The study of muscles

Movement Facilitation Thermogenesis Postural Support Regulation of Organ Volume Protects Internal Organs Pumps Blood (HEART)

Contractility – able to shorten

Extensibility (Flexibility) – able to lengthen

Elasticity – able to return to original shape

Excitability (Irritability) – able to respond to a stimulus

Attached to bones Striated appearance under a microscope Voluntary control (conscious control) Multinucleated Myofilaments - contractile elements of each

muscle fiber Functions:• movement

• thermogenesis

• posture

• protection of internal organs

Forms the bulk of heart wall (Myocardium) Striated Involuntary Fibers are quadrangular and branching Cardiac fibers typically have a centrally located nucleus Require a constant supply of oxygen Autorhytmicity

• Built-in rhythym—the heart has a pacemaker that initiates each contraction

Sarcolemmas connected by intercalated discs• Strengthens cardiac muscle tissue• Propagates an action potential from cell to cell through specialized

structures on the intercalated discs called gap junctions Function:

• contractions of the heart

Located in walls of hollow internal surfaces such as:• blood vessels• stomach• urinary bladder• intestines

Non-striated in appearance Involuntary (typically) Can be stretched to great lengths Allows for tremendous size variability Slowest contracting muscle type Functions:

• controls diameter of blood vessels• Peristalsis• Muscular contractions to push urine out the urinary bladder

Myofilaments - structural components of myofibrils

• Myosin - thick myofilaments

• Actin - thin myofilaments

Structure of muscle

Thick myofilaments Occupy the A Band of the sarcomere Overlap free ends of the actin myofilament Shaped like a golf club

• Long, thick protein molecule (tail)

• Globular head at the ends

Thin myofilaments Anchored to the Z Line Two stranded protein molecule intertwined around

each other Associated with two regulatory proteins

• Tropomyosin –• long stranded protein molecule that follows the contour of actin

• When the muscle fiber’s sarcomere is relaxed, tropomyosin blocks actin’s active sites preventing cross-bridge formation with myosin

• Troponin - protein located at regular interval along the tropomyosin that covers the active sites on actin. Has three subunits, one that binds with actin, another with tropomyosin, and the last bind to Ca++

An electrical impulse that originates at the motor end plate, travels along the length of the sarcolemma, down a transverse tubule, and causes the muscle to contract.

Due to an action potential, the actin and myosin myofilaments slide past one another shortening the sarcomere

No change in length of myofilaments H Zone narrows or disappears I Band narrows or may disappear A Band remains the same length

Neuron - nerve cellAxon - long, threadlike process that transmits impulse away from cell body (may be up to 1 meter in length)Motor Unit - motor neuron and all the muscle fibers it innervatesNeuromuscular Junction - junction between axon terminal and muscle fiber

Motor End Plate - location on the muscle fiber at the end of an axon terminal

Synaptic End Bulb - distal end of axon terminal

Synaptic Vesicles - membrane enclosed sacs within the synaptic end bulbs that store neurotransmitters

Synaptic Cleft - space between axon terminal and motor end plate

Subneural Clefts - folds in sarcolemma along the synaptic gutter

Acetylcholine (Ach) - neurotransmitter released from synaptic vesicles that initiates an action potential in a muscle

All or None Principle• Impulse from motor neuron will cause contraction in

ALL muscle fibers it innervates or none

• Threshold Stimulus - the weakest stimulus from a neuron that will initiate a muscular contraction

• An action potential travels down the motor neuron. When it arrives at the synaptic knob, the membrane of the nerve at the synaptic cleft is depolarized, thereby increasing the Ca++ permeability of the membrane.

• Ca++ diffuses from outside of the synaptic knob to inside the synaptic knob.• The influx of Ca++ into the nerve causes the release of Ach.• Ach is ejected into the synaptic cleft, diffuses across the cleft, and depolarizes the

muscle membrane.• This increases the permeability of the muscle membrane to Na+.• Na+ rushes into the muscle cell, depolarizing the membrane as it travels away

from the motor end plate thus initiating an action potential.• Ach is quickly broken down in the cleft by Ach-ase so that each action potential

arriving from the nerve initiates only one action potential within the muscle.• The action potential spreads across the muscle membrane and down the T-tubules

deep into the muscle cell.• The action potential of the T-tubules depolarizes the membrane of the nearby

sarcoplasmic reticulum which results in the release of Ca++ into the sarcoplasm.• Ca++ is very quickly removed out of the sarcoplasm by the sarcoplasmic reticulum

so the effects of one action potential are very short lived and produce a very small contraction.

• Many action potentials are necessary to produce enough force to produce a strong or prolonged muscle contraction.

• The Ca++ released from the sarcoplasmic reticulum binds with troponin and cause troponin to change shape.

When troponin changes shape, it physically moves the other regulatory protein, tropomyosin, out of the way exposing the active sites on the actin myofilament.

Since the heads or cross-bridges of myosin have a very strong affinity for the active sites on actin, they make contact immediately after the active sites have been exposed.

The acto-myosin complex has ATPase activity and ATP is split into ADP + P and energy is released.

The energy released by the splitting of ATP is used to produce movement of the cross-bridges, sliding the actin and myosin filaments past one another which causes the sarcomere to shorten and the muscle to contract and produce force.

The myosin cross-bridge has a low affinity for ADP but a very high affinity for ATP.

It discards the ADP and becomes recharged with a new ATP.

The myosin then releases its hold on the active sites on actin, swivels back to its original position, and is ready to respond to another action potential.

When another action potential comes along the entire process is repeated.

It takes many action potentials to produce enough shortening of the sarcomeres to generate enough force to produce movement of a body segment.

Origin• Body segment with most mass

• Usually more proximally located

• Usually larger surface area of attachment

• Remains stationaryInsertion

• Body segment with least mass

• Usually more distally located

• Usually smaller surface area of attachment

• Attached to the part that movesGaster (Belly)

• Fleshy portion of the muscle between the tendons of the origin and insertion

Agonist (Prime Mover)• Muscle responsible for the majority of force

Antagonist• Performs the opposite movement

Synergist• Muscle that assists the agonist• provides additional force

• redirects the force of the agonist

Fixator (Stabilizer)• Stabilizes a body segment so the prime mover can

act more effectively

• Masseter• Biceps brachii• Triceps brachii• Brachialis• Rotator cuff

• Supraspinatus• Infraspinatus• Teres minor• Subscapularis

• Sternocleidomastoid• Trapezius• Deltoid• Diaphragm• Rectus abdominis• External oblique• Pectoralis major• Latissimus dorsi

• Gastrocnemius• Tibialis Anterior• Soleus• Hamstrings

• Semimembranosus• Semitendidnosus• Biceps femoris

• Quadriceps• Rectus femoris• Vastus lateralis• Vastus medialis• Vastus intermedius

• Gluteus maximus• Gluteus medius• Sartorius• Gracilis• Flexors• Extensors• Pronator• Supinator

Muscles whose contractions bend a limb or other part of the body

Any of a number of specific muscles in the arm, hand, leg, or foot

Muscles whose contractions extend or straighten a limb or other part of the body.

Any of a number of specific muscles in the arm, hand, leg, and foot

Aponeurosis a strong flat sheet of fibrous connective tissue that serves as a

tendon to attach muscles to bone or as fascia to bind muscles together or to other tissues at their origin or insertion

Bursa a fluid-filled sac or saclike cavity situated in places in tissues

where friction would otherwise occur Flaccid

weak, lax, lacking normal muscle tone Hypertrophy

enlargement or overgrowth of an organ or part due to increase insize of its constituent cells

Atrophy a wasting away; a diminution in the size of a cell, tissue, organ, or

part

Painful disorders of muscles, tendons, and surrounding soft tissue

Muscle destroying diseases characterized by the degeneration of individual muscle fibers

Leads to progressive atrophy of skeletal muscles

Due to a genetic defect

Autoimmune muscle disease characterized by muscular weakness and chronic fatigue

Caused by a lack of Ach Body sends antibodies to destroy AchThe action potential cannot be sent to the

skeletal muscles

Occurs a few hours after death when the skeletal muscles undergo a partial contraction that causes the joints to become fixed

Seems to result from an increase in membrane permeability to calcium ions, which promote contraction and decrease in the availability of ATP, which prevents relaxation

The actin and the myosin filaments remain linked together until the muscles begin to decompose

Approximate times for algor and rigor mortis in temperate regions

Body temperature Body stiffness Time since death

warm not stiff dead not more than three hours

warm stiff dead 3 to 8 hours

cold stiff dead 8 to 36 hours

cold not stiff dead more than 36 hours

SOURCE: Stærkeby, M. "What Happens after Death?" In the University of Oslo Forensic Entomology [web site]. Available from http://folk.uio.no/mostarke/forens_ent/afterdeath.shtml.

Connective tissue sheath of the tendon becomes inflamed and swollen following an injury or repeated stress of athletic activity

Most commonly affected are those of the shoulder, elbow, and hip

A form of food poisoning that results when the bacteria have not been heated high enough to inactivate the toxin

Caused by a toxin (made by Clostridium botulinum) that can prevent the release of Ach from the motor nerve fibers at the neuromuscular junctions.

When the muscle fibers fail to be stimulated, the body, including the muscles responsible for breathing, may be paralyzed.

Without prompt medical attention, death may result.

This is when the tendinous attachments or muscle belly are torn as a result of strenuous activity

The painful injury is accompanied by internal bleeding from damaged blood vessels that supply the muscles

Hypertrophy• Muscle growth

• Caused by using the muscle

Hypotrophy • Better known as atrophy

• Decrease in muscle size and strength

• Caused by NOT using the muscle

• Muscle wasting

Pain in the lower leg Tendonitis of the tibialis posterior muscle Inflammation of the periosteum Stress fracture of the tibia Pulling away of the periosteum from the

underlying bone Treatment:

• RICE

• strengthen tibialis anterior muscle

The forcible wrenching or twisting of a joint with partial or complete rupture or injury to joint attachments without dislocation

1st Degree Sprain = stretching of ligaments

2nd Degree Sprain = partial tearing of ligaments

3rd Degree Sprain = complete tear of ligaments

Pulling or overstretching a muscle Soft tissue (muscle) injury