Focuses on the structure and function of muscle tissue.
Includes various muscle types (skeletal, cardiac, smooth) and their contraction mechanisms.
Review: Structure of Skeletal Muscles
Motor Unit
Events at the Neuromuscular Junction
Excitation-Contraction Coupling
Sliding Filament Mechanism
Twitch, Summation, and Tetanus
Smooth and Cardiac Muscle Contraction
Attached to bone on each end by tendons.
Insertion: more movable attachment.
Origin: less movable attachment.
Contraction of muscles causes tension on tendons, moving bones at a joint.
Flexors decrease the angle of joints; Extensors increase it.
Muscle fibers: muscle cells, multinucleated, striated.
Sarcolemma: plasma membrane of muscle fibers.
Distinctive striations visible due to the arrangement of myofibrils.
Each muscle fiber consists of myofibrils (1μm in diameter).
Myofibrils: filled with myofilaments (thick and thin filaments).
Thick filaments: made of myosin.
Thin filaments: made of actin.
Sarcolemma and sarcoplasm also present in muscle fibers.
Organelles containing protein fibers essential for contraction.
Composed of sarcomeres arranged end to end.
A band: dark area; contains thick filaments (myosin).
H band: area in the center of the A band where actin and myosin don't overlap.
I band: light area; contains thin filaments (actin).
Z line/disc: center of the I band, where actin attaches.
Each motor neuron branches to innervate multiple muscle fibers.
A motor unit consists of one motor neuron and all fibers it innervates.
Activation leads to all muscle fibers in the motor unit contracting sequentially.
Innervation Ratio: varying from 1:100 to 1:2000, indicating fine control.
Recruitment: process of activating more motor units for smooth muscle operation.
Ca2+ influx: opens voltage-gated channels.
Exocytosis of ACh into the synaptic cleft.
ACh binds to receptors, causing muscle depolarization and action potential.
ACh is broken down, leading to muscle relaxation.
Contractile Proteins: Myosin and Actin.
Regulatory Proteins: Troponin and Tropomyosin.
Structural Proteins: Titin, Nebulin, Alpha-actin, Myomesin, Dystrophin.
Genetic disorders causing skeletal muscle degeneration and replacement with scar tissue.
Duchenne Muscular Dystrophy: most common form, X-linked, leads to muscle necrosis.
Step 1: Sarcolemma conducts action potentials from ACh release.
Step 2: Depolarization leads to T-tubule action potential.
Step 3: VG Ca2+ channels in sarcoplasmic reticulum (SR) cause Ca2+ release.
Contraction initiated by tropomyosin movement exposing myosin binding sites.
Relaxation: Ca2+ pumped back into SR, blocking myosin sites.
Muscle contractions involve the sliding of thin filaments over thick filaments, causing sarcomere shortening.
A bands move closer; I bands shorten during contraction.
ATP is crucial for contraction and relaxation; limited to a few seconds without replenishment.
Methods of ATP production include:
Creatine phosphate (15 seconds)
Anaerobic glycolysis (2 minutes)
Cellular respiration (>2 minutes).
Muscle Fatigue: results from inadequate Ca2+, nutrient depletion, lactic acid accumulation.
Slow Oxidative (SO): endurance; high mitochondria.
Fast Glycolytic (FG): power; fatigue easily.
Fast Oxidative-Glycolytic (FOG): intermediate properties.
Recruitment order: SO → FOG → FG.
Cardiac Muscle: striated, involuntary, branched, intercalated discs.
Smooth Muscle: no striations, more actin than myosin, contracts as a single unit (visceral) or individually (multi-unit).
Contraction regulated through Ca2+ and influenced by hormones and local factors.