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Skeletal muscles
Over 600 in the body; responsible for movement and contraction in living animals.
Tendon vs Ligament
Tendon connects muscle to bone; ligament connects bone to bone.
Connective tissue layers
Epimysium (muscle), Perimysium (muscle bundle), Endomysium (muscle fiber).
Muscle organization hierarchy
Muscle → Muscle bundle → Muscle fiber (myofiber) → Myofibril → Myofilament (actin/myosin).
Myofibril structure
Contains repeating units called sarcomeres; made of actin (thin) and myosin (thick) filaments.
Sarcomere structure
Smallest functional unit of a muscle fiber; bounded by Z-lines and contains A-band (myosin) and I-band (actin).
Actin
Thin filament protein; interacts with myosin during muscle contraction.
Myosin
Thick filament protein; most abundant muscle protein; forms crossbridges with actin.
Z-line
Defines the boundaries of a sarcomere; where actin filaments anchor.
M-line
Center of sarcomere; connects thick filaments together.
Titin
Elastic protein that stabilizes myosin and contributes to elasticity of muscle.
Desmin
Intermediate filament linking Z-lines; maintains structural integrity.
Sarcoplasmic reticulum (SR)
Organelle regulating calcium ion release and reuptake during contraction and relaxation.
Sarcolemma
Plasma membrane surrounding the muscle fiber; involved in electrical excitation.
T-tubules
Invaginations of sarcolemma that transmit action potentials deep into the muscle fiber.
Motor neurons
Axons that control skeletal muscle contraction.
Action potential
Rapid rise and fall in electrical membrane potential that triggers muscle excitation.
Acetylcholine (ACh)
Neurotransmitter released at neuromuscular junction; binds to receptors on sarcolemma to trigger depolarization.
Resting membrane potential
Approx. -70 mV; maintained by Na+/K+ ATPase pump (3 Na+ out, 2 K+ in).
Depolarization
Voltage-gated Na+ channels open, Na+ enters cell, making inside more positive.
Repolarization
Voltage-gated K+ channels open, K+ exits cell, restoring negative potential.
Hyperpolarization
Membrane potential briefly more negative than resting potential (~-90 mV).
Actomyosin
Complex of actin and myosin formed during crossbridge cycle; responsible for contraction.
Excitation-contraction coupling
Link between action potential and muscle contraction; involves Ca2+ release from SR.
Calcium role
Ca2+ binds to troponin, causing tropomyosin to shift and expose binding sites on actin for myosin attachment.
ATP in contraction
ATP binds myosin head to release crossbridge; hydrolysis provides energy for power stroke.
Rigor mortis
Postmortem process where muscles stiffen due to ATP depletion and permanent actomyosin crossbridges.
Rigor mortis stages
Delay (ATP present), Onset (stiffening), Completion (actomyosin fixed), Resolution (proteolytic degradation).
Muscle fiber types
Red (Type I), White (Type IIB), and Intermediate (Type IIA) fibers with distinct functions and metabolism.
Type I fibers
Slow-twitch, oxidative, high myoglobin, small diameter, many mitochondria, high endurance.
Type IIA fibers
Fast oxidative-glycolytic, intermediate diameter and color, balanced metabolism.
Type IIB fibers
Fast-twitch, glycolytic, low myoglobin, large diameter, low endurance, rapid contraction.
Color differences in fibers
Red = more myoglobin and mitochondria; White = less myoglobin, anaerobic metabolism.
Red muscle function
Slow, sustained contractions (posture muscles); fatigue-resistant.
White muscle function
Fast, powerful contractions (locomotion); easily fatigued.
Myoglobin function
Oxygen storage and transport protein in muscle; influences color.
Comparative examples
Marathon runner = more red fibers; sprinter = more white fibers.
Animal examples
Duck breast = red (sustained flight); Chicken breast = white (short bursts).
Chewing vs eye muscles
Chewing muscles = red, slow, sustained; Eye muscles = white, fast, short bursts.
Fiber type and species
Rabbit, Pig, Ox show varying fiber distributions (pig muscles have red fibers grouped centrally).
White fiber prevalence
Most muscles contain majority white fibers, even in red muscles.
Structure-function relationship
Red fibers have more mitochondria, capillaries, lipids, and smaller diameters for heat/waste dissipation.
White fiber structure
Larger diameter, more myofibrils, high glycogen, adapted for anaerobic metabolism and rapid contraction.
Feel the burn
During intense activity, limited oxygen leads to lactic acid accumulation and burning sensation.
Effect of training
Endurance training increases oxidative capacity; sprint training enhances glycolytic fibers.
Rigor mortis and meat texture
Permanent actomyosin crossbridges increase toughness until proteolysis softens tissue.
Protein degradation postmortem
Desmin, titin, and myosin heavy chain degrade over time, aiding tenderness.
Cooking and carcinogens
High-temperature cooking produces HCAs, PAHs, and nitrosamines linked to cancer risk.
HCAs (Heterocyclic amines)
Formed from Maillard reaction between creatine, amino acids, and sugars at high heat; carcinogenic.
PAHs (Polycyclic aromatic hydrocarbons)
Formed from incomplete fat combustion (grilling/broiling); carcinogenic potential.
Nitrosamines
Formed when proteins react with nitrite/nitric oxide at high temperatures or acidity; found in cured meats.
Factors affecting HCA formation
Cooking temperature/time, method, moisture, lipid content, and meat type.
Cooking methods and HCAs
High: grilling, broiling, pan-frying; Low: roasting, baking, boiling.
Inhibiting HCA formation
Lower cooking temps, microwave precooking, antioxidants (BHA, BHT, polyphenols), phosphates.
Cancer risk chemicals in cooked meat
HCAs (burned), PAHs (incomplete combustion), nitrosamines (cured meat).