticulum lateral sacs through active transport via ATP hydrolysis
- Ca2+ removal restores troponin-tropomyosin inhibitory action. With ATP present, actin and myosin remain in the dissociated relaxed state.
The contractile response
“Twitch” contraction
- muscle twitch contraction
- happens fast
- single twitch
An electrical pulse occurs - takes time to get to neuromuscular junction from skin
Then its not just Ca2+ released, thats why there is a curve on its way up, everything is released together
Length-tension relationship
Force from highest to lowest, the muscle is super shortened then lengthens a lot when there’s low force
Increase cross-bridge interactions + increase shortening capability = increase force (4,3,2)
Decrease cross-bridge interactions + increase shortening capability = decrease force (1)
Increase cross-bridge interactions + decrease shortening capability = decrease force (5) - strongest force
The contractile response
“Tetanic” contraction
A) series of twitch contractions - no increase in frequency
B) unfused tetanic contraction
C) fused tetanic contraction - increase frequency in twitches (more electrical impulses, more force)
Dynamic contractions
Regardless of the circumstances of the contraction, the interactions between the myosin heads and the actin filaments remain the same: cross-bridges engage the actin filaments and attempt to slide along them
Isometric:amount of filament overlap depends on the length of the muscle prior to activation. Cross-bridges repeatedly make and break connections with actin producing tension equal to the external load
- muscle contractions but does not shorten
- no change, maintaining the contraction
Concentric: in shortening contractions with a manageable external load, the sliding movement allows myosin to become completely overlapped by actin
- shortening contractions
Eccentric: in lengthening contractions, cross-bridges collectively generate less tension than the external stretching force applied to the muscle and the opposing actin filaments in the sarcomeres are pulled away from each other
- lengthiness contraction
Force-Velocity Relationship
Force (N) = load (kg) x gravitational constant (9.81m/s^2)
Po (Pmax = the highest force one can produce)
- lowest velocity, highest force
Vmax (how quickly Ca2+ can move in and out of—> creates velocity)
- highest velocity, lowest force
F=ma
N= (kg)(9.81m/s^2)
Power Output of Muscle
Power = force x velocity
Almost like a parabola
Fatigue
A loss in the capacity of the muscle to develop force and or velocity resulting from muscle activity under load and that is reversible by rest
Occurs from interrupting the chain of events between the CNS —> PNS —> NMF —> muscle fibres
Mechanisms are complex; some examples:
- alterations in CNS neurotransmitters (e.g. serotonin or dopamine)
- reduced stored muscle energy (e.g. glycogen)
- disturbance in T-tubule system
- impaired calcium release and re-uptake
If you rest long enough you can restore force
