Muscular Systems

Duration of muscle contraction in muscle types

Skeletal - reaches peak tension quickly (fast muscle action), sustained constrictions, a-delta fibres

Cardiac - reaches peak tension little less quickly than skeletal, no sustained contractions, reaches max HR

Smooth - reaches peak tension slowly as contraction spreads

Levels of organization

Muscle group - eg. Gastrocnemius

Muscle fascicles - bundles

Muscle fibres (start of striation) - muscle cells

Myofibrils (start of striation)

Myofilaments - actin, myosin

Connective tissue organization (and what they surround and their function)

Endomysium - muscle fibres (inner)

Perimysium - muscle fascicles (middle)

Epimysium - muscle group (outer)

Transfer tension to tendons

Muscle Fascicle Arrangement (and types of fascicles)

Muscles consist of fascicles - muscles fibres are parallel to fascicles

Fascicles form patterns with respect to tendons - parallel, fusiform, circular, triangular, pennate

Lever system for bone-muscle relationships (how parts in the body function in system)

Bones - act as levers

Joints - act as fulcrums

Muscle Contraction - provides effort, applies force where muscle attaches to bone

Load - bone, overlying tissue → anything lifted

First Class Lever

Not common in body → fulcrum is between the effort and load

Eg. Lifting head off of chest → fulcrum is where skull connects to atlas (Atlanto-occipital joint), load is the facial skeleton that needs to be lifted, and the posterior neck muscles provide the effort (also seesaws and scissors)

Second class lever

Uncommon in body → load is between fulcrum and the effort

Eg. Standing on tip toe → effort is exerted by calf muscles, joints on ball of foot are the fulcrum, weight of body is the load

Third class lever

Common → effort is between fulcrum and the load, always at a mechanical disadvantage

Eg. Flexing forearm at biceps brachii → effort exerted by proximal radius of the forearm, fulcrum is elbow joint, load is hand and distal end of forearm

Myofibrils (what is it surrounded by and composed of)

Composed of many myofilaments - actin (thin), myosin (thick)

Surrounded by sarcoplasmic reticulum

Sarcomere (what it is, where its found and describe structure)

Found in striated muscle → contractile unit

From Z-line to Z-line (pulled together during shortening/cross-bridging), called repeater units

Structure → composed of m-line and thin/thick filaments, also has A-bands and H-zones

A Band

Dark zone in Myofibrils

Length of myosin

In sarcomeres

I Band

Light zone in Myofibrils

Non-overlap zone (Z-line)

end of one sarcomere into the start of another

H-zone

Only myosin in A Band (includes m-line)

In Myofibrils in the sarcomeres

M-line

In sarcomeres and A Band

Runs through myosin but not actin

Stabilizes core of myosin

Contains myomesin

Z-line

Made of connective tissue

Two z-lines create one sarcomere

Myosin

Thick filament, always activated due to bound ATP, binding sites for actin and ATP

Found in Myofibrils

Actin

Double helix, binding sites for myosin → covered by tropmyosin, activated when Ca+ binds troponin

Muscle Proteins

Contractile - myosin, actin

Regulatory - troponin, tropomyosin

Structural - titin, nebulin, myomesin, dystrophin

Role of titin and nebulin

Titin - stabilizes myosin

Nebulin - aligns actin (actin wraps around nebulin)

Role of myomesin and dystrophin

Myomesin - part of the m-line → stabilizes core of myosin

Dystrophin - attaches myofilaments to sarcolemma (membrane) and fascia, helps transmit tension and shortening to muscle group

Sliding filament mechanism

Myosin head attaches to actin then pivots to pull actin inwards, causing z-lines to pull closer together which causes more overlap and sarcomere shortening which causes tension

Muscle at rest

Calcium pumps remove Ca back into the SR → needs ATP

Tropomyosin slides over actin sites → no cross-bridges

Actin and myosin go back to resting length

Relaxation is an active process

Activation of actin

Ca2+ binds troponin → shifts tropomyosin, reveals actin binding sites, cross-bridges are now possible

Excitation-Contraction Coupling (what it is)

How a contraction is initiated → through the release of calcium

Neuromuscular junction (nerve meeting muscle)→ axon terminal ends, muscle end-plate (post synaptic membrane)

Excitation-Contraction Coupling steps

AP arrives at end-plate from motor neuron → acetylcholine is released from axon end

• binds to receptors on the muscle endplate → EPP or End-plate potential aka muscle GP (from opening sodium gates and sodium rushing into cell → just like regular AP)

• EPP travels to side of end-plate, becomes muscle AP

• AP moves down T-tubules to inner core of muscle (close to sarcoplasmic reticulum - SR)

• AP voltage change in T-tubules triggers release of Ca2+ from SR (after DHP receptor activation)

• AP activates DHP receptor → opens Ryanodine gate in SR, calcium is released into muscle

• Calcium binds to troponin, shifts tropomyosin, cross-bridging and shortening now possible

T-tubules function

muscle AP travels down t-tubules, changes voltage in t-tubules which will trigger SR

Sarcoplasmic reticulum function

Releases Ca2+ from voltage change in t-tubules

How is a contraction initiated in skeletal muscle

excitation-contraction coupling process

Cross-bridge cycle steps

Step 1 → energized myosin binds to actin (myosin has ADP + Pi bound already)

Step 2 → myosin head pivots, increases overlap of actin and myosin (sarcomere shortening) aka the Power Stroke (uses up the bound ADP + Pi)

Step 3 → myosin binds to new ATP so the myosin head can detach

Step 4 → ATP hydrolyzes into ADP + Pi, this allows myosin to re-pivot, myosin is now re-energized and ready to attach to another actin molecule

Sequence repeats as long as Ca2+ is present

Role of ATP in cross-bridge cycle

Detaches myosin head from actin, provides energy to myosin head to re-pivot to a high energy state, powers release of ADP and Pi which prepares myosin head for next cycle

Effects of contraction in sarcomere

Sarcomere decreases in size as z-lines get closer, I band decreases as overlap increases, H zone decreases, A band stays the same since length of myosin is constant, overlap zones increase in size as myosin pulls actin inwards

isotonic contractions

Create force / move load

Concentric - shortening the muscle (decreasing angle)

Eccentric - lengthening the muscle (increasing angle)

Isometric contractions

Create force without moving a load

Happens before isotonic contractions as it builds the tension before the movement

If load is too heavy you’ll have increase isometric contractions but no isotonic contractions

Phases of contraction

Isometric tension: no visible shortening, increasing tension, length is constant → building cross bridges, making tension=load (first phase)

Isotonic shortening: visible shortening, tension is constant (second phase)

Muscle twitch

A single contraction-relaxation cycle

• latent period → time between AP and contraction

Latent period

Time for → excitation-contraction coupling, build-up of isometric tension

As load increase, latent period gets longer → needs to build more tension

Tetanus

High frequency of action potentials

• ensures that no relaxation happens during sustained contraction

What muscles are always doing during movement → held until muscle fatigues

Motor unit summation

Increased voltage, increased # of fibres stimulated, increased contraction size → load size determines which fibres are stimulated

Used when there’s an increased load → more fibres contracting = more force

Effects of load

Increased load → more tension needed, longer latent period, decreased contraction distance, back-slippage (need more myosin constantly attached to prevent), slower cross-bridge recycling (less myosin heads moving at once), decreased contraction velocity, if tension can’t overcome load → isometric contraction

Factors that determine muscle force

Muscle fibre diameter → actin and myosin cross-bridges (more myofilaments whcih builds diameter)

Muscle fibre length → length - tension relationship

Energy sources in muscle

ATP → used for contraction and relaxation

creatine phosphate → stored ATP (used when muscle is wokring)

glycogen → goes through glycolysis to make ATP

Muscle fibre types

Slow oxidative (type I), fast oxidative (IIa), fast glycolytic (IIb)

• based on fuel source and contraction type

Slow oxidative fibres (type I)

Slow cross-bridging cycling

Uses oxidative metabolism for energy (aerobic) → Myoglobin, mitochondria, high blood flow

“Red Fibres” → due to factors above

Low intensity and high endurance → maintain w/out fatigue and needs less ATP

Lower constant force with no fatigue

Eg. High proportion in core muscles

Fast oxidative fibres (IIa)

Faster cross-bridging cycling, higher intensity but lower endurance

Builds more force than oxidative but fatigues quicker

Present all over body (eg. Arms, legs, etc)

Fast glycolytic fibres (IIb)

Uses glycolysis for energy → anaerobic

Highest intensity but lowest endurance → fatigue quickly but create lots of force

“Emergency fibres” → used as last resort

“White fibres” → less blood flow

Muscle fatigue

Depends on oxidative ability

Due to → increased lactic acid, decreased ATP, increased wastes, Ca2+ changes (low calcium causes cramping/spasms or can’t create enough force for contraction)

Aerobic exercise effects

Glycolytic fibres convert to oxidative

• more mitochondria

• Increased blood flow

• More myoglobin and glycoge

Fast oxidative increase their endurance levels → increased blood flow and myoglobin

Resistance exercise effects

More actin and myosin within muscle fibres → increased diameter (“bulk up”)

Muscle cells don’t divide (G0) so fibres get bigger but don’t increase in #

Muscle training

Weight training produces increased muscle strength and size

Fast contractions tends to build up muscle endurance instead

Short term effects of exercise

Increased blood supply

Increased temperature

Increased lactic acid and wastes

Long term effects of exercise

More maintained blood flow to muscles

Larger muscle fibre diameter

More mitochondria

Conversion of fast glycolytic fibres to fast oxidative fibres

More actin and myosin

Anabolic steroid effects

Increases # of actin and myosin filaments → similar to testosterone

If too large, can overload tendon → pull tendon off of bone

Cardiac hypertrophy → build up of cardiac muscle

Golgi tendon organ

Prevents over-contraction and over stretch of tendon

• triggers a reflex relaxation

• Eg. Muscle failure with high load

Muscle Spindle

With an Increased load → stretches spindle, triggers reflex, increased contraction strength

Stretch receptor reflex (contracts muscle instead of relaxing like GTO)

Smooth muscle

Involuntary → Walls of hollow organs and tubes, gut, blood vessels

No striations → filaments don’t form Myofibrils, cells usually arranges in sheets

Spindle-shaped cells → single nucleus

Types of filaments in smooth muscle

Thick myosin filaments → longer than in skeletal muscle

Thin actin filaments → tropomyosin but no troponin

• shorten in every direction and makes cell more round instead of short

Intermediate filaments → not part of contraction, cytoskeleton- supports cell shape

Smooth muscle arrangement

Diagonal arrangement of actin and myosin → reinforced by dense bodies

Activation of myosin instead of actin

Smooth muscle contraction activation

Ca2+ from extracellular space binds to calmodulin which triggers second messenger response that activates myosin kinase and phosphorylates myosin, binding of actin and myosin in cross bridges → contraction

How are smooth muscle and skeletal muscle different?

Skeletal → voluntary, striated, use troponin and tropomyosin and cross-bridging with myosin and actin

Smooth → involuntary, non-striated, only uses tropomyosin, activates actin instead of myosin

Multi unit smooth muscle

Neurogenic

Discrete units function independently→ each must be stimulated (varicosities run between each cell to stimulate and there are few to no gap junctions)

Large blood vessels and airways to lungs, ciliary body muscle (eye), iris of eye, base of hair follicles

Single unit smooth muscle

Also called visceral smooth muscle contraction → gut, Urogenital tract

Self-excitable → doesn’t require nervous stimulation

Fibres contract as single unit → gap junctions spread the impulse (varicosities are only along top cells)

Contraction is slow

Cardiac muscle

Striated, involuntary, intercalated discs , cardiac cells (interconnected by gap junctions, innervated by autonomic NS)

Intercalated discs

Desmosomes → withstand stress

Gap junctions → spread impulses

Helps maintain contractions

Initiation of AP in cardiac muscle

Pacemaker initiated → neurogenic influence (para/sym)

Initiation of muscle contraction in cardiac muscle

AP from pacemaker initiates opening of calcium+ channels and Ca2+ comes in and triggers more calcium from SR → spread by gap junctions and special fibres, calcium activates actin

How does cardiac differ from smooth and skeletal

Striated, only in heart, has intercalated discs for synchronized contractions, involuntary

Muscular dystrophy

X-linked genetic disorder of skeletal muscle

• missing dystrophin → can’t transmit force

• Death of muscle fibres

• Degeneration of shoulder and pelvic muscle

Muscle as age increases

Connective tissue increases in muscles, number of muscle fibres decrease

Loss of muscle mass → decreased muscle strength is 50% by age 80

• sarcopenia → muscle wasting (loss of muscle strength)