BIO 4

CHAPTER 10: MUSCLE TISSUE

LECTURE NOTES

I. OVERVIEW OF MUSCLE TISSUE

Muscle is one of the four primary tissue types of the body.

Three types of muscle tissue:

1. Skeletal muscle

2. Cardiac muscle

3. Smooth muscle

Common property: Excitability

 Ability to change electrical states (polarized to depolarized)

 Transmits an electrical signal called an action potential

Nervous System Interaction

 Skeletal muscle: Depends entirely on nervous system signals.

 Cardiac and smooth muscle: Can also respond to hormones and local stimuli (e.g., stretch,
chemicals).

Muscle Contraction Process

Triggered when actin is pulled by myosin.

In skeletal and cardiac muscle:

 Requires Ca²⁺, troponin, and tropomyosin

 Ca²⁺ exposes binding sites on actin

In smooth muscle:

 Ca²⁺ activates enzymes that activate myosin heads

  ATP (adenosine triphosphate) is required for contraction.
 Relaxation: Ca²⁺ is removed, binding sites are re-covered.

Properties of Muscle Tissue

1. Excitability: Responds to stimulation.

2. Contractility: Can shorten with force.
3. Extensibility: Can stretch.
4. Elasticity: Returns to original length after stretching due to elastic fibers.

Structural Differences

Striations:

 Present in skeletal and cardiac muscle (due to organized actin and myosin)
 Absent in smooth muscle (no regular arrangement)

Nuclei:

 Skeletal muscle: Multinucleated

 Cardiac muscle: 1–2 nuclei per fiber
 Smooth muscle: Single nucleus

II. SKELETAL MUSCLE

Functions of Skeletal Muscle

 Movement: Primary function is to contract and produce movement.

 Posture Maintenance: Constant minor contractions help resist gravity and maintain balance.
 Joint Stabilization: Prevents excessive movement and dislocation by stabilizing joints.
 Substance Control: Located at openings of internal tracts to control voluntary actions like:
1. Swallowing
 2. Urination
3. Defecation
 Organ Protection: Acts as a shield for internal organs, especially in the abdominal and pelvic
regions.
 Heat Generation:
1. Muscle contraction breaks down ATP, releasing heat.
2. Seen during exercise and shivering (in cold conditions).

Skeletal Muscle as an Organ

Composed of:

 Skeletal muscle fibers

 Blood vessels
 Nerve fibers
 Connective tissues

Connective Tissue Layers (Mysia)

1. Epimysium:

 Outer layer
 Dense irregular connective tissue
 Surrounds the entire muscle
 Allows powerful contractions while maintaining integrity
 Separates muscle from other organs/tissues

2. Perimysium:

 Middle layer
 Surrounds fascicles (bundles of muscle fibers)
 Enables specific movements by targeting groups of fibers

3. Endomysium:

 Inner layer
 Thin layer surrounding each individual muscle fiber
 Contains collagen, reticular fibers, extracellular fluid, and nutrients

Muscle Attachment and Force Transmission

Tendon Connection:

 Collagen fibers from all three mysia layers merge with tendons
 Tendons attach to the periosteum of bones
 Transfers force for skeletal movement

Aponeurosis:

 Broad, flat tendon-like sheet

 Example: Lower back latissimus dorsi attachment

Fascia:

 Connective tissue linking skin to bones/muscles

SKELETAL MUSCLE FIBER

 Skeletal muscle cells are also called muscle fibers due to their long, cylindrical shape.
 They are large compared to other human cells:
 Diameter: up to 100 μm
 Length: up to 30 cm (e.g., Sartorius muscle in the thigh)

Development and Structure

 Muscle fibers are multinucleated:

 Formed by the fusion of multiple embryonic myoblasts
 Each myoblast contributes a nucleus
 This allows for the production of large amounts of proteins and enzymes necessary for
contraction

Terminology (Greek root: “sarco” = flesh)

 Sarcolemma: The plasma membrane of a muscle fiber

 Sarcoplasm: The cytoplasm of the muscle fiber
 Sarcoplasmic Reticulum (SR):
1. A specialized smooth endoplasmic reticulum
2. Stores, releases, and retrieves calcium ions (Ca²⁺) for muscle contraction
Sarcomeres – functional units of contraction

Contain organized contractile proteins:

 Actin (thin filaments)

 Myosin (thick filaments)
 Supported by structural proteins
 Sarcomeres are aligned end-to-end along the length of the myofibrils

THE SARCOMERE

 A sarcomere is the functional unit of a skeletal muscle fiber.

 It is responsible for the striated appearance of skeletal muscle due to the organized
arrangement of actin and myosin filaments.

Structure

 Sarcomeres are bundled within myofibrils, which extend the entire length of the muscle fiber.
 Each muscle fiber contains hundreds to thousands of myofibrils, and each myofibril contains
thousands of sarcomeres.
 Size: Approximately 2 μm in length
 Shape: Cylindrical and organized in a three-dimensional array

Components

1. Z-discs (Z-lines):

 Define the boundaries of each sarcomere

 Serve as the anchor points for actin (thin) filaments

2. Thin Filaments:

 Composed of actin, troponin, and tropomyosin

 Extend from the Z-discs toward the center of the sarcomere
 Called "thin" due to their narrow diameter

3. Thick Filaments:

 Composed of myosin
 Positioned at the center of the sarcomere
 Have multiple heads that interact with actin for muscle contraction
  Called "thick" due to their greater mass and size

Muscle Contraction

 As myofibrils contract, entire muscle fibers contract.

 Contraction is the result of the interaction between actin and myosin within each sarcomere.

EXCITATION-CONTRACTION COUPLING

 All living cells have an electrical charge difference across their membranes called the membrane
potential.
 For most cells, the inside is negative (around -60 to -90 mV) compared to the outside.
 Muscle and nerve cells are electrically excitable, meaning they can use this charge difference to
send signals through action potentials.

What is Excitation-Contraction Coupling?

 Excitation-contraction coupling is the process that links the nerve signal to muscle contraction.
 For contraction to occur, the muscle fiber must first be excited by a nerve impulse, which causes
an action potential in the sarcolemma.
 This excitation leads to the release of calcium ions (Ca²⁺) from the sarcoplasmic reticulum (SR)
inside the muscle fiber.
 Calcium binds to troponin, moving tropomyosin away from actin’s binding sites, allowing myosin
to attach and pull the actin filament—resulting in contraction.

Nervous System Involvement

 Skeletal muscle excitation always begins with the somatic motor division of the nervous system.
 Motor neurons originate in the spinal cord (and brainstem for face, head, and neck muscles).
 These neurons send signals via long extensions called axons that reach the muscle fibers.

The Neuromuscular Junction (NMJ)

1. The axon terminal of a motor neuron reaches the neuromuscular junction (NMJ).
 2. The neuron releases a chemical called acetylcholine (ACh) into the synaptic cleft.
3. ACh binds to ACh receptors on the motor end-plate of the sarcolemma.
4. This opens channels for positive ions to enter the muscle fiber, depolarizing the membrane
(making it less negative).
5. Voltage-gated sodium channels open, creating an action potential that spreads along the
sarcolemma.

Rapid Signal Transmission and Control

 The action potential spreads rapidly, and immediately afterward, the membrane repolarizes
(returns to resting potential).
 Acetylcholinesterase (AChE) breaks down ACh in the synaptic cleft to prevent prolonged
stimulation of the muscle.

Role of T-Tubules and Triads

 T-tubules (transverse tubules) are invaginations of the sarcolemma that penetrate deep into the
muscle fiber.
 They carry the action potential to the sarcoplasmic reticulum (SR).

 The triad is a structure formed by one T-tubule and two adjacent areas of the SR.
 This setup ensures synchronized release of calcium ions, surrounding the myofibrils that contain
actin and myosin filaments.

III. MUSCLE FIBER CONTRACTION AND RELAXATION

Initiation of Muscle Contraction

 Signal Source: The process begins with a neural signal—an action potential from a motor
neuron.
 Neurotransmitter Involved: Acetylcholine (ACh) is released at the neuromuscular junction
(NMJ).
 Depolarization: ACh binds to receptors on the motor end-plate of the muscle fiber, causing Na⁺
ions to enter and depolarize the sarcolemma.
  Propagation: The action potential travels along the sarcolemma and into the T-tubules, reaching
the sarcoplasmic reticulum (SR).

Calcium Release and Role

 Triggering Calcium Release: Depolarization of the T-tubules causes voltage-gated calcium

channels in the SR to open.
 Calcium Function: Ca²⁺ ions are released into the sarcoplasm, where they bind to troponin.
 Uncovering Binding Sites: This binding causes tropomyosin to shift, exposing the myosin-binding
sites on actin filaments.

Sliding Filament Model of Contraction

 Cross-Bridge Formation: Myosin heads attach to the exposed binding sites on actin.
 Power Stroke: With the help of ATP, myosin pulls the actin filaments toward the center of the
sarcomere, shortening the muscle fiber.
 Cross-Bridge Cycling: This cycle continues as long as:
1. Ca²⁺ is present in the sarcoplasm.
2. ATP is available to power the movement and release of myosin heads.

Muscle Relaxation

 End of Signal: When the motor neuron stops signaling, ACh is broken down by
acetylcholinesterase (AChE).
 Repolarization: The muscle fiber membrane repolarizes, closing the calcium channels in the SR.
 Calcium Reuptake: Ca²⁺ is actively pumped back into the SR using ATP-powered calcium pumps.
 Restoration: Tropomyosin returns to its original position, covering the binding sites, and
preventing further cross-bridge formation.

Structural Basis of Contraction – The Sarcomere

Sarcomere Components:

 Z-discs: Anchor the ends of thin (actin) filaments.

 M-line: Center of the sarcomere; anchors thick (myosin) filaments.
 Zone of Overlap: Area where actin and myosin overlap—critical for contraction.
 Contraction: As sarcomeres shorten, myofibrils and entire muscle fibers contract.
Muscle Fatigue

Contraction ends when:

 Neural stimulation ceases.

 ATP supply is exhausted.
 The muscle enters a state of fatigue, reducing contractile function.

THE SLIDING FILAMENT MODEL OF MUSCLE CONTRACTION

 The sliding filament model explains how skeletal muscle fibers contract by thin filaments (actin)
sliding past thick filaments (myosin) within each sarcomere.
 This process starts when a motor neuron signals the muscle fiber, causing Ca²⁺ ions to enter the
sarcoplasm.

Role of Regulatory Proteins

A. Tropomyosin

 A long, thread-like protein that wraps around actin filaments.

 Function: Blocks the myosin-binding sites on actin, preventing contraction when the muscle is at
rest.

B. Troponin

 A globular protein complex attached to tropomyosin.

 Has a binding site for Ca²⁺ ions.
 When Ca²⁺ binds to troponin, it changes shape, causing tropomyosin to shift and expose myosin-
binding sites on actin.

Initiation of Contraction
  Calcium Release: Ca²⁺ is released into the sarcoplasm from the sarcoplasmic reticulum.
 Calcium Binding: Ca²⁺ binds to troponin.
 Tropomyosin Movement: This causes tropomyosin to move away from the myosin-binding sites
on actin.
 Cross-Bridge Formation: Myosin heads bind to exposed sites on actin, forming cross-bridges.

Cross-Bridge Cycling

 Power Stroke: Myosin heads pull the actin filaments toward the center of the sarcomere.

ATP Role:

 ATP is needed to detach the myosin head from actin.

 The hydrolysis of ATP re-cocks the myosin head to repeat the cycle.
 This cycle repeats, shortening the sarcomere and producing muscle contraction, as long as Ca²⁺
and ATP are available.

ATP AND MUSCLE CONTRACTION

Energy and the Cross-Bridge Cycle

 Muscle contraction depends on the sliding filament mechanism, driven by the interaction of
actin and myosin filaments.
 This repeated interaction is called the cross-bridge cycle, which is ATP-dependent.

Cross-Bridge Cycle Steps

A. Formation

 Myosin head binds to actin while still holding ADP + Pi.

 This creates a weak bond at first.

B. Power Stroke

 Pi is released, strengthening the actin-myosin bond.

 The myosin head bends, pulling actin 10 nm toward the M-line.
 This pulling motion is the power stroke.
 C. Detachment

 After the power stroke, ADP is released, but myosin still remains attached to actin.
 ATP binds to the myosin head, causing it to detach from actin.

D. Re-Cocking

 ATP is hydrolyzed to ADP and Pi by myosin’s ATPase activity.

 Energy from hydrolysis re-cocks the myosin head to a high-energy position.
 The cycle repeats as long as ATP and Ca²⁺ are present.

Energy Demand in Muscle Cells

 Each thick filament has about 300 myosin heads, each capable of forming cross-bridges.
 Multiple cross-bridges form and break continuously during contraction.
 This high frequency of activity across thousands of sarcomeres and muscle fibers requires
enormous ATP supply.

Rigor Mortis: A Result of ATP Absence

 After death, ATP production ceases.

 Without ATP, myosin heads cannot detach from actin.
 Muscles stiffen as a result of continuous cross-bridge attachment—this is called rigor mortis.

SOURCES OF ATP FOR MUSCLE CONTRACTION

 ATP and Muscle Contraction Overview

 ATP is essential for cross-bridge cycling and Ca²⁺ reuptake into the sarcoplasmic reticulum (SR).
 Muscles store limited ATP, enough for only a few seconds of contraction.
 Continuous ATP regeneration is crucial for sustained activity.

Three Main Sources of ATP:

1. Creatine Phosphate (CP) System

 Immediate energy source (first ~15 seconds).

  In resting muscles, ATP transfers phosphate to creatine → creatine phosphate + ADP.
 During contraction, CP donates phosphate to ADP → ATP + creatine (via creatine kinase).
 Rapid but short-term ATP production.

2. Anaerobic Glycolysis and Fermentation

 Occurs without oxygen.

 Breaks down glucose (from blood or glycogen) → 2 ATP + 2 pyruvic acid.
 If O₂ is insufficient, pyruvic acid → lactic acid, regenerating NAD⁺.
 Provides energy for ~1 minute of high-intensity effort.
 Less efficient and leads to muscle fatigue due to lactic acid buildup.

3. Aerobic Respiration

 Oxygen-dependent, occurs in mitochondria.

 Substrates: glucose, pyruvic acid, fatty acids.
 Produces ~36 ATP per glucose.
 Supports 95% of ATP needs in resting/moderate activity.
 Slower, but efficient and long-lasting.
 Myoglobin stores O₂ in muscle for better endurance.
 Aerobic training enhances O₂ delivery and usage.l

Muscle Fatigue

 Inability of muscle to contract despite continued neural stimulation.

Causes:

 Depleted ATP.
 Lactic acid accumulation → ↓pH → enzyme inhibition.
 Na⁺/K⁺ imbalance affects Ca²⁺ release.
 Possible SR or sarcolemma damage from prolonged activity.
 Oxygen Debt (Post-Exercise Recovery)
 Extra O₂ needed after exercise to:
 Replenish ATP & CP stores.
 Convert lactic acid → pyruvic acid → glucose/glycogen (via liver).
 Support recovery of other systems.
 Explains heavy breathing after exercise.

RELAXATION OF A SKELETAL MUSCLE

  Initiation: Begins when the motor neuron stops releasing acetylcholine (ACh) at the
neuromuscular junction (NMJ).
 Repolarization: The muscle fiber repolarizes, leading to the closure of calcium (Ca²⁺) release
channels in the sarcoplasmic reticulum (SR).

Calcium Reuptake:

 ATP-powered Ca²⁺ pumps actively transport calcium ions back into the SR.
 This lowers cytoplasmic Ca²⁺ levels.

Blocking Cross-Bridge Formation:

 Low Ca²⁺ levels cause tropomyosin to cover actin-binding sites again.

 Without exposed binding sites, cross-bridge cycling stops, and the muscle relaxes.

MUSCLE STRENGTH

Fixed Number of Muscle Fibers:

 Determined genetically; does not increase with training.

Strength Depends On:

 Number of myofibrils and sarcomeres per fiber.

 These can increase with training, a process known as hypertrophy.

Hypertrophy:

 Triggered by hormones, resistance training, or anabolic steroids.

 Results in increased muscle mass and force production.

Atrophy:

 Occurs with disuse or disease.

 Leads to loss of myofibrils and sarcomeres, not muscle fibers.
 Common in immobilized limbs or conditions like polio.

IV. NERVOUS SYSTEM CONTROL OF MUSCLE TENSION

Types of Muscle Contractions

1. Isotonic Contractions – Muscle changes length while tension remains constant:

 Concentric: Muscle shortens as it contracts (e.g., lifting a weight).

 Eccentric: Muscle lengthens while maintaining tension (e.g., lowering a weight slowly).

2. Isometric Contractions – Muscle produces tension without changing joint angle or muscle length:

 Occurs when force cannot overcome the load.

 Important in posture and joint stability.

Example: Trying to lift an immovable object still activates sarcomeres, but no movement occurs.

Muscle Tension and Load

 Load: The object that muscle tension attempts to move.

 Muscle Tension: Force generated by sarcomere contraction.
 Movement occurs only when muscle tension exceeds the load.

 Most real-life actions involve both isotonic and isometric contractions working together.

MOTOR UNITS AND NEURAL CONTROL

Motor unit: A single motor neuron and all the muscle fibers it innervates.

Type of contraction

1. Concentric Contraction

 A type of isotonic contraction where the muscle shortens as it contracts to move a load.

Example: Lifting a dumbbell upward during a bicep curl.

2. Eccentric Contraction

 A type of isotonic contraction where the muscle lengthens while still producing tension.

Example: Lowering a dumbbell slowly during a bicep curl.

3. Isometric Contraction
  The muscle produces tension but does not change in length and no joint movement occurs.

Example: Holding a heavy object in place without moving it.

Three Phases of a Muscle Twitch:

1. Latent phase: During this time, action potentials travel, and calcium ions are released from the
sarcoplasmic reticulum

2. Contraction phase: This is when the actual contraction happens.

3. Relaxation phase: The muscle returns to its resting state.

 Wave Summation: Increased force due to rapid, repeated stimuli.

 Tetanus: Sustained muscle contraction from high-frequency stimulation.
 Treppe: Gradual increase in contraction strength after repeated stimuli.

LENGTH-TENSION RELATIONSHIP

This refers to how the initial length of a sarcomere (the basic unit of muscle fiber) affects the amount of
tension a muscle can produce during contraction.

 Optimal sarcomere length (80%–120% of resting length) allows maximum overlap between thick
(myosin) and thin (actin) filaments, leading to strongest tension.
 If the sarcomere is too stretched (>120%), there’s less overlap, fewer cross-bridges form, and
tension decreases.
 If it’s too compressed (<80%), filaments overlap too much, limiting movement and reducing
tension.
 If there's no overlap at all, no tension can be produced because no cross-bridges can form.

THE FREQUENCY OF MOTOR NEURON STIMULATION

1. Muscle Twitch

 A single, brief contraction caused by one action potential.

 Measured by a myogram.
 Duration: few ms to 100 ms depending on muscle type.

Phases of a Twitch:

 Latent Period: AP propagates; Ca++ released from SR; no contraction yet.

 Contraction Phase: Ca++ binds to troponin; cross-bridges form; sarcomeres shorten.
  Relaxation Phase: Ca++ reabsorbed into SR; cross-bridge cycling stops; muscle returns to rest.

2. Graded Muscle Response

 Real muscle contractions require repeated stimuli.

Controlled by:

 Frequency of action potentials.

 Number of motor units activated.
 Allows muscles to vary in strength and duration of contraction.

3. Wave Summation

 Occurs when a second stimulus hits before relaxation ends.

 Ca++ accumulates, increasing tension.
 Results in stronger contraction due to summation of effects.

4. Tetanus

Incomplete Tetanus:

 Rapid stimulation with brief relaxation phases.

 Muscle tension builds; wavelike pattern.
 Tension = 3–4× that of a single twitch.

Complete Tetanus:

 Very high frequency stimulation.

 No relaxation between stimuli.
 Smooth, sustained maximal contraction.

TREPPE

 A phenomenon where a muscle that has been inactive contracts more forcefully with repeated
stimulation.
 The force of contraction increases gradually with each stimulus, resembling a staircase pattern.
 Initial contractions are weaker, while later contractions are stronger and more efficient.
 Also called the “staircase effect.”

Cause:

 Repeated stimulation leads to increased Ca++ concentration in the sarcoplasm.

  More Ca++ enhances cross-bridge cycling and muscle contraction strength.
 Requires adequate ATP to sustain the effect.

MUSCLE TONE

 A state of continuous, partial contraction in resting muscles.

 Maintains posture and joint stability even when muscles appear at rest.
 Controlled by the nervous system through cyclical activation of motor units.

Key Features:

 Prevents complete fatigue by allowing some motor units to rest while others are active.
 Ensures readiness of muscles for sudden movement.

Disorders:

1. Hypotonia (Low Muscle Tone)

 Causes: CNS damage (e.g., cerebellum), nerve damage (e.g., polio).

 Characteristics: Flaccid muscles, weak reflexes, muscle atrophy.

2. Hypertonia (Excessive Muscle Tone)

Cause: Damage to upper motor neurons (CNS).

Types:

 Rigidity: Constant resistance to movement (e.g., Parkinson’s disease).

 Spasticity: Sudden resistance then release of a limb (e.g., post-stroke).

Often accompanied by hyperreflexia (exaggerated reflexes).