Skeletal= Primarily attached to bones; it is striated and voluntary

Cardiac= forms the wall of the heart; it is striated and involuntary

Smooth (visceral)= located in viscera; it is non-striated (smooth) and involuntary

Produce body movements

Stabilize body positions

Regulate organ volumes

Movement of substances within the body (blood, lymph, urine, air, food and fluids, sperm)

Produce heat

Excitability (Ability to respond to stimuli and produce electrical signals)

Contractility (Ability to shorten and generate force once excited)

Extensibility (Ability to stretch without damaging the tissue)

Elasticity (Ability to return to normal length after being extended)

Thermal (Ability to produce heat energy)

attaches to bone, skin or fascia

Striated with light and dark bands

Voluntary control of contraction and relaxation

Multi-nucleated

Epimysium

Perimysium

Endomysium

All of these extend beyond the muscle belly to form the tendon

outermost layer

Surrounds the whole muscle

middle layer

Surrounds bundles (fascicles) of 10-100 muscle cells

Innermost layer

Separates individual muscle cells

Skeletal Muscle

Perimysium

Epimysium

Fascicle

Myofibril

Sarcoplasm

Sarcolemma

Stiations

Muscle fiber

Nucleus

Endomysium

Blood Capillary

Motor Neuron

Endomysium

Perimysium

Fascicle

Epimysium

• Muscle cell cytoplasm
• Contains lots of glycogen for energy production and myoglobin for oxygen storage

• Tiny invaginations of the sarcolemma
• Filled with ECF and quickly spread the muscle action potential to all parts of the fiber
• Connects the outside of the cell to the inside

W/o the T Tubule we would only have the perimeter of the muscle working.  They allow us to use the inside AND outside of muscles

• System of tubule sacs
• Stores Calcium when relaxed
• Release of Calcium triggers contraction

Thick and Thin filaments

Z disc

Contractile proteins: Does the contracting (myosin and actin)

Regulatory proteins: Turns contraction on and off (troponin and tropomyosin

Structural proteins: keeps everything aligned (titin, myomesin, nebulin and dystrophin)

Thick filament

Each molecule resembles two gold clubs twisted together

Myosin heads (cross bridges) extend toward the thin filaments and bind

Held in place by the M line proteins

made of actin, troponin, and tropomyosin

 Held in place by Z-lines

Blocks release of neurotransmitter at the NMJ so muscle contraction can not occur

 muscle paralysis by blocking the ACh receptors

Used to relax muscle during surgery

One motor neuron and all the skeletal muscle cells it innervates (10-2000 cells)

 1 muscle fiber can only receive impulses from 1 neuron

1 motor neuron can control MANY muscle fibers

Motor nerve impulse must meet or exceed the threshold.

If the threshold is not met no fibers in that unit act

Amount of contraction at any given time

Maintaining posture

maintaining blood pressure

• Release of Calcium from the SR is triggered and the muscle cell will shorten and generate force
• Calcium binds to troponin and causes troponin-tropomyosin complex to move and reveal myosin binding sites on actin
• The contraction cycle begins

Calcium

ATP

Nerve signal

Calcium releases and channels close

Troponin holds tropomyosin in position to block myosin-binding sites on actin

Calcium release channels open.

Calcium binds to troponin uncovering the myosin-binding sites on actin

myosin cross bridges pull on thin filaments

Thin filaments slide inward

Sarcomeres, muscle fiber and muscle shorten

Z discs pulled toward M line-shortening the sarcomere length

H zone shortens

I band shortens

A band remains the same

thick and thin filaments overlap

1. AP reaches axon terminal in nerve
2. Voltage-gated Ca²⁺ channels open, causing Ca²⁺ influx
3. Ca²⁺ causes releases of ACh (exocytosis) into synaptic cleft
4. ACh crosses synaptic cleft and binds to receptors on motor end plate
5. Causes ligand-gated sodium channels to open, sodium rushes in
6. Sodium influx causes inside of muscle to become positivel triggers muscle AP
7. AP spreads over sarcolemma and down into T Tubules
8. AP causes Ca²⁺ to be released from SR
9. Ca²⁺ binds to troponin moves tropomyosin away from binding site on actin
10. Myosin heads become reoriented (requires ATP) and myosin heads bind to actin (forms crossbridge)
11. Myosin crossbridges rotate toward center of sarcomere (power stroke) and pull actin (sarcomere shortens)
12. ATP needed to detach myosin and actin
13. continues as long as Ca²⁺ and ATP present

AChE breaks down ACh in synaptic cleft

Muscle AP stops

Ca²⁺ release channels close and Ca²⁺ is pumped back into SR

Troponin and tropomyosin move to cover actin's binding site

Sarcomeres return to resting length

Type l, slow oxidative, slow-twitch

Type lla, fast oxidative-glycolytic, (FOG)

Type llb, fast glycolytic fibers, fast-twitch

1 slow red ox

Red in color (lots of mitochondria, myoglobin, and blood vessels)

Prolonged, sustained contractions for maintaining posture (low intensity, long duration-aerobic)

FOG

Pinkish(lots of mitochondria, BV, and myoglobin)

split ATP at very fast rate; used for walking or sprinting

2 fast white sugar

White (few mitochondria, BV, and myoglobin)

Anaerobic movements for short duration; weight lifting

hypertrophy- growth enlargement of existing cells

Hyperplaga- increasing the number of muscle fibers

What do anabolic steroids do?

what are the side effects?

increases muscle size, strength and endurance

liver cancer

 kidney damage

heart disease

mood swings

facial hair and deeper voice in females

atrophy of testicles and baldness in amles

concentric (lifting-shortens)

eccentric (extending- lengthens)

isometric (tension but no muscle shortening or lengthining)

1. number of motor units activated
2. type of motor units activated
3. size of muscle
4. muscle length
5. joint angle
6. speed of action

what force production is changed during #1

Number of motor units activated

Increase motor units activated

Increase force

Type of motor unit Activated

increase fast-twitch motor neurons activated

increase force

Size of Muscle

increase fiber size

increase force

Muscle length

impacts cross bridge interaction (more interaction=more force)

Muscle and connective tissue have elastic properties

joint angle

force generated in muscle transferred to bone via tendon insertion

optimal joint angle maximizes the force transmitted to bone

speed of action

Force velocity curves

Decreased/increase load, increased/decreased velocity

• Latent period (2 msecs)
• Contraction period (10-100msec)
• Relaxation period (10-100msec)
• Refractory period (5 msec in skeletal; 300 in cardiac)

second stimulus applied before muscle has completely relaxed

Increased strength of contraction

creatine phosphate (CP)

Anaerobic Cellular respiration/gylcolysis

Aerobic cellular respiration (require O₂₎

Cardiac contractions las longer (prolonged delivery of Ca²⁺ ions)

Stimulated by their own autorhythmic fibers

larger mitochondria to generate ATP aerobically (require more O₂)

visceral (single unit) gap junctions, unison

Multiunit- no gap junctions, not in unison