Muscle Physiology

• Somatic motor pathways control voluntary movements by transmitting signals from the central nervous system (CNS) to skeletal muscles

Upper Motor Neurons (UMNs)

• Located in the primary motor cortex (precentral gyrus) of the frontal lobe
• Initiate voluntary movement by sending impulses down the spinal cord
• Travel via descending tracts, mainly the corticospinal tract (controls limb and trunk muscles) and the corticobulbar tract (controls muscles of the face and head via cranial nerves)

Lower Motor Neurons (LMNs)

• Located in the brainstem (for cranial nerves) and anterior horn of the spinal cord (for spinal nerves)
• Directly innervate skeletal muscles and cause contraction
• Receive input from UMNs and transmit signals through spinal nerves or cranial nerves to muscles

Neuromuscular Junction (NMJ) Structure

• A specialized synapse between a lower motor neuron and a skeletal muscle fiber
• Responsible for converting electrical nerve impulses into muscle contractions
• Presynaptic Terminal (Axon Terminal of LMN) contains synaptic vesicles filled with acetylcholine (ACh)
• When an action potential reaches the terminal, voltage-gated calcium (Ca2+) channels open, allowing Ca2+ influx
• The Ca2+ influx triggers the release of ACh into the synaptic cleft via exocytosis
• Synaptic cleft: A small gap between the motor neuron and the muscle fiber where ACh diffuses across and binds to receptors on the muscle cell membrane
• Postsynaptic Membrane (Motor End Plate of Muscle Fiber) contains nicotinic acetylcholine receptors (nAChRs), which are ligand-gated ion channels
• When ACh binds, Na+ (sodium) ions enter the muscle cell, causing depolarization
• If the depolarization reaches the threshold, an action potential propagates along the muscle fiber, leading to contraction
• Acetylcholinesterase (AChE) Enzyme is located in the synaptic cleft and rapidly breaks down ACh into acetate and choline to prevent continuous stimulation
• Choline is reabsorbed into the presynaptic neuron to synthesize more ACh

Function of the NMJ

• Step 1: Action Potential Arrival: A nerve impulse reaches the axon terminal of the LMN
• Step 2: Calcium Influx: Voltage-gated Ca2+ channels open, and Ca2+ enters the neuron
• Step 3: ACh Release: Synaptic vesicles release ACh into the synaptic cleft
• Step 4: ACh Binding: ACh binds to nicotinic receptors on the motor end plate
• Step 5: Na+ Influx & Depolarization: The receptor opens, allowing Na+ influx, generating an end-plate potential (EPP)
• Step 6: Muscle Action Potential: If EPP reaches threshold, voltage-gated Na+ channels open, propagating an action potential
• Step 7: Muscle Contraction: The action potential spreads via T-tubules, triggering calcium release from the sarcoplasmic reticulum, leading to contraction
• Step 8: ACh Breakdown: Acetylcholinesterase degrades ACh, stopping the signal

Skeletal Muscle

• Structure: Striated, elongated, multinucleated myofibers
• Responsible for voluntary movement and controls the movement of joints
• Attached to bones

Cardiac Muscle

• Structure: Striated, short, branching cells with a single centrally placed nucleus; Intercalated discs and gap junctions allow synchronized contractions
• Involuntary control
• Autorythmic pacemaker cells maintain a rhythmic heartbeat without nervous system input
• Found only in the heart

Smooth Muscle

• Structure: Non-striated, spindle-shaped cells with a single central nucleus and no sarcomeres; actin and myosin are anchored to dense bodies and lacks T-tubules
• Involuntary control and controlled by the autonomic nervous system
• Stretches and contracts, maintains contraction without fatigue (e.g., sphincters)
• Found in walls of hollow organs (e.g., stomach, intestines, bladder, blood vessels)

Contractile Proteins

• Generate Force for Contraction
• Myosin (thick filament) has heads that form cross-bridges with actin and uses ATP to generate movement
• Actin (thin filament) contains myosin-binding sites and interacts with myosin for contraction
• Thousands of myosin filaments lie along actin filaments in a muscle fiber

Regulatory Proteins

• Control Contraction
• Tropomyosin covers actin's binding sites at rest, preventing myosin from attaching
• Troponin binds calcium (Ca2+) and moves tropomyosin, allowing myosin to bind actin for contraction

Structural Proteins

• Provide Alignment, Stability, and Elasticity
• Titin (molecular "spring") helps return muscle to resting length after stretching, contributing to elasticity
• Alpha-Actinin anchors actin filaments to the Z-line, maintaining sarcomere structure
• Myomesin links intermediate filaments to the M-line, stabilizing thick filaments
• Nebulin acts as a thin filament "ruler," regulating actin filament length during sarcomere assembly
• Dystrophin connects the muscle fiber's cytoskeleton to the extracellular matrix, helping transmit force and maintain structural integrity but defects in dystrophin lead to muscular dystrophy

The Sliding Filament Mechanism

• Muscles contract by the interaction between thick (myosin) and thin (actin) filaments within the sarcomere. The filaments do not shorten but instead slide past each other, leading to muscle shortening
• Muscle contraction occurs when the sarcomere shortens
• Thick (myosin) and thin (actin) filaments overlap but do not change in length
• Cross-bridge cycling pulls actin toward the center of the sarcomere
• Z-discs move closer together, reducing sarcomere length

Steps of Muscle Contraction (Sliding Filament Theory)

• Step 1: Cross-Bridge Formation: Myosin heads bind to actin, forming cross-bridges
• Step 2: Power Stroke: Myosin pulls actin toward the M-line, shortening the sarcomere; ATP is used to release and reset the myosin head
• Step 3: Detachment & Resetting: New ATP binds to myosin, causing detachment from actin; ATP hydrolysis resets the myosin head for the next cycle
• Step 4: Repeat: The process continues as long as calcium (Ca2+) and ATP are available

Structure Change During Contraction

• Sarcomere Shortens
• Z-Discs move closer together
• A-Band remains the same (thick filaments do not shorten)
• I-Band shortens (thin filaments slide inward)
• H-Zone narrows or disappears

The Sliding Filament Mechanism Significance

• Explains how muscle fibers shorten without changing filament length
• Demonstrates the role of ATP in contraction and relaxation
• Describes the importance of calcium ions (Ca2+) in regulating contraction
• Forms the basis of all voluntary and involuntary muscle movement

Steps of the Contraction Cycle

• Step 1: Cross-Bridge Formation: Calcium (Ca2+) binds to troponin, causing tropomyosin to shift and expose myosin-binding sites on actin; Myosin heads attach to actin, forming cross-bridges
• Step 2: Power Stroke: Myosin heads pivot, pulling actin filaments toward the M-line (center of the sarcomere); ADP (Adenosine Diphosphate) and Pi (inorganic phosphate) are released, generating force
• Step 3: Cross-Bridge Detachment: ATP binds to myosin, causing it to detach from actin; Without ATP, myosin remains attached (as seen in rigor mortis)
• Step 4: Myosin Reset (Cocking of Myosin Head): ATP is hydrolyzed (split into ADP + Pi), re-energizing myosin heads; Myosin returns to its pre-stroke "cocked" position, ready for another cycle

Excitation-Contraction Coupling

• A process linking an action potential in the muscle fiber to muscle contraction: This involves electrical signaling, calcium release, and the initiation of crossbridge cycling
• Neuromuscular Junction Activation (Excitation): The action potential travels down the motor neuron, acetylcholine gets released into the synaptic cleft, ACh binds to receptors that open ligand-gated channels that allow more Na+ to enter than K+ exits causing depolarization that forms an end plate potential.
• Action Potential Propagation: The action potential travels down the sarcolemma and into T-tubules where DHP receptors detect voltage changes and activate ryanodine receptors on the sarcoplasmic reticulum (SR).
• Calcium Release from the SR & Crossbridge Formation & Contraction: Ryanodine receptors open, allowing Ca2+ to flood the cytosol from the SR causing a calcium induced calcium release that amplifies the Ca2+ release, the now free Ca2+ binds to troponin, causing tropomyosin to shift, exposing myosin-binding sites on actin which allows the myosin heads to bind to actin, initiating crossbridge cycling and muscle contraction.

Steps of Muscle Relaxation

• Nerve signal stops & the action potential ceases
• Acetylcholinesterase then breaks down acetylcholine in the synaptic cleft, stopping muscle fiber excitation
• Calcium is then reabsorbed back into the sarcoplasmic reticulum (SR) by Ca2+-ATPase pumps, reducing cytosolic calcium levels
• Troponin releases Ca2*, causing tropomyosin to block myosin-binding sites on actin
• Subsequently, Crossbridges detach because there is no more calcium available
• Muscle returns to resting length

Motor unit Description

• Consists of one motor neuron and all the muscle fibers it innervates, the human body has ~250 million muscle fibers but only 420,000 motor neurons, meaning each neuron controls multiple fibers.
• A single motor neuron can innervate 1 to 150+ muscle fibers, depending on the muscle's function, as well as having synchronized contraction where fibers in a motor unit contract and react the same time as the stimulus.
• Small motor units (few fibers per neuron) facilitate precise movements (e.g., eye muscles) & large motor units (many fibers per neuron) generate powerful movements (e.g., leg muscles)
• Different motor units are recruited in rotation to delay fatigue in muscles (especially in postural muscles)
• More motor units are activated when more force is needed (called recruitment) that follows the size principle where smaller units (slow-twitch, fatigue-resistant) are activated first, then larger units (fast-twitch, high-power) & motor units work together to ensure smooth, controlled movements instead of jerky, uncoordinated contractions

Muscle Tension and Force Factors

• More motor units = Greater force production.
• Size Principle (Small motor units recruited first, then larger as needed)
• Force is proportional to size and Larger fiber size produces more force
• Determined by it's ability to produce and use energy through oxidative capacity increasing the amount of ATP from Aerobic metabolism
• Speed of contraction is determined by the myosin ATPase activity
• Force id relational to the cross sectional area

Types Muscle Isotonic Contraction

• Isotonic Contraction, where the Muscle's length Changes, the force generates while changing length can then split into two types:
• Concentric Contraction: Muscle Shortens, Force is greater than resistance (lifting a dumbbell in a bicep curl)
• Eccentric Contraction: Muscle Lengthens, Resistance is greater than force (lowering a dumbbell in a bicep curl) and generates more force but also cause more damage
• Isometric Contraction: where the length does not change, and generates a force without changing length (Holding a plank), it occurs when resistance equals force and stabilizes help joints
• Isokinetic Contraction: (Constant Speed, Specialized Equipment), Muscle contracts at a constant speed with varying resistance using specialized machines.

Fast-Twitch Fibers (Type II)

• Rapid energy generation for quick, powerful muscle actions and has high amounts of Myosin & sarcoplasmic reticulum that contracts 3 - 5 times quicker relying on anaerobic glycolysis
• Suited for sprinting, jumping, and explosive movements that are important stop-and-go sports
• Subtypes of Type II Fibers: Fast-Oxidative-Glycolytic (FOG), Intermediate & Fast-Glycolytic (most anaerobic, highest speed & force) MYH Gene

Slow-Twitch Fibers (Type I)

• Generate ATP through aerobic metabolism with large mitochondria but with low & slow amounts of ATPase & calcium while having slower speed and function and MYH Gene
• Highly fatigue-resistant, ideal for prolonged endurance activities for long duration exercising and also help when sustaining and bettering posture.
• Classification of Smooth Muscle - Based how muscle fibers are activated.
• Single Unit Muscle are in tract, blood and respiratory vessels that interact as as single electrical.

Muscle Types Cont.

• Smooth/Cardiac striations are similar in slow/fatigue, sarcoplasmic reticulum and action for potential conduction.
• Gap function allow coordinates contraction with pacemaker cells and autothonomic for modulation. - Smooth muscle found in hollow organs such as intestines or blood vessels contract involuntarily and regulares in smooth muscles/Cardiac.
• Multi Unit Smooth fiber acts independent

Reflex Arcs

• Arc- 5 parts: Receptor detects stimuli, Afferent/sensitive(carries to spinal), Integration Center in the spine for monosunaptic and polysunaptic efferent to muscle Effector responds.
• Stretch- Knee jerk reflex function Prevent over -stretch of muscle spindle sends motor neurons contraction by alphabeta
• With Drawl Limb reflex to avoid pain, withdraw sends signals with 4 receptors & neruron activate .
• Internerons contact Flexion motor contact

Sensory organs

• Structure Muscle fibers Changes & stretch, made off fibres, motor neurson adjustment
• Golgi detect tension with fibres
• contract muscle- & fiber contract , adjusted sensitivity with y motor nuersom alpha controls to contract .

Explore muscle fiber types, contraction mechanisms, and ATP production in this quiz. Key topics include fast-twitch vs. slow-twitch fibers, smooth muscle characteristics, and the role of acetylcholine at the neuromuscular junction. Test your knowledge on excitation-contraction coupling and rigor mortis.