Muscle Tissues: Types, Properties & Functions

• Study notes regarding muscle tissues

Types of Muscle Tissue

• Skeletal muscle tissue attaches to bones, 40% of body mass, long, cylindrical, multinucleated, voluntary, striated, quick twitch, short contractions, and has many functions
• Cardiac muscle tissue found only in the heart, short and branched cells, usually uninucleated, involuntary, striated with intercalated discs, intermediate twitch, and maintains blood pressure
• Smooth muscle tissue found in hollow organ walls, short, spindle-shaped cells, single nucleus, slow twitch, long contractions, moves substances, and regulates vessel diameter

Skeletal Muscle Properties

• Excitability: responds to stimuli
• Contractility: shortens when stimulated
• Extensibility: lengthens when relaxed
• Elasticity: returns to resting length

Functions of Skeletal Muscle Tissue

• Produces Skeletal Movement: Muscle contractions pull on tendons and move bones in various coordinated movements
• Maintains Posture and Body Position: Tension in muscles maintains posture
• Supports Soft Tissues: Abdominal wall muscles support visceral organs
• Guards Entrances and Exits: Sphincters control swallowing, defecation, and urination
• Maintains Body Temperature: Heat from muscle contractions keeps body temperature within normal range, and 85% of body's heat comes from skeletal muscle tissue
• Provides Nutrient Reserves: Contractile proteins break down into amino acids for energy or glucose synthesis

Gross Anatomy of Skeletal Muscles

• Skeletal muscles are organs composed of skeletal muscle tissue plus connective tissues, nerves, and blood vessels
• Skeletal muscle tissue is highly vascularized and innervated which is a high metabolic rate and voluntary control
• Muscle is composed of large bundles called fascicles
• Each fascicle contains numerous muscle cells or myocytes (muscle fibers)
• Each muscle fiber is composed of myofibrils
• Each myofibril is composed of myofilaments: myosin (thick) and actin (thin)
• Myofilaments arranged in sarcomeres, the functional units

Connective Tissue Layers

• Epimysium: Dense collagen layer surrounding entire muscle, separates it from tissues
• Perimysium: Fibrous layer dividing muscle into fascicles, containing blood vessels and nerves for blood flow
• Endomysium: Connective tissue surrounding individual muscle fibers

Attachments

• Tendons: Collagen fiber bundles attaching muscle to bone
• Aponeurosis: Broad collagen fiber sheet attaching muscle to bone

Microscopic Anatomy of Skeletal Muscle Cells

• Sarcoplasm: Cytoplasm of muscle cell
• Contains more mitochondria and myoglobin (oxygen storage) than average cells
• Sarcolemma: Plasma membrane of muscle cell
• T tubules: Invaginations in sarcolemma forming passageways
• Sarcoplasmic reticulum (SR): Tubular network storing calcium ions
• Terminal cisterna: The storage of calcium ions
• Triad: One T tubule with two terminal cisternae

Sarcomere Anatomy

• Sarcomere: Functional unit with actin and myosin arrangement
• A band: Dense region of overlapping thick and thin filaments
• I band: Area with only thin filaments (actin)
• H band: Area within the A band with only thick filaments (myosin)
• M line: Anchors central portion of thick filaments inside of H band
• Z lines: Boundary between adjacent sarcomeres and anchors the thin filaments

Myofilament Anatomy

• Thin Filament (Actin): Composed of interacting proteins
• F-actin: Twisted strand of G-actin molecules
• G-actin: Molecule with an active site for myosin binding
• Tropomyosin: Covers G-actin active sites
• Troponin: Binds calcium ions, changes shape, and moves tropomyosin
• Thick Filament (Myosin): Myosin subunits twisted together
• Myosin subunits have a tail and a free head connected by a hinge
• 300 myosin molecules arranged with tails pointing to M line and heads forming a spiral

Neuromuscular Junction

• Skeletal muscle cells are stimulated by a motor neuron
• Motor neuron axon branches into synaptic terminals
• Synaptic terminals interact with muscle fiber sarcolemma at the neuromuscular junction
• Action potential reaches synaptic terminals that open calcium channels
• Calcium influx causes synaptic vesicles to release acetylcholine (ACh) into the synaptic cleft via exocytosis
• ACh binds to receptors (ion channels) on the motor end plate
• ACh binding opens channels, causing sodium influx and sarcolemma depolarization for an action potential and subsequent contraction
• Acetylcholinesterase breaks down ACh, preventing continuous contraction

Generating Action Potential

• Resting sarcolemma is polarized
• Extracellular environment is positive (Na+), and intracellular is negative (K+)
• Sarcolemma is relatively impermeable to both ions at rest
• Depolarization occurs when ACh binds and the motor end plate's Na+ ion channels open
• Sodium rushes into the cytoplasm localizing inside of the membrane
• Propagation: Positive charge changes adjacent sarcolemma permeability, opening more Na+ channels, and causing depolarization to spread
• Repolarization: The permeability of the sarcolemma changes once again
• The influx of sodium stops, but K+ begins to leak out, switching the outside of the membrane back to positive (charge)
• Since more K+ ions eventually leave, the membrane becomes hyperpolarized
• Sodium-Potassium Pump restores ion concentrations (3 Na+ out, 2 K+ in) to reach resting membrane potential
• Muscle fibers are in a refractory period during repolarization
• Action potentials are all or none responses

Excitation-Contraction Coupling

• Action potential moves along sarcolemma through the T tubules
• Terminal cisternae release Calcium ions into sarcoplasm
• Calcium ions are available to myofilaments of the sarcomere

Sliding Filament Mechanism

• Tropomyosin inhibits myosin cross-bridge attachment in resting muscle
• Calcium ions released from terminal cisternae bind to troponin which changes shape
• Troponin then exposes the binding sites on actin
• High-energy myosin heads attach to actin forming cross-bridge formation
• ADP + P release causes the myosin head to pivot and pull the actin filament towards the midline which is called the power stroke
• New ATP binds to myosin head and head detaches from actin
• ATP splits into ADP + P transferring energy to the myosin head
• Head is in the high-energy position (cocked or reactivated)
• Calcium is reabsorbed back into the terminal cisternae and tropomyosin covers active sites and cross-bridge formation stops and the muscle relaxes

Nervous System Control of Muscle Tension

• Tension production is greatest at optimal muscle length
• Amount of tension produced can not be regulated by changing amount of contracting sarcomeres
• Calcium ions are released by all triads which means the muscle is either contracting or relaxed

Myograms

• Myogram: Recording of muscle contractions (force vs. time)
• Twitch: Single stimulus-contraction-relaxation sequence
• Latent Period: Action potential spreads, calcium ions are released, and no tension is produced
• Contraction Period: Cross-bridge formation occurs and tension increases
• Relaxation Period: When calcium ions are no longer present, then attachment sites are covered and tension decreases.

Motor Units

• Motor unit: All muscle fibers controlled by a single motor neuron
• Varying number of fibers in motor units for fine or gross motor activities
• Recruitment is a smooth increase in muscle tension via increasing active motor units
• Muscle Tone: Variable number of active motor united creating resting tension
• Asynchronous Motor Unit Summation: Motor units activated on a rotating basis

Factors Determining Tension

• Tension depends on single muscle fiber tension amount and amount of stimulated muscle fibers
• Treppe: Gradual increase in contraction force after complete relaxation occurring, and is sometimes call the "staircase effect"
• Wave Summation: Stimuli arrive as relaxation begins, causing larger contractions
• Incomplete Tetanus: Almost peak tension during rapid contraction/relaxation cycles until a plateau
• Complete Tetanus: Rapid stimulation with no relaxation time

Muscle Contraction Force

• Optimum overlap is 80-120% of resting length
• Less than 80% overlap means an inability to add new cross bridges
• Greater than 120% means a lack of cross bridges and sarcomere stretching

Energy for Contraction

• Muscle contraction requires ATP from aerobic or anaerobic production
• Mitochondrial activity is the ultimate energy source
• Stored ATP is in limited amounts providing 2 seconds/10 twitches of energy.
• Creatine phosphate (ADP + creatine phosphate = creatine + ATP) creates 15 seconds/70 twitches of energy
• Glycolysis (anaerobic) produces 2 ATP for 130 seconds/670 twitches energy
• Aerobic pathways (citric acid cycle/ETS) requires oxygen but produces 36 ATP providing 2400 seconds/12,000 twitches energy
• Oxygen debt occurs when high exertion causes lactic acid build up
• Oxygen, lactic acid, glycogen, ATP, creatine phosphate must be resynthesized for recovery

Muscle Fatigue

• Fatigue is when muscles can not perform at required levels
• Decline in pH, decreasing calcium ion binding to troponin, altering enzyme activities
• Recovery period returns muscle fiber conditions to normal
• Moderate activity recovery takes a few hours; higher levels take a week

Types of Muscle Fibers

• Slow Fibers (Type I): Small, slow peak tension and contraction, high fatigue resistance, red, high myoglobin, high vascularization, many mitochondria, few glycolytic enzymes. Also called slow twitch, oxidative, red, Type I, slow, or slow oxidative (SO)
• Intermediate Fibers (Type IIa): Intermediate diameter/peak tension/fatigue resistance, fast contraction, pink, low myoglobin, intermediate vascularization/mitochondria, many glycolytic enzymes. Also called fast-twitch oxidative (FO), fast resistant (FR), or Type II-A.
• Fast Fibers (Type IIb): Large, rapid peak tension/contraction, low fatigue resistance, white, low myoglobin/blood supply/mitochondria, high glycolytic enzymes. Also called fast-twitch muscle, glycolytic, white, Type II-B, and fast-fatigue (FF)

Effect of training

• Hypertrophy: Enlargement of stimulated muscle via fiber diameter increases
• Atrophy: Muscle becomes flaccid, loses tone/power, decreases in diameter due to lack of use
• Paralysis: Loss of muscle control

Muscle Diseases

• Polio is a viral infection attacking motor neurons
• Tetanus is a bacterial infection releasing toxins, which interferes with motor neuron communication
• Botulism is a bacterial infection that blocks acetylcholine release
• Anticholinergics are drugs that block Ach receptors and preventing motor end plate potential

Rigor Mortis

• Rigor mortis is sustained contraction after death because of ATP loss in muscle
• Actins cannot detach resulting in prolonged contraction
• It Begins after 2-7 has passed since death and disappears after 1-6 days

Smooth Muscle

• Smooth muscle cells are long and slender
• Actin/myosin contraction differently arranged vs skeletal/cardiac muscle
• Lack of sarcomeres/myofibrils results into smooth and unstriated muscle
• Thin fibers (actin) attached to dense bodies vs z lines
• More heads per thick filament, scattered throughout sarcoplasm
• No T-tubules and loose sarcoplasmic reticulum network
• Calcium ions enters from outside and inside the cell
• No troponin but has tropomyosin with calmodulin to bind to Ca2+
• Visceral smooth muscle cells have no direct contact with motor neurons and have caveolae
• Connected by gap junctions to spread signals
• Peristalsis: Two layers of smooth muscle alternate contract, constricting and causing contraction
• Calcium causes contraction Steps: Neurons/chemicals stimulate, Calcium ions enter using channels, Calcium opens SR, Calcium binds calmodulin, activating myosin kinase enzymes (phosphorylate myosin), activated myosin forms bridges, shortening, and contractions stop when Calcium is not available