Skeletal Muscle Contraction Quiz

Skeletal Muscle Contraction

• Flexors: Muscles that shorten, bringing attached bones closer together.
• Tendons: Attach skeletal muscles to bones.
• Origin: The stationary end of a skeletal muscle.
• Antagonistic Muscles: Flexors contract while their opposing extensors relax for limb movement.
• Transverse Tubules (T-tubules): Rapidly conduct action potentials to the muscle fiber interior.
• Actin: Globular molecules polymerized into filaments.
• Myosin & Actin: Interconnected by cross-bridges that span the gap.
• Striated Muscles: Muscle fibers with repeating light and dark bands called sarcomeres.
• I bands: Contain only thin filaments (actin).
• H zone: Contains only thick filaments (myosin).
• Titin: Stabilizes the position of contractile filaments.
• Sarcomere Shortening: Occurs during muscle contraction, along with I band shortening.
• Cross-bridge Formation: Proportional to the generated tension in a muscle fiber.
• Calcium's Role: Binds to troponin, which moves tropomyosin, allowing high force cross-bridge formation.
• Myosin Head Function: Binding sites for actin and ATP; detaches from actin when ATP binds.
• Power Stroke: Release of ADP immediately follows the power stroke.
• ATP Hydrolysis: Causes myosin to rotate, repositioning it to bind to actin.
• Force Decrease: Lower intracellular calcium levels reduce force.
• DHP Receptor: Detects action potentials traveling along the T-tubule.
• Neuromuscular Junction: Acetylcholine binding opens a channel for Na+ and K+, triggering an action potential.
• Sarcoplasmic Reticulum (SR): Ca2+ release from SR triggers the contraction cycle.
• Ca2+ ATPase: Crucial for muscle relaxation, removing Ca2+ from the cytoplasm.
• Latent Period: Delay between action potential and muscle contraction.
• Phosphocreatine: Backup energy molecule quickly converted to ATP in active muscles.

Muscle Energy & Fatigue

• Exercise & ATP: Carbohydrate metabolism during heavy exercise meets ATP needs.
• Muscle Fatigue: Primarily from excitation-contraction coupling failures.
• Extended Exercise Fatigue: Glycogen stores depletion is a primary cause.
• Slow-twitch Fibers: Long contraction duration, high capillary density.
• Myosin ATPase Isoform: Determines the speed of force development.
• Sarcomere Length & Twitch: Sarcomere length before contraction affects twitch tension.
• Motor Unit: One neuron controlling multiple muscle fibers.
• Fast-twitch Motor Units Activation: Activated by weak contractile stimuli.
• Fast-twitch vs Slow-twitch: Fast twitch fibers generate more force, and fatigue faster.
• Isotonic vs Isometric: Isotonic = movement; Isometric = no movement/equal load.

Smooth Muscle

• Smooth Muscle Contraction: Slower and more sustained than skeletal muscle.
• Troponin Lack: Smooth muscle lacks troponin.
• Myosin Light Chain Kinase (MLCK): Ca2+-calmodulin complex activates this enzyme; phosphorylates myosin light chains.
• IP3 Receptor Channel: Opened by increased phospholipase C activity, releasing Ca2+.
• Pharmacomechanical Coupling: Change in smooth muscle tension without electrical potential change.
• Twitch Duration: Determined by the rate of Ca2+ removal.
• Smooth Muscle Energy Use: Low energy use for force generation, sustained contractions with no fatigue.
• Skeletal vs Smooth Muscle Calcium Source: Both sarcoplasmic reticulum and extracellular calcium involved
• Energy Source: Smooth muscle uses a variety of sources, not just oxidative phosphorylation

Muscle Fiber Types & Recruitment

• Fiber Recruitment Order (Weak to Strong Stimulus): Fatigue-resistant slow twitch, fatigue-resistant oxidative fast twitch and glycolytic fast twitch
• Fiber Force Increase: Increasing action potential frequency.
• Fiber Endurance: Oxidative phosphorylation.
• Lever System: Bones act as levers, joints as fulcrums for muscle-bone interactions.