An Introduction to Muscle Tissue

Three main classes of muscle

• Skeletal muscle = voluntary = connect bones

are used for complex coordinated activities.
Around digestive & urinary (sphincters)-can control when we go

• Smooth muscles = involuntary = surround

internal organs such as the large and small
intestines, the uterus and large blood vessels
Helps digest food in small intestine
• Cardiac muscle: Striated muscle of the heart.
Beats on its own
Muscular Tissue
Properties of Muscular Tissue

• Excitability
• Contractility =can extend
• Extensibility= goes back to its original place
• Elasticity

Functions
• Produce skeletal movement Bones are the levers
• Maintain body position = stay up; hold head
• Support soft tissues =protect organs
• Guard openings = mouth, digestive system, and urinary system
• Maintain body temperature = we can shiver
• Store nutrient reserves = glycogen Nutrient we can use during muscle contraction
Muscular Tissue - Contractility
Isometric Contraction = The muscle develops tension but does not
shorten. These are important to maintain posture and
support loads. Pushing against the wall & it cannot move. You are not the Hulk!

Isotonic Contraction = movement occurs.

o Eccentric isotonic contractions involve the lengthening of a muscle
during a contraction- i.e. putting down the weight
o A concentric isotonic contraction occurs when a muscle shortens
and pulls on another structure -- like a lifting a weight Shorting
Skeletal Muscle Structures
Muscles have three layers of connective
tissues
• Epimysium = An overcoat of dense irregular
connective tissue

• Perimysium = surrounds muscle fiber

bundles = fascicles = is made of dense
irregular connective tissue that surrounds
groups of 10- 100 or more individual muscle
fibers

• Endomysium = surrounds individual muscle

cells = muscle fibers
When we need to lift heavier things=recruit more muscle fibers

If I have to lift something light I might only have to use 10 muscle fibers, but
if I lift something heavy i might have to use 100 muscle fibers
Types of muscle fibers

Muscle fibers = muscle cells. Fibers are categorized based on the rate of
ATP hydrolysis, methods of ATP production, and rate of fatique.

Anerobic, fast
twitch

Runner would have more slow twitch fibers

If you do weight lifting you will have fast oxidative glycolytic fiber
Usian bolt will have more fast oxidative glycolytic fiber
Types of muscle fibers
Type I
Slow twitch oxidative fibers = are the smallest of the muscle fibers.
These fibers are fatigue resistant and have high amounts of ATP
o These fibers also have high amounts of myoglobin, and are usually
reddish in color.
o Slow twitch or type I fibers are dominant in muscles that help to
maintain posture. Running a marathon Keep upright=position

Dark red=lots of blood supply

Lots of myoglobin=holds onto O2 locally in your muscle
Lots of mitochondria to make ATP

Think of the tuna fish

Types of muscle fibers

Fast twitch oxidative fibers = intermediate fibers = are also fairly

fatigue resistant.
o These fibers are also red, with aerobic generation of ATP, and contain
many mitochondria
o Contractions are faster than in type I fibers. Sprinters have more
of these
o Used when walking
Usian bolt probly doesnt even relay on fast twitch oxidative fibers (type 2)

Fast twitch glycolytic fibers are the largest fibers that fatigue very easily,
with high levels of glycogen and low levels of mitochondria & myoglobin
(white).
Anaerobic = mostly used when doing short burst stuff like lifting weights
Look white like chicken breasts
Think the fish tilapia, not a very athletic fish
Muscle soreness

o Muscle soreness is a result of tiny tears in the muscle fibers- not

lactic acid build-up. Due to H+ accumulation Micro tears & H+ acculination
o When these tears happen, an inflammatory reaction occurs which
causes swelling =edema.
o Swelling and soreness peak 48h post workout, causing your muscles
to hurt more the second day.
o Micro-tears actually cause the muscle to become stronger when it is
rebuilt. ☺
Dehydration is also a factor. You hydrolyzes lots of ATP during muscle contraction

What helps with muscle soreness? (These can also help prevent soreness)
-Creatine
-Hydrate
-Magnesium=helps with muscle relaxation
-Electrolytes

Coldness brings down inflammation it does not help with healing

Skeletal Muscle Fibers anatomy
Not a lot of detail in the anatomy of muscl fiber

Internal Organization of Muscle Fibers

• The sarcolemma is the cell membrane of a muscle fiber (cell)
• Surrounds the sarcoplasm = cytoplasm of muscle fiber

• Transverse tubules (T tubules) = Transmit action potential through cell =

allow for electrical signals
Pathway for action potential all inside the muscle

• Myofibrils = bundles of protein filaments = myofilaments = Myofilaments

are responsible for muscle contraction = actin and myosin

• Sarcoplasmic reticulum (SR) = Forms chambers = terminal cisternae

attached to T tubules = Cisternae = concentrate Ca2+ (via ion pumps) and
release Ca2+ into sarcomeres to begin muscle contraction
Skeletal Muscle Fibers anatomy

Storff!
Muscle spindles and Golgi tendon organs

Two types of proprioceptors in muscles and tendons monitor muscle length and
force of contraction = communicate this information to spinal cord, cerebellum, and
cerebral cortex
• Muscle spindles = tapered structures found scattered among regular contractile
muscle fibers = are composed of a few intrafusal muscle fibers that lack actin
and myosin in their central regions, are non-contractile, and serve as receptive
surfaces. Ultimately causes muscle to contract
Cause muscle to contract
• Golgi tendon organs = mechanoreceptors located within tendons near muscle-
tendon junction
o Monitor tension generated by a muscle contraction = prevents skeletal
muscle from tensing excessively.
o Consist of an encapsulated bundle of collagen fibers
o Contain a single somatic sensory axon that fires more rapidly as greater
tension is generated with each contraction = information is sent to CNS =
inhibits motor neurons and allows muscle to relax = protect muscle and
tendon
Lead to muscle rexlation
Muscle spindles and Golgi tendon organs

D.it, Mihorize
I this part

Note: Extrafusal = outside the spindle; Intrafusal = within the spindle

o Intrafusal fibers = do not contribute to the overall tension of the muscle. They regulate the excitability of the
sensory afferent spindle nerves by mechanically deforming the receptors = innervated by gamma motor neurons.
o Extrafusal fibers = innervated by alpha motor neurons and are responsible for developing muscle tension.

Muscle spindles respond to stretch, length, or position of the muscle = will lead to
Muscle contraction
This allows you to hold up an object
Golgi tendon organs = within tendons = respond to force = cause muscle relaxation
Knee jerk response, protective mechanism
Muscle spindles
Example
Golgi tendon organs
Example-knee jerk response
Skeletal Muscle Fibers – Sacromere
Will talk about proteins involved not the anatomy

Sarcomeres = The contractile units of

skeletal muscle
Thin and thick filaments
Skeletal Muscle Fibers – thin filaments
Actin = thin filaments = microfilaments

Four Thin Filament Proteins - know

1. F-actin (Filamentous actin) = Two twisted rows of globular G-actin

2. Nebulin = Holds F-actin strands together

Held together by nebulin
3. Tropomyosin = Is a double strand = Prevents actin–myosin interaction

4. Troponin = A globular protein = Binds tropomyosin to G-actin (Globular

actin) Attached to tropomyosin
Skeletal Muscle Fibers – thick filaments

Thick Filaments
• The myosin molecule Tail = binds to other myosin molecules
• Head = made of two globular protein subunits
• Contain titin strands that recoil after stretching Titin like a spring
• Myosin head is an ATPase = hydrolyzes ATP
ATP + H2O —- ADP + Pi + H

Activated myosin head

Neuromuscular junction

The neurons that stimulate the

skeletal muscle to contract are
called somatic motor neurons.
Mylenitated neurons

The structural point of contact and

functional site of communication
between the motor neuron and the
sarcolemma of muscle fiber is
called the neuromuscular junction
at motor end plate
https://www.youtube.com/watch?v=f2PmP
Dc990Y

https://www.youtube.com/watch?v=5QzfMJ
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https://www.youtube.com/watch?v=sIH8uO
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Why does calcium come in & what is the transport process?
Faciated diffusion, comes in because of concentration gradient

The action potential of neuron & action potential of muscle both lead to the opening of calcium
channels

*Some video 3 notes to answer*

When does the sarcomere shorten?

Binding of what cause troponin to change shape?

The mysosin head must be activated before what can happen?

When does crossbridge cycling end?

In order to get Ca+2 to get back into the sarcolemma, we use ATP & go against the gradient
The big picture during muscle contraction
Firts need an action potential by the neuron
Neuromuscular junction steps

1.Action potential arrives at neuromuscular junction

2.This opens voltage gated Ca2+ channels and Ca2+ rushes in
3.Ca2+ “tells” the vesicles to release Acetylcholine by exocytosis
Neuromuscular Junction Steps
1. Action potential arrives at neuromuscular junction
2. This opens voltage gated Ca2+ channels & Ca2+ rushes in
3. Ca2+ “tells” the vesicles to release ACh by exocytosis
Pathway to contraction

1.Acetylcholine binds to receptors on motor end plate

2.This will open ligand gated channels (the receptors)
Pathway to Contraction
1. ACh binds to receptors on motor end plate=activate area on muscle
2. This will open ligand gated channels (the receptors)=nicotinic receptors
3. Na+ rushes in=that is your graded potential=leads to graded depolarization
4. This leads to action potential which zooms down T tubules
T Tubules and Ca2+

Graded depolarization leads to an action potential in the muscle which zooms

down the T tubules
7. This opens voltage gated Ca2+ channels in the muscle & Ca2+ is being released from
sarcoplasmic reticulum
Pathway to contraction
Why we need Ca2+

Ca2+ will bind to Troponin which will move tropomyosin to expose the myosin
binding site on actin
Now myosin can bind to actin

Ca2+ binds to troponin & mysosin binds to actin

Like a rope pulling actin

Mysosin is activated by the hydrolyzes of ATP

Pathway to contraction
Last slide of thurs Lecture

To activate Myosin, need ATP

When an ATP binds to myosin, it detaches from actin
Then myosin hydrolyzes ATP to ADP + Pi + H+ = this activates the ATP
And it can bind again to actin
At rigor mortis what happens?
Get stiff, no more O2, no more ATP
No detaching from actin
Muscle relaxation
Left off

Events in muscle relaxation:

o Termination of nerve signal and ACH release from motor neuron
o Hydrolysis of ACH by acetylcholinesterase = breaks down ACH
o Closure of ACH receptor causes cessation of end plate potential
o No further action potential generation
o Closure of calcium channels in sarcoplasmic reticulum
o Return of Ca2+ to sarcoplasmic reticulum by pumps = active = need
ATP = why? Against the gradient
o Return of troponin to original shape
o Return of tropomyosin blockade of actin’s myosin binding sites
o Return of muscle to original position due to its elasticity
Clinical View: Myasthenia Gravis

• Autoimmune disease = primarily in women. Autoimmune = your own cells

are attacked
• Antibodies bind to ACH receptors in neuromuscular junctions – ACH cant
bind and so no contraction
• Receptors removed from muscle fiber by endocytosis
• Results in decreased muscle stimulation
• Rapid fatigue and muscle weakness
• Eye and facial muscles often involved first
• May be followed by swallowing problems, limb weakness, breathing is
affected
Supplying Energy for Skeletal Muscle Contraction

Muscle cells have only a little ATP in storage

• Stored ATP is spent after about 5 seconds of
intense exertion
• ATP is made on demand

• Three ways to generate ATP in skeletal muscle

fiber
• Immediate supply via phosphate transfer
• Short-term supply via glycolysis
• Long-term supply via aerobic cellular respiration
Supplying Energy for Skeletal Muscle Contraction

Immediate supply of ATP: phosphate (Pi) transfer = local in muscle

• Myokinase transfers Pi from one ADP to another = know enzyme
in muscle to make ATP
• Creatine kinase transfers Pi from creatine phosphate to ADP =
Creatine phosphate is used to transfer Phosphate to make ATP
• This can be used only shortly
Supplying Energy for Skeletal Muscle Contraction

Short-term supply of ATP: glycolysis in muscle = also may a minute to

minutes = uses glycogen which is converted to glucose to use in
glycolysis = anaerobic
• Does not require oxygen = anaerobic
• Glucose (from muscle’s glycogen or through blood) is converted to
two pyruvate molecules
• 2 ATP released per glucose molecule
• Lasts about one minute depending on glycogen amount

Long-term supply of ATP: aerobic cellular respiration = last hours

• Requires oxygen and increased blood flow; Breathing increases
• Occurs within mitochondria
• Need to increase breathing to bring in O2, blow off CO2; increase
blood flow via increase in heart rate and force of contraction
• Lasts hours
Metabolic Processes for Generating ATP
Muscle Metabolism
Oxygen Consumption After Exercise
• After exercise, heavy breathing continues and oxygen consumption
remains above the resting level

Excess post-exercise oxygen consumption (EPOC) = The added oxygen

that is taken into the body after exercise = This added oxygen is used to
restore muscle cells to the resting level
1) to convert lactic acid into glycogen/glucose in liver
2) to synthesize creatine phosphate and ATP
3) to replace the oxygen removed from myoglobin.
4) Returning Ca2+ back into SR or removing Ca2+ via ATPases
5) Recycle ACH
Lactic acid and muscle Contraction

The Cori Cycle = The removal and recycling of lactic acid/lactate by the liver
• Liver converts lactic acid to pyruvic acid and then glucose
• Glucose is released to recharge muscle glycogen reserves
Ultimately lactic acid to glucose in the liver
Muscle and changes to activity
Muscle Fatique
Muscle Fatigue
• Inability of muscle to maintain force of contraction after prolonged activity
• Factors that contribute to muscle fatigue
• Inadequate release of calcium ions from the SR
• Depletion of creatine phosphate
• Insufficient oxygen = if blood supply is insufficient
• Depletion of glycogen and other nutrients such as glucose, fatty acids
• Buildup of lactic acid and ADP = has to be lots of lactic acid = it’s a weak
acid
• Acidosis is due to H+ from ATP hydrolysis but only if you cant remove
them
• Failure of the motor neuron to release enough acetylcholine or not enough
Ca2+ to release ACH
Muscle Twitch
Twitch Contraction = The brief contraction of the muscle fibers in a motor unit
in response to an action potential

Latent period (2 msec) = A brief delay between the stimulus and muscular
contraction. Why do we see this delay? All the steps

Contraction period (10–100 msec)

Relaxation period (10–100 msec)

Tension Production
Wave summation = Increasing tension or summation of twitches
• Repeated stimulations before the end of relaxation phase. Muscle no longer
completely relaxes. Mostly due to Ca2+ staying in the muscle and
increasing

Incomplete tetanus = Sustained but wavering contraction

Complete Tetanus = If stimulation frequency is high enough, muscle never

begins to relax, and is in continuous contraction. Do not get tetanus in
heart. In the heart that is a heart attack
Twitches and tetanus
Exercise and lactate
Two diagrams representing energy metabolism in skeletal muscle
during two different exercise intensities. A: steady state at ∼60% V̇o2
max. Note that macronutrients are a mix of blood glucose, muscle
glycogen, blood free fatty acids, and intramuscular lipid. Blood free
fatty acids and intramuscular lipolysis eventually yield the activated
fatty acid molecules (FA-CoA). Pyruvate, NADH, and protons produced
from substrate flux through glycolysis are predominantly consumed by
the mitochondria as substrates for mitochondrial respiration. The
same is true for the products of ATP hydrolysis (ADP, Pi, H+). Such a
metabolic scenario can be said to be pH neutral to the muscle cells. B:
short-term intense exercise at ∼110% V̇o2 max, causing volitional
fatigue in ∼2–3 min. Size of the arrows approximate relative
dependence/involvement of that reaction and the predominant fate
of the products. Note that Pi is also a substrate of glycogenolysis. In
this scenario, cellular ATP hydrolysis is occurring at a rate that cannot
be 100% supported by mitochondrial respiration. Thus there is
increased reliance on using cellular ADP for ATP regeneration from
glycolysis and creatine phosphate. For every ADP that is used in
glycolysis and the creatine kinase reaction under these cellular
conditions, a Pi and proton is released into the cytosol. However, the
magnitude of proton release is greater than for Pi due to the need to
recycle Pi as a substrate in glycolysis and glycogenolysis. As explained
in the text, the final accumulation of protons is a balance between the
reactions that consume and release protons, cell buffering, and proton
transport out of the cell. This diagram also clearly shows that the
biochemical cause of proton accumulation is not lactate production
but ATP hydrolysis.
Biochemistry of exercise-induced metabolic acidosis
Robert A. Robergs , Farzenah Ghiasvand , Daryl Parker
American Journal of Physiology - Regulatory, Integrative and Comparative
PhysiologyPublished 1 September 2004Vol. 287no. R502-R516DOI:
10.1152/ajpregu.00114.2004
Exercise and lactate
Lactate produced is removed from the cell by the monocarboxylate transporter. The
lactate is circulated away from the origin cell where it can be taken up and used as a
substrate for metabolism in other tissues, such as other muscle cells (skeletal and
cardiac), the liver, and kidney.

Effects of acute and chronic exercise

on sarcolemmal MCT1 and MCT4
contents in human skeletal muscles:
current status
Claire Thomas , David J. Bishop ,
Karen Lambert , Jacques Mercier ,
George A. Brooks
American Journal of Physiology -
Regulatory, Integrative and
Comparative PhysiologyPublished 1
January 2012Vol. 302no. R1-R14DOI:
10.1152/ajpregu.00250.2011
Exercise and Immunity

Cardiovascular exercise stimulates

Endorphins which stimulate
Immune cells, especially Natural killer
Cells
Natural killer cells are very potent immune cells
Introduction to Cardiac Muscle Tissue

Cardiac muscle is striated, found only in the heart

• Have a single nucleus
• Have short, wide T tubules
• Have no triads
• Have SR with no terminal cisternae
• Are aerobic = high in myoglobin, mitochondria
• Have intercalated discs = communication pathway
Introduction to Cardiac Muscle Tissue
Cardiac Muscle Tissue

Intercalated Discs = allow cardiac muscle to contract as unit

Are specialized contact points between cardiocytes
• Join cell membranes of adjacent cardiocytes (gap junctions, desmosomes)
• Functions of intercalated discs
• Maintain structure
• Enhance molecular and electrical connections
• Conduct action potentials

Because intercalated discs link heart cells mechanically, chemically and

electrically, the heart functions like a single, fused mass of cells
Introduction to Smooth Muscle Tissue
Smooth Muscle in Body Systems = involuntary = contracts in all directions
• Forms around other tissues
• In blood vessels = Regulates blood pressure and flow
• In reproductive and glandular systems = Produces movements
• In digestive and urinary systems = Forms sphincters and produces
contractions. Sphincters are round muscles
• In integumentary system = Arrector pili muscles cause “goose bumps”