Muscular System

ORGANIZATION OF SARCOMERES

Actin (thin) myofilaments

  • F-actin forms double helix attached to the sarcomere.

  • Made of G-actin monomers with myosin-binding active sites.

  • Tropomyosin covers the active sites of actin.

  • Troponin has 3 binding sites:

    • Binds to actin

    • Binds to tropomyosin

    • Binds to Ca²+

Troponin-tropomyosin complex regulates actin-myosin interaction during contraction.


Myosin (thick) myofilaments

- Thick filaments consist of many myosin molecules with rods and heads.

Myosin Heads

  • Binds to actin to form cross-bridges

  • Pivot at the hinge, producing muscle movements

  • ATPase enzymes that break down ATP to provide energy for contraction.


NEUROMUSCULAR JUNCTION STRUCTURE

- Synapse between motor neurons and skeletal muscle fiber that initiates muscle contraction.

Components:

  • Presynaptic terminal - axon terminal containing Acetylcholine in synaptic vesicles.

  • Synaptic cleft - gaps where acetylcholine diffuses.

  • Postsynaptic terminal - contains acetylcholine receptors that generate a muscle action potential.


Sliding Filament Model

  • Actin filaments slide over myosin filaments.

  • Actin and myosin do not shorten.

  • Sarcomeres shorten , causing muscle contraction.

  • During relaxation, sarcomeres lengthen due to external forces (e.g., antagonistic muscles).


Sarcomere Shortening

Relaxed Muscle

  • Actin and myosin overlap slightly

  • H zone is visible

  • Sarcomere is at resting length

Contracted Muscle

  • Actin slides toward at the center over myosin

  • Z disks move closer together

  • Sarcomere shortens

  • A band remains the same length

  • H zone disappears as filament overlap increases


SKELETAL MUSCLE FIBER PHYSIOLOGY

Resting Membrane Potential

Resting membrane potential is required before an action potential and muscle contraction can occur.

  • Cell membrane are polarized.

  • K+ (Potassium) , Inside highly negatively charged ions.

  • Na+ (Sodium) , Outside highly positively charged ions.

  • Sodium-Potassium maintains ion distribution.


Review Membrane Permeabilities

Phospolipid bilayer

  • Hydrophobic(water fearing)

  • Preventing free water movement of charged ions.

Transport proteins

  • Ion channels

  • Allow ions to cross the membrane.

Ion movement through channels creates the electrical properties of resting and active cells.


ION CHANNELS

Types

Ligand-Gated

- Molecules that bind to receptors.

Receptors:

  • Protein

  • Glycoprotein with a receptor sites

Example: Acetylcholine(neurotransmitter)

Voltage-Gated

- Open and close in response to small voltage changes across plasma membrance.

Both are specific for certain ions.


MEASURING THE RESTING MEMBRANE POTENTIAL

  • K+ leaks out faster than Na+ enters thru leak channels.

  • Negative protein remains inside, making the inside of cell negative.

  • 3 Na+ pump out, 2 K+ pump in

This maintains the resting membrane potential.


3 Phases

  1. Depolarization : Voltage-gated Na+ channels open → Na+ enters → inside becomes positive.

  2. Repolarization : Na+ channels close → K+ enters → K+ exits → membrane returns negative.

  3. Hyperpolarization : Membrane becomes more negative before returning to resting potential. Na+ pump restores resting ion distribution.


Key Concepts

All-or-none principle

- Once threshold is reached, a full action potential occurs.

Propagation

-Action potential spreads along the membrane.

Frequency

  • Number of action potentials produced per unit time.


STEPS IN A MUSCLE CONTRACTION (SLIDING FILAMENT THEORY)

  1. An action potential travels down motor neuron to presynaptic terminal causing Ca²+ channels to open.

  2. Ca²+ causes synaptic vesicles to release acetylcholine into synaptic cleft.

  3. Acetylcholine binds to receptor sites on Na+ channels, Na+ channels open, and Na+ rushes into postsynaptic terminal (depolarization).

  4. Na+ causes sarcolema and t-tubules to increase the permeability of sarcoplasmic reticulum which releases stored calcium.

  5. Ca²+ binds to troponin which is attached to actin.

  6. Ca²+ binding to troponin causes tropomyosin to move exposing attachment sites for myosin.

  7. Myosin heads bind to actin.

  8. ATP is released from myosin heads and heads bend toward center of sarcomere.

  9. Bonding forces acting to slide over myosin.

  10. Acetylcholinesterase (enzyme breaks down acetylcholine) is released, Na+ channels close, and muscle contraction stops.


ATP and MUSCLE CONTRACTION

  • Energy for muscle contractions supplied by ATP

  • Energy is released as ATP →ADP+P

  • ATP is stored in myosin heads

  • ATP help form cross bridges formation between actin and myosin

  • New ATP must bind to myosin before cross-bridge is released

Rigor mortis :

  • A person dies and no ATP is available to release cross-bridge.

  • Muscle stiffness occur hrs after death.

Muscle Soreness

  • Inflammation and microscopic muscle injury after exercise.

OTHER INFORMATION

  • ATP is made in mitochondria from aerobic or anaerobic respiration.

  • During a muscle contraction, H zone and I band are shorten but A band stays the same.

  • Striations of skeletal and cardiac muscle are due to sarcomeres (actin and myosin).


CROSS-BRIDGE MOVEMENT


During one muscle contraction, myosin repeatedly undergoes:

  • Cross-bridge formation

  • Power stroke

  • Cross-bridge release

  • Recovery Stroke

These cycles continue as long as ATP and Ca²+ are available.


MUSCLE RELAXATION

ATP - Dependent Events

  1. Na+/K+ pump restores the resting membrane potential.

  2. ATP detaches myosin from actin, ending cross-bridge attachment.

  3. Ca²+ is pumped back into the Sarcoplasmic reticulum.

  4. Ca²+ decreases → tropomyosin covers the actin binding sites → muscle relaxes.


MUSCLE TWITCH and PHASES

Muscle twitch

- the response of a muscle fiber to a single action potential along its motor neuron.

PHASES

Lag or latent Phase

- from the stimulus to the beginning of contraction.

Contraction Phase

- Ca²+ released and cross-bridging cycling occurs.

Relaxation Phase

- Ca²+ returns to SR(sarcoplasmic reticulum) and muscle fiber returns to precontraction length.


TYPES OF MUSCLE CONTRACTIONS

Isometric

- no change in length but tension increases.

  • Postural muscles of the body


Isotonic

- change in length, but tension is relatively constant.

Types of Isotonic Contractions

  • Concentric - overcome opposing resistance and muscle shortens.

  • Eccentric - tension maintained but the opposing resistance is great enough to cause the muscle to lengthen.


Motor Units

- A motor unit is consists of one motor neuron and all the muscle fibers it innervates.

Types

Large muscle

- large motor units with many muscle fibers.

Small muscle

- small motor units with few muscle fibers.


Force of Contraction in Individual Muscle Fibers

Graded muscle contraction

- muscle force varies depending on the number of cross-bridges formed.

Factors affecting Force

1.Frequency of stimulation (Treppe) Staircase Effect

Repeated stimulation → more Ca²+ available increases cross-bridges formation → becomes slightly stronger → muscle tension reaches a plateau(maximum level)

2.Muscle fiber diameter

3.Muscle fiber length at the time of contraction

Active tension - force produced during muscle contraction.

Optimal length - the muscle is at the best length for contraction, so it produces the strongest force.

Passive tension - forced produced when a muscle is stretched withouth contracting.

Total tension - active + passive


WAVE SUMMATION and TETANUS


Wave summation

- Rapid stimulation increases muscle tension because contractions overlap.

Incomplete Tetanus

- Muscle partially relaxes between contractions.

Complete Tetanus

- No relaxation, muscle remain continously


RECRUITMENT

  • Sub-threshold stimulus

- no action potential; no contraction.

  • Threshold stimulus

- have action potential; contraction.

  • Submaximal stimuli

-stronger contraction.

  • Maximal stimulus

- all motor units are activated → maximal contraction


MUSCLE FIBER TYPES

Type I (Slow-Twitch Fibers)

  • Contract slowly

  • Fatigue slowly

  • Posture and endurance activities(long-distance runners)

  • Use aerobic respiration

  • High myoglobin(dark)

  • Many mitochondria

  • Rich blood supply


Type II (Fast-Twitch Fibers)

  • Contract rapidly

  • Fatigue quickly

  • Powerful, rapid movements (sprinting)

  • Use anaerobic respiration

  • Low myoglobin(white)

  • Fewer mitochondria

  • oxidative and glycolytic subtypes

Anaerobic respiration

  • Occurs in absence of oxygen

Aerobic respiratison

  • Required oxygen and breaks down glucose

  • More efficient than anaerobic


MUSCLE FATIGUE

Muscle Fatigue

- Reduced ability of muscles to generate force.

Types of Muscle Fatigue

Physiological contracture

- Lack of ATP prevents contraction and relaxation.

Psycological fatigue

- Fatigue originating from the CNS.


Mixed Fiber Distribution

  • Humans have both types of fibers

  • Distribution of fibers is genetically determined

  • Neither type can be converted, but capacity can be increased through intense exercise.


Effects of Exercise

Hypertrophy

  • Increased in muscle size

  • Increased myofibril

  • Addition of nuclei from satellite cells

  • Increased strength and enzyme production


Atrophy

  • Decreased muscle size

  • Caused by disuse, aging, and diseases

  • Usually reversible unless muscle cells die


Heat Production

Exercise

- metabolic rate and heat production increase.

Post-exercise

- metabolic rate stays high due to oxygen debt

Shivering

- uncoordinated contraction of muscle fibers resulting in shaking and heat production.


MUSCLE ATTACHMENT (FUNCTION ROLES OF MUSCLES)

Origin → nonmovable end/fixed end

Insertion → movable end

Belly → middle part of the muscle

Synergist → muscles that work together to produce a movement

Antagonist → muscle that oppose each other