Muscle tissue Flashcards
Recall: 3 types of muscular tissue found throughout the body
Smooth (non-striated, involuntary) – found in organs (e.g. stomach, blood vessels, arrector pili, esophagus, uterus etc.).
Cardiac (striated, involuntary) – found only in the heart (more on this later and in AP200).
Skeletal (striated, voluntary) – most numerous (you’ve learned the names, origins, insertions, actions, innervation, & blood supply of these in Myo100).
4 Functions of muscular tissue:
Produces the body movements necessary for survival as humans. I.e. Walking, running, grasping, talking, digestion, movement of food, manipulation etc.
Postural and stabilization of form. I.e. Standing and sitting erect. The erector spinae muscles keep your spine erect. The posterior cervical muscles keep your head upright.
Storage and transference of substances within the body. Our muscles store ions, glycogen (body’s stored form of energy), and enzymes used throughout the body during normal metabolism. Also, muscles act as gate keepers – sphincters – to regulate movement of substances from one area to the next. (e.g. esophageal & urinary sphincter)
Thermoregulation. Heat is released as a by-product of normal muscle metabolism.
Shivering is an involuntary response of skeletal muscle to generate body heat to raise body temp when the environment is cold (it is an involuntary response using voluntary muscles).
You cannot stop yourself from shivering if you are cold.
4 key properties of Muscle Tissue
Excitability – the ability to respond to a stimulus – e.g. electrical signals from the nervous system or chemical signals from the endocrine system.
Contractility – the ability to shorten and contract, forcefully. This in turn generates movement.
Extensibility – the ability to stretch (lengthen) without damage to its own tissue.
Elasticity – the ability to return to its original length.
C. Skeletal Muscle Tissue Anatomy:
Periosteum – recall the layer of connective tissue that acts as the skin for the bone. This is continuous with the outer layer of the tendon and the muscle itself (epimysium) which is made of dense irregular connective tissue.
Fascia – connective tissue that surrounds muscles and lies under the skin
2 types of fascia
Superficial fascia – separates muscle from the skin (1st layer we encounter when pealing back the epidermis and dermis) – also known as the subcutaneous layer or hypodermis. Recall that this layer is densely packed with nerves, blood vessels, adipose tissue, connective tissue, & lymphatic vessels.
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Deep (investing) fascia – dense (fibrous) connective tissue which surrounds a muscle or a group of muscles (forming fascial compartments). Allows for free movement of muscles and fills the space between them.
Deeper to the investing fascia are the following layers specific to muscles:
Epimysium – tissue layer that encircles the entire muscle (dense irregular connective tissue) i.e. The entire biceps brachii muscle.
Tendon
– dense regular connective tissue that extends from the muscle to attach to the bone (can be continuous with epimysium, perimysium, and endomysium) – typically shaped as long, cylindrical, and tubular.
Aponeurosis
– similar to a tendon (same type of tissue) however it is broad and flat. It serves to attach muscles to bone or muscles to muscles. For e.g. Epicranial aponeurosis, thoracolumbar fascia.
Synovial tendon sheaths
– “skin for tendons”. In certain areas of the body, certain tendons are subject to high levels of stress, therefore require an extra layer of connective tissue to prevent wear and tear.
Muscle fiber
– AKA – “muscle cell” – stores each of the individual muscle filaments (thick and thin)
Microscopic Anatomy of Muscle Fibers
[Diagram 10.2 pg 306] – microanatomy
Muscle fibers develop from myoblasts (immature muscle cells) and are the fundamental unit of muscles. The terms ‘muscle fiber’ and ‘muscle cell’ are interchangeable.
The number of muscles fibers is predetermined at birth and therefore these cells DO NOT subsequently undergo mitosis. They may grow, heal, and adapt but NOT increase in number (they undergo hypertrophy but NOT hyperplasia).
Hypertrophy
– Increase in size of the muscle (E.g. lifting weights). The excessive stress causes microscopic muscle tears, stimulating repairs and causing the cells to increase in size.
Hyperplasia –
Increase in the number of fibers (this occurs only for a limited time frame during embryonic development)
Muscle cells exit the cell cycle at G0 phase
“Atrophy”
– loss of myofibrils and therefore size of the muscle fiber (due to lack of use). For example, after a muscle has been in a cast for 2 months due to a fractured bone.
Fibrosis (scar tissue
) – damage to muscle fibers and replacement by fibrous scar tissue. Causes include strains, tears, overuse, & most acute traumas to muscles.
. Histology:
Satellite cell
– mature myoblast that persist to help with muscle repair
Myoblasts
– immature muscle cells derived from mesenchymal cells that fuse to form mature muscle cells.
Sarcolemma
– plasma membrane of a muscle cell
Sarcoplasm
– cytoplasm of the muscle cell
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Myoglobin
– protein found only in muscle fiber; binds O2 which is needed for ATP production
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Myofibrils
– contracting organelles of a skeletal muscle fibe
Sarcoplasmic reticulum (SR
) – smooth membranous sacs that encircle and surround each myofibril. Stores Ca2+ for release into the myofibril (very similar to the endoplasmic reticulum in other cells).
Sarcoplasmic reticulum (SR
) – smooth membranous sacs that encircle and surround each myofibril. Stores Ca2+ for release into the myofibril (very similar to the endoplasmic reticulum in other cells).
Triad: consists of: Transverse tubules (T-tubules)
– tiny invaginations of the sarcolemma which allow nerve impulses to activate the SR.
Surrounded by:
Terminal cisternaes – enlargements of the SR.
Filaments
– found in the myofibril (organelle) – 2 main types (named after their size)
- Thick – 15 nm in diameter – made of myosin protein.
- Thin – 7 nm in diameter – made of actin, troponin, & tropomyosin proteins.
1 nm (nanometer) is 1/1,000,000,000 of a meter (10-9)
(FYI – 1 HIV virus has a diameter of 140 nm)
Note: Thick and thin filaments are arranged in a staggered pattern within a sarcomere (functional unit of a muscle). This is what gives skeletal muscles their characteristic striations.
F. Muscle Proteins
– divided into 3 main categories:
Contractile – main components that generate the force – includes:
i) Myosin
– makes up thick filaments; shaped like “golf clubs” twisted together
ii) Actin
– makes up thin filaments; akin to “golf balls” that are the attachment sites of the myosin heads
B. Regulatory
– helps alternate between contraction & relaxation
i) Troponin – found on thin filaments; functions as a calcium binding site
ii) Tropomyosin – found on thin filaments; functions to block the myosin binding site during muscle relaxation.
i) Troponin
– found on thin filaments; functions as a calcium binding site
ii) Tropomyosin
– found on thin filaments; functions to block the myosin binding site during muscle relaxation.
C. Structural – helps stabilize the entire structure and provide elasticity and extensibility
i) Titin (3rd most plentiful) – anchors a thick filament from m-line to z-disc; helps return the filaments to the original positions after full stretch or contraction.
ii) Myomesin
– forms the M-line; helps stabilize thick filaments
iii) Nebulin
– helps anchor the thin filaments to the Z-discs
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Anatomy of a Sarcomere: (you need to know this!!!)
A-band –
entire length of thick filaments with ends overlapping thin filaments (“a” in dark b/c of both types of filaments overlapping each other)
I-band
– light b/c of thin filaments only, no thick filaments (“i” in light [not dark], no thick filaments)
Z-discs
– protein structures located on the Z-line (they help stabilize the filaments)
Z-line
– the lines that dictate the terminal ends of 1 sarcomere unit.
M-line
– the middle of the sarcomere (“midline”) – passes through the middle of thick filaments
H-zone
– the middle portion of the A-band of thick filaments only, no thin filaments.
Zones during contraction:
Z-lines/discs come closer together, as sarcomere shortens.
H-zone shrinks/disappears
I-band shrinks
A-band – remains the same size (it never changes length!!!)
Sliding filament theory:
Currently the most widely accepted model of muscle contraction:- Myosin heads attach to each actin ball, and slide the 2 Z-lines closer together, thus shortening the sarcomere (and the overall muscle).
4 key steps:
- ATP hydrolysis - ATPase cleaves ATP into ADP and releases a high energy P+ group
- Formation of cross bridges - Ca++, from the SR binds to troponin and changes troponin-tropomyosin complex shape and slides it out of the way to allow myosin and actin to bind
- Power stroke – cross bridge rotates towards center of sarcomere and slide the complex towards the middle
- Breaking of cross bridges - another molecule of ATP binds to the cross bridge and releases the myosin from actin.
This process continues as long as
ATP and Ca2+ are readily available.
Length–tension relationship:
Explains how the overlap between thick and thin filaments determines the amount of force that is generated by the muscle contraction
See [Fig 10.9 pg 302]
When a muscle is in its optimal range of overlap (b/w thick and thin filaments), there is the potential to achieve maximum force during contraction (ideal sarcomere length is about 2.0-2.4 µm).
When the sarcomere lengths are too short or too long there is less potential to achieve maximum force during contraction.
G. Excitation-Contraction coupling
:
Ca2+ ions are the key to muscle contraction. Ca2+ ions are found everywhere in muscle, however in a relaxed state, there are HUGE amounts stored in the SR. When an action potential reaches the SR, it signals a HUGE release and influx of Ca2+ into the sarcoplasm. This is done via Ca2+ release channels. Ca2+ binds to troponin, tropomyosin slides out of the way, myosin is now able to bind to actin => contraction follows. This is excitation/contraction coupling!!!
Post contraction Ca2+ is restored in the SR via Ca2+ active transport pumps in the SR membrane (recall primary active transport from cell biology).
Also, a binding protein called
calsequestrin helps bind to and store Ca2+ in the SR for the next muscle contraction phase.
Resting muscles have a [Ca2+] 10,000X more in the SR than in the cytosol!!!
this allows a continuously stored amount of calcium available for muscle contraction. (recall that Ca2+ must be tightly regulated between 9-11mg/100ml of blood). Hypocalcemia will result in lack of Ca2+ available for muscle contractions.
Rigor mortis
– state of total muscle rigidity – there is no muscle relaxation b/c there is no energy (ATP) left to fuel the detachment of cross bridges. This happens hours post mortem and disappears in about 24 hours d/t enzymes
Strain
– excessive force on muscles that cause the fibers to tear. Can have accompanying bleeding, pain, lack of function and fibrosis. (Muscles strain, ligaments sprain!!!)
Cramps
– painful, sudden, spasmodic contraction of muscle fibers due to extended usage, lack of blood flow, dehydration, lactic acid and other toxic build ups.
