What are the three types of muscle tissue?
Smooth (non-striated, involuntary)
Cardiac (striated, involuntary)
Skeletal (striated, voluntary)
What are the four functions of muscle tissue?
- produce movement
- posture and stability
- storage and transference of substances (ions, glycogen, enzymes; sphincters)
- heat generation
What are the 4 key properties of muscle tissue?
- excitability
- contractibility
- extensibility
- elasticity
Periosteum
The layer of dense, irregular connective tissue that surrounds the bone and is continuous with synovial tendon sheath of the muscle.
Fascia
Fibrous connective tissue that surrounds the muscle.
What are the two fascial layers?
Superficial
Deep
Superficial fascia
Separates muscle from skin.
AKA subcutaneous or hypodermis fascia
Deep (investing) fascia
Surrounds muscle or a group of muscles and lines body wall.
Holds muscle of similar function together. Allows for free form movement of muscles.
Epimysium
Dense irregular connective tissue layer that encircles the entire muscle.
Perimysium
Dense irregular connective tissue that encircles a fascicle
Fascicle
A bundle of (ten or more) muscle fibres
Endomysium
Tissue layer that encircles and separates each individual muscle fibre within a fascicle
Tendons
Dense regular connective tissue that connect muscle to bone.
Can be continuous with epimysium, permysium and endomysium.
Long, cylindrical and tubular
Aponeurosis
Similar to a tendon, but broad, thin and flat.
Attaches muscle to muscle, or muscle to bone.
Synovial tendon sheaths
Skin for tendon.
Present where tendons are subject to high levels of stress.
Muscle fibre
AKA. Muscle cell
Stores each of the individual muscle filaments (thick and thin)
Develop from myoblasts and are the fundament unit of muscles
Hypertrophy
Increase in size. Muscles do this.
Hyperplasia
Increase in number. Muscles don’t do this.
Atrophy
loss of myofibrils and therefore size of muscle fibre.
Fibrosis
Damage to muscle fibres and replacement by fibrous scar tissue. Occurs when the number of satellite cells can’t keep up with the demand for new myofibrils.
Satellite cell
A mature myoblast that hasn’t transformed.
Aids in muscle repair. Still capable of mitosis (to create more satellite cells).
Myoblasts
Immature muscle cells derived from mesenchymal cells that may fuse with each other to form a mature muscle fibre (or may persist as satellite cell)
Sarcolemma
Plasma membrane of a muscle cell
Sarcoplasm
Cytoplasm of a muscle cell
Myoglobin
Protein found only in muscle cells, that bind O2 for ATP production
Myofibrils
Contracting organelles of skeletal muscle cells.
Myofibril vs muscle fibre
Muscle fibre: muscle cell. Contains myofibrils
Myofibrils: contractile organelles within muscle fibres
Parenchyma
Functional tissue of an organ
Muscle triad
One transverse tubule (T tubule), plus
Two terminal cisternae
Transverse (T) Tubules
Invagination of the sarcolemma, which go from the surface toward the centre of each muscle fibre
Filled with interstitial fluid
Muscle action potentials travels through the T tubules
Terminal cisternae
Enlargement of the sarcoplasmic reticulum, which butt up against T tubule
Ca2+ stored in the SR are released through the terminal cisternae, triggering muscle contraction.
Sarcoplasmic Reticulum
Smooth membranous sac that encircle and surround each myofibril
Stores and releases Ca2+ into the sarcoplasm to help with muscle contraction
Filaments
Contained within myofibril. Two types: Thick and thin.
Arranged in a staggered pattern within 1 sarcomere (z-line to z-line)
Overlap of thick and thin filaments give muscles their striated appearance
Thick and thin filaments pulling on each other are effectively muscle contractions
Thick filaments
1-2 micrometers long. 16 nanometers wide.
Made up of MYOSIN protein
Thin filaments
1-2 micrometers long. 8 nanometers wide.
Made up of ACTIN, TROPONIN, and TROPOMYOSIN proteins
What are the three types of muscle proteins?
Contractile
Regulatory
Structural
Contractile Proteins
Main components that generate force.
- Myosin
- - make up thick filaments - Actin
- - make up thin filaments
Structural Proteins
Help stabilize the entire structure
- Titin
- Mysomesin
- Nebulin
- Dystrophin
Titin
Third most plentiful structural protein
Anchors thick filament from m-line to z-disc.
Helps return filaments to their original position after contraction.
Myomesin
Structural protein.
Forms the M-line. Helps stabilize thick filaments
Nebulin
Structural protein
Anchors thin filaments to z disc
Dystrophin
Structural protein
Help link thin filaments to sarcolemma for stability.
Lacking in muscular dystrophy
Sarcomere
Arrangement of filaments inside a myofibril.
Smallest contractile unit of muscle.
Z disc to Z disc
A Band
Entire length of thick filament with ends overlapping thin filaments. Dark.
I band
Section with only thin filaments. Light.
A Z-band passes through the centre of each I-band
Z Disc
Protein structures located on the Z line.
Help stabilize filaments.
Z line
Lines that dictate the terminal end of one sarcomere unit.
M Line
The exact middle of the sarcomere. Passes through the middle of thick filaments.
Formed by myomesin
H Zone
The middle portion of the A Band of thick filaments only.
No thin filaments.
What happens during the zones during contraction?
Z lines/discs: come together as sarcomere shortens
H zone: shrinks/disappears
I band: shrinks
A band: NEVER CHANGES LENGTH
What are the four steps to the Sliding Filament Theory?
- ATP hydrolysis
- Formation of cross bridge
- Power stroke
- Breaking of cross bridges
Continues as long as ATP and Ca2+ are available.
ATP hydrolysis
First step of contraction. ATP is attached to myosin head. ATPase cleaves ATP into ADP and releases P. Myosin is energized and reoriented.
Formation of cross bridges
Second step of contraction. Ca2+ from the SR binds to the troponin, changes troponin-tropomyosin complex, and slides tropomyosin out of the way to allow myosin and actin to bind.
Regulatory proteins
Help alternate between contraction and relaxation
Troponin
Tropomyosin
Troponin
Found on thin filaments. Ca2+ binding site.
Assists tropomyosin in blocking myosin binding site during relaxation.
Tropomyosin
Found on thin filaments. Functions to block the myosin binding site during relaxation. Needs to be moved out of the way for contraction to occur.
Power stroke
Third step of contraction. Cross bridge rotates towards centre of sarcomere.
Breaking of cross bridges
Forth (and final) stage of contraction. Another molecule of ATP binds to the cross bridge, causing the conscious uncoupling of myosin and actin.
Length-tension relationship
The degree of overlap between thick and thin filaments will determine the amount of force generated by the contraction. Optimal range is around 2-2.4 microns
Calsequestrin
Binds to and helps to store Ca2+ in the SR for the next contraction phase.
Excitation-Contraction Coupling
Describe the steps that connect excitation to contraction.
Ca2+ stored in SR when muscle relaxed.
When Action Potential reaches SR, Ca2+ release channels in the SR open, and CA2+ floods the sarcoplasm.
– Ca2+ levels in sarcoplasm raise tenfold
One Ca2+ molecule binds with one troponin molecule, causing it to change shoe, which moves tropomysosin away from the myosin binding sites on actin.
Power stroke –> contraction
When AP stops, Ca2+ pumps move Ca2+ back into the SR
Rigor Mortis
Total muscle rigidity, occurring within hours of death, because without ATP the muscles don’t relax.
In around 24hrs, enzymes breakdown the cross bridges and so rigor mortis stops.
DOMS
Delayed Onset Muscle Soreness
Satellite cells use amino acids to create new protein for repairs. Hence all those protein recovery drinks.
Strain
Damage to muscles, caused by excessive force which tear fibres.
Cramps
painful, sudden, spasmodic contraction of muscle fibres due to extended usage, lack of blood flow, dehydration or other toxic build up.
Action Potential
Electric impulse that causes changes in the membrane. Different channels open/close, and different chemicals are released.
Somatic motor neurons
Extend from central nervous system. Responsible for body movements.
Neuromuscular junction
Synapse between the axon of a neuron and muscle fibre. Usually at midpoint of the muscle fibre.
Not always 1:1
Synaptic cleft
Micro gap between axon terminal and muscle
Neurotransmitters
Chemicals that propagate a signal across the synaptic cleft
Acetylcholine (ACh)
The main NT active at the NMJ. Stored in synaptic vesicles on axon terminal side
Motor end plate
The side of the sarcolemma that contains the ACh receptors (ligand-gated).
AKA the post-synaptic side
What are the steps involved in generating an Action Potential at the NMJ?
- Release of ACh
- Activation of ACh receptors
- Production of AP
- Termination of ACh
Release of ACh
Arrival of nerve impulse at synaptic end causes voltage-gated Ca2+ channels to open. Ca2+ flows in (down concentration gradient), which stimulates ACh vesicles to undergo exocytosis. ACh then diffuses across synaptic cleft.
Activation of ACh receptors
Two molecules of ACh bind to a receptor on motor end plate, which opens an ion channel in the ACh receptor. Small cations (namely Na+) flow down electrochemical gradient across membrane.
Production of muscle action potential
The influx of Na+ makes inside of muscle fibre more positively charged, generating a post-synaptic action potential, which propagates along the sarcolemma in both directions (towards origin and insertion).
AP eventually travels down T-tubules, causing Ca2+ to be released from the sarcoplasmic reticulum => sliding filaments
Termination of ACh
ACh is broken down by acetylcholinesterase (ACHE), an enzyme attached to collagen fibres in the ECM of the synaptic cleft.
Botox
Derived from clostridium botulism. Blocks release of ACh from axon terminal, preventing contraction.
How long can cardiac muscle contractions last?
10-15 x longer than skeletal muscle (due to lots of Ca2+ in SR and interstitial fluid.
Autorhythmicity
Cardiac muscle’s ability to generate its own action potential. Also present in visceral smooth muscle
What are the two cardiac nodes?
Sino-Atrial (upper half, atrium, natural pacemaker)
Atrial-Ventricular (lower half, ventricles)
What do cardiac nodes do?
Responsible for electrical signals of the heart => staggered lub dub rhythmical contractions
Average heart rate
75 bpm
Intercalated Discs
In cardiac muscle, increased/thickened areas of the sarcolemma made up of gap junctions and desmosomes.
Unique to cardiac muscle
Connect ends of muscle fibres to each other.
Fasciculation
Small, voluntary, local, muscle contraction and relaxation visible under the skin arising from the discharge of a bundle of fascicles. Benign, mostly harmless, many causes.
What are the two types of smooth muscle?
Visceral (single unit)
Multi-unit
Why doesn’t smooth muscle appear striated?
Thin and thick filaments don’t have a regular pattern of overlap.
Dense bodies
What smooth muscle thin filaments and intermediate filaments attach to. Functionally similar to z discs
Intermediate filaments
In smooth muscle.
Bundles of intermediate filaments connect dense bundles. Makes fishnets for muscle fibre.
During contraction, tension transferred to intermediate filaments.
Caveolae
In smooth muscle, pouch-like invaginations that contain Ca+
Calmodulin
In smooth muscle, a protein that binds to Ca+ (functionally similar to troponin)
How is smooth muscle different from skeletal muscle?
Autorhythmicity (in visceral)
Dense bodies instead of Z discs
Not striated (irregular placement of thick and thin filaments)
Intermediate filaments
Caveolae instead of SR (present, but scarce)
Dense bodies instead of Z discs
Calmodulin instead of troponin
Slower contractions (onset and duration)
Can stretch and distend a lot more.
Three forms of muscle metabolism
Creatine Phosphate
Anaerobic metabolism
Aerobic metabolism
Creatine Phosphate
Produced in liver, pancreas and kidneys; stores in muscle.
Provides enough energy for about 15 seconds of activity
ATP + creatine –CK–> ADP + creatine phosphate (at rest – storing excess Energy)
Contraction: Creatine phosphate + ADP –CK–> creatine + ATP
Creatine Kinase
The enzyme that catalyzes both the formation of creatine phosphate and it’s breakdown into creatine + ATP
Anaerobic metabolism
Occurs in absence of oxygen, in cytoplasm of cells.
Breakdown of glucose (glycolysis) into 2 molecules of ATP + 2 molecules of pyruvic acid (which goes into aerobic metabolism).
30-40 seconds of activity.
Aerobic metabolism.
Requires oxygen
Occurs in mitochondria.
Pyruvic acid (from glycolysis) and fatty acids and amino acids –> Krebs Cycle & Electron transport chain –> many ATP
Also produces heat, H2O and CO2
O2 from hemoglobin and myoglobin
Muscle fatigue
Inability to maintain forceful contraction after prolonged periods.
Oxygen debt
Aka recovery oxygen uptake
The period following strenuous exercise following strenuous exercise where the body continues to attempt to replenish the normal resting values of O2 in tissues.
Motor unit
A somatic motor neuron and all the muscle fibres it innervates.
In general, the finer the movement, the fewer muscle fibres per motor neuron.
Averages 1 neuron/150 muscle fibres.
Twitch Contraction
brief contraction of all the muscles in a motor unit.
Very brief (20-200 msec)
Electromyography
Electrodes used to determine muscle activity and to diagnose certain conditions. Prints out a myogram.
Wave summation
Muscle stimuli arriving at different times. Cause larger than normal contractions.
Unfused tetanus
aka incomplete tetanus
Sustained but wavering contraction due to stimuli arriving 20-30 times/second.
Fused tetanus
aka complete tetanus
Completely sustained contraction due to stimuli arriving 80-100 times/second. Fibre has no time to relax
What are the four stages of contraction?
Latent
Contraction
Relaxation
Refractory
Latent Period
Action potential sweeps the sarcolemma and Ca2+ is released
Contraction Period
Ca2+ binds to tropomyosin, cross bridges form, contraction occurs
Relaxation period
Cross bridges break, Ca2+ is taken up and restored
Refractory period
Period in which a subsequent AP will not be able to generate a muscle contraction. A period of lost excitability
Motor Unit Recruitment
Recruit smaller fibres first, then larger – increase the number of motor units used to meet duration/force demanded. Allows for smooth, fluid contraction
Muscle tone
The amount of tension/tautness of a muscle during contraction or at rest.
Flacid paralysis
Loss of muscle tone, loss of reflexes, atrophy and degeneration.
West Nile virus, polio, myaesthenia gravis, spinal cord injury
Rigidity
increased muscle tone with no effect on reflexes (i.e. Tetanus)
Red Muscle Fibres
Have lots of myoglobin, mitochondria, blood supply. Dark meat.
White Muscle Fibres
Not so much myoglobin, mitochondria, blood supply. White meat.
Slow Oxidative (SO) Fibres
smallest in diameter (least amount of myofibrils)
Weakest
Appear dark red. Many mitochondria, capillaries –> aerobic metabolism
Slow contractions, but good endurance. Marathons
Fast oxidative glycolytic (FOG) fibres
Intermediate in diameter.
Appear red. Many mitochondria and capillaries (aerobic), and also high levels of glycogen so also anaerobic. Sprints.
Fast Glycolytic (FG) fibres
Largest in diameter (most myofibrils)
Fewest myoglobin, capillaries, mitochondria. Generate ATP from glycolysis
Strongest contraction for the shortest amount of time.
Power lifters, pitchers.
What are the three types of leverage?
Ist class EFL (see saw/posterior neck) 2nd class FLE (wheelbarrow; calf muscles) 3rd class FEL (biceps brachii)
Muscle spindles
Proprioceptors found in muscles that adjust to changes in muscle length
Intrafusal muscle fibres
In muscle spindles.
3-10 specialized fibers in muscle belly that deliver sensory information to the nervous system.
Gamma motor neuron
Terminates near the ends of the intrafusal fibres.
Adjust the tension of the muscle spindle.
As the frequency of gamma neurone stimulation increases, the muscle spindle becomes more sensitive to stretching.
Extrafusal muscle fibres
Ordinary contractile muscle fibres found outside the muscle spindle
Alpha motor neuron
Motor neurons that innervate the extrafusal fibres.
Golgi Tendon Organs
Monitor the tension/force that is translated from muscle contraction and help the muscle relax.
Located at músculo-tendonous junction.
Muscular Dystrophy
X-linked, recessive disorder in which the protein responsible for muscle stability during contraction is lost –> unstable sarcolemmas. Self-limiting.
Causes loss of coordinated movement, cardiac and respiratory failure.
Myasthenia Gravis
An autoimmune disorder in which the body produces antibodies which block the ACh receptors, preventing contraction. Possible thymus involvement.
Fibromyalgia
Idiopathic musculoskeletal condition involving muscles and connective tissue. Pain, headaches, insomnia, fatigue, depression.