B1.3 muscular function
π’ Overview
600 muscles in the human body
Vary in size, shape & structure
Account for ~40β50% of body weight
𧬠Types of Muscle
𦴠Skeletal Muscle
Voluntary control
Striated appearance (dark & light bands)
Attached to bones via tendons
β Main function β move the skeleton
β€ Cardiac Muscle
Found in the heart
Striated
Involuntary control
Contracts without conscious effort
π« Smooth Muscle
Lines blood vessels & hollow organs (e.g. stomach, intestines)
Involuntary control
β Not striated
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β Functions of Muscle
π Movement
Skeletal muscle contracts β pulls on tendons β moves bones at joints
π Movement of Substances
Smooth muscle β moves food through digestive tract
Cardiac muscle β pumps blood
Skeletal muscle β aids venous blood return
π§ Posture & Stability
Postural muscles maintain body position
Muscles can be active with no visible joint movement
π₯ Heat Production
Muscle contraction (e.g. shivering)
Can generate up to 85% of body heat
π― Chapter Focus
Emphasis on large skeletal muscles
Importance in joint movement
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Properties of muscles:
β Key Properties
Contractility β ability to contract and generate force when stimulated by a nerve
β Unique to muscle tissue
Muscles usually work in pairs (one shortens, the other stretches)
β Extensibility
Ability of muscle to be stretched beyond resting length
π Elasticity
Ability to return to original resting length after stretch is removed
π¦Ύ Example: Elbow Movement
π§ Nerve signal β biceps brachii contracts (contractility)
π Elbow bends β triceps brachii stretches (extensibility)
β¬ Arm lowers β triceps returns to resting length (elasticity)
π Muscle Fibre Capacity
Can shorten to ~50% of resting length
Can stretch to ~150% of resting length
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Neuromuscular function:
β‘ Nervous System Overview
Made up of millions of nerve fibres carrying electrical signals
Central Nervous System (CNS) π§ : brain and spinal cord β sensing and control
Peripheral Nervous System π: nerves extending from spinal cord to limbs and body
π¦Ύ Motor Neurons
Carry signals from CNS to muscles
Tell muscles to contract or relax
~200,000 motor neurons in the human body
Also called the efferent system
π Muscle Activation
Nerve cells send electrical impulses from the brain
Enables coordinated muscle contractions
π Energy for Contraction
ATP (adenosine triphosphate) = main energy βcurrencyβ β
PCr (phosphocreatine) helps fuel contraction
ATP transfers chemical energy for metabolic reactions
Structurally: adenosine + three phosphate groups
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Structure of neurons:
π§© Main Components
Soma (cell body) π§
Located in the spinal cord or in ganglia
Dendrites πΏ
Connect neurons to each other
Allow information flow between nerves
Axon β‘
Main pathway for nerve signal transmission
Functions like an electrical wire
π‘ Myelin Sheath
Axon covered by myelin β insulates electrical signals β
Nodes of Ranvier β
Gaps in myelin
Help speed up signal transmission β
π Neuromuscular Junction
Axon becomes unmyelinated at the muscle
Connects to muscle fibre at the motor endplate
Synapse = small gap between neuron and muscle
β electrical signal triggers muscle stimulation β
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Neurons:
The end of a motor neuron reaches a muscle
Branches of the end plate reach out to various muscle cells of the muscle
Space between end of neuron and muscle cell called the synapse
Neurotransmitters released at synapse recognized by muscle cell
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π What is a Motor Unit?
β One motor neuron + all muscle fibres it innervates
π Innervation Ratio
High ratio (β2,000 fibres) β large force, less precision
e.g. gluteus maximus
Low ratio (β10 fibres) β small force, high precision
e.g. eye muscles
β Force vs Precision
β Fibres per neuron β β force
β Fibres per neuron β β control & precision
β‘ All-or-None Principle
When a motor neuron fires β all fibres in that motor unit contract
Fibres are either fully relaxed or fully contracted β
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Types of motor units
π’ Type I (Slow-twitch)
β Slow nerve transmission
β Small force production
β Highly fatigue resistant
π Best for endurance activities (walking, jogging)
π‘ Type IIa (Fast-twitch, fatigue-resistant)
β Fast neural transmission
β Moderateβhigh force
β Relatively fatigue resistant
π΄ Best for sustained power activities (swimming, cycling)
π΄ Type IIx (Fast-twitch, high force)
β Fastest contraction speed
β Largest force production
β Fatigue quickly
π Best for explosive activities (sprinting, jumping, throwing, weightlifting)
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𧬠Muscle Fibre Distribution
β 50% Type I
β 25% Type IIa
β 25% Type IIx
β Proportions vary by muscle and individual
π’ Type I Muscle Fibres (Slow-twitch / Fatigue-resistant)
β High aerobic endurance
β Efficient ATP production via oxidation (carbohydrate & fat)
β Sustain activity as long as oxygen is available
π Suited to long-duration, low-intensity exercise
π‘ Type IIa Muscle Fibres (Fast-twitch, fatigue-resistant)
β Greater force than Type I
β Moderate aerobic & anaerobic capacity
β Fatigue faster than Type I
π Used in high-intensity endurance (e.g. 1500 m run, 400 m swim)
π΄ Type IIx Muscle Fibres (Fast-twitch, fast-fatiguing)
β Largest force production
β Predominantly anaerobic
β Fatigue very quickly
β‘ Used in explosive events (e.g. 100 m sprint, 50 m swim)
π Key Idea
Fibre type β determines energy system use, force, and fatigue rate
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Orderly recruitment:
π§ Motor Unit Activation
β When a motor unit is activated β all its muscle fibres contract
β More force = more motor units recruited
β Low force = fewer motor units recruited
π Recruitment with Increasing Intensity
Force demand increases β motor units recruited in a set order:
β Type I
β Type IIa
β Type IIx
𧬠Motor Unit Size
β Type IIa & IIx motor units = more muscle fibres
β Type I motor units = fewer muscle fibres
β Larger motor units β β force production
π Key Principle
β Recruitment order depends on motor neuron size
β Smaller motor neurons recruited first
β Known as the principle of orderly recruitment
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π Hypertrophy (Increase in Muscle Size)
β Fibre hypertrophy = increase in size of existing muscle fibres
π Two types:
Transient hypertrophy β short-term β size due to fluid accumulation
π§ Fluid from blood plasma
β Returns to normal within hours
Chronic hypertrophy β long-term β size from resistance training
β Size of muscle fibres (Fibre Hypertrophy)
β Possible increase in number of fibres (Fibre Hyperplasia)
π§ Strength Gains & Neural Adaptations
β Early strength gains = neural factors (stronger, more powerful signals)
β Motor unit recruitment
β Rate of motor unit recruitment
β± First 8β10 weeks β neural adaptations dominate
β© After ~10 weeks β muscle fibre hypertrophy becomes major contributor
π Atrophy (Loss of Muscle Size)
β Occurs with disuse or immobilization
e.g. casts, stopping training
β Associated with loss of strength
β Greater effect in Type I muscle fibres
π Recovery
β Muscle size and strength can recover when training resumes
β³ Recovery time longer than immobilization period
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Muscle contractions:
Β General Principle
Muscle ends are drawn towards the centre of the body
Movement depends on:
π₯ Force of contraction
π Line of action relative to the joint
π§ Isometric Contraction (Static)
β Muscle contracts without movement
β Muscle length stays the same
Example: arm wrestle held static
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π Isotonic Contractions (Movement Occurs)
β¬ Concentric Contraction
β Muscle shortens
β Body segment moves
Speed controlled by performer
β¬ Eccentric Contraction
β Muscle lengthens while contracting
β Muscle force < resistance
Example: plyometric movements (jumping, bounding)
β Isokinetic Motion
β Movement at constant speed
π§ͺ Rare in sport β usually requires special equipment
β Useful in rehabilitation
β Constant joint speed β constant muscle shortening speed
π Muscle Relaxation
β No contraction force
β Some resistance may still occur due to:
Elasticity
Extensibility
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Muscle roles in joint movement:
π― Agonist (Mover)
β Contracts concentrically to produce movement
β Muscle torque > resistance torque
Levels:
Prime mover
Assistant
Emergency
Example: biceps brachii during elbow flexion
β Antagonist
β Contracts eccentrically
β Controls or slows movement
Acts opposite to usual concentric action
Example: biceps brachii slowing the descent in a bicep curl
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π§± Fixator (Stabilizer)
β Contracts (usually isometrically) to hold one segment steady
β Allows movement at the desired joint
π Important for core stability
Example: trunk muscles stabilising the body while limbs move
π§ Synergist (Neutralizer)
β Prevents unwanted movements
Usually contracts isometrically
Example: pronator muscles preventing supination when biceps brachii contracts
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π§ Identifying Muscle Contraction Types in Movement
β¬ Against Resistance (e.g. gravity)
β Limb moves opposite to resistance
β Agonist performs isotonic concentric contraction
β¬ With Resistance (controlled)
β Limb moves in the same direction as resistance
β Antagonist performs isotonic eccentric contraction
βΈ No Visible Movement
β Muscle contracting with no joint movement
β Isometric contraction
β½ Soccer Kicking Example (Knee Joint)
Preparation phase (knee flexion):
β Hamstrings = agonists
β Quadriceps = antagonists
Ball strike phase (knee extension):
β Quadriceps = agonists
β Hamstrings = antagonists (β slow/stop movement)
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πΌ Agonist (Prime Mover)
β Deltoid
Responsible for arm abduction
π½ Antagonist
β Latissimus dorsi
Resists the abduction movement
π§± Fixator (Stabiliser)
β Trapezius
Holds the scapula in place
π§ Synergist
β Teres minor
Eliminates unwanted joint actions
π Summary
β Agonist β main muscle producing movement
β Synergists β assist the agonist
β Fixator β stabilising synergist
β Antagonist β opposite action; relaxes or contracts eccentrically to control movement
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Reciprocal inhibition:
π§ What It Is
β Automatic neural reflex during movement
β When an agonist contracts, the antagonist relaxes
β How It Works
β Agonist motor neuron is stimulated
β Antagonist motor neuron is inhibited
β Prevents opposing muscle torque
β Allows maximum force at the joint
π Example: Biceps Curl
Upward phase:
β Biceps brachii β concentric contraction
β Triceps brachii β relaxes
Downward (controlled) phase:
β Biceps brachii β eccentric contraction
β Triceps brachii β still relaxed
β Common Misconception
β Antagonists do not usually contract eccentrically during agonist concentric action
β This would β net joint torque
π€ Co-activation
β Agonist + antagonist contract together
β Used to:
β Joint stiffness
β Balance
Support skill learning
π§ Voluntary control overrides reciprocal inhibition
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Mechanics of muscle contraction:
π§΅ Muscle Structure
β Muscle made of parallel muscle fibres
β Fibres contain myofibrils
β Myofibrils give muscle a striated (striped) appearance
β Filaments
𧬠Thin filaments β actin
𧬠Thick filaments β myosin
β 2 thin filaments : 1 thick filament
π Sarcomeres
β Filaments arranged into sarcomeres
β Sarcomeres = functional units of muscle fibres
β Do not run the full length of the fibre
π Striations
β Caused by overlap of actin and myosin
β Degree of overlap changes when muscle is:
Contracted
Relaxed
Stretched
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Sliding filament theory:
β‘ Neural Activation
β Electrical impulse travels along motor neuron
β Reaches neuromuscular junction
π§ͺ Acetylcholine released into the synapse
β Triggers an action potential in the muscle fibre
π Calcium Release
β Action potential travels along fibre and T-tubules
β Sarcoplasmic reticulum releases CaΒ²βΊ
β Calcium exposes binding sites on actin
π Cross-Bridge Formation
β Myosin heads attach to actin
β ATP attached to myosin is split β ADP + phosphate
β Myosin head bends and pulls actin inward
β‘ Sliding Action
β Actin slides past myosin
β New ATP binds β myosin detaches
π Cycle repeats while:
Neural signal continues
Calcium remains available
π Relaxation
β Neural signal stops
β Acetylcholine broken down
β Calcium returns to sarcoplasmic reticulum
β Myosin heads return to resting position
π Key Outcome
β Muscle contracts through repeated sliding of actin over myosin
β This mechanism is the sliding filament theory
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With tropomyosin no longer inhibiting muscle contraction, actin and myosin can interact and allow cross-bridge
M and Z lines move closer
I and H shrink
A band remains same size
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Cross bridge cycle:
𧬠What It Is
β Repeating sequence of events between myosin heads and actin filaments
β Occurs during muscle contraction
β Cross-Bridge Formation
β Myosin heads bind to actin
β Binding occurs when contraction begins
π₯ Power Stroke
β Myosin head tilts
β Pulls actin toward the centre of the sarcomere
β Shortens the sarcomere
β Generates muscle force
π Detachment & Reattachment
β Myosin head detaches after tilting
β© Rotates back to original position
β Reattaches to a new site on actin
π« When Muscle Is Relaxed
β Bonding blocked by tropomyosin
β Myosin remains near actin but cannot bind
β‘ Key Outcome
β Repeated power strokes β filaments slide past each other
β Basis of the sliding filament theory
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Role of troponin and tropomyosin:
π§± Filament Structure
β Thick filament β myosin (tails form shaft, heads project outward)
β Thin filament β made of:
Actin
Tropomyosin
Troponin
βΈ Muscle at Rest
π« Tropomyosin covers myosin-binding sites on actin
β Myosin heads cannot bind
β Muscle remains relaxed
β‘ Initiation of Contraction
π§ Nerve impulse β CaΒ²βΊ released from sarcoplasmic reticulum
β Calcium binds to troponin
β Troponin moves tropomyosin away
β Myosin-binding sites exposed
π Muscle Contraction
β Myosin heads bind to actin
β Force is generated
β Muscle contracts
π On / Off Control
β Calcium concentration β contraction starts
β Calcium concentration β contraction stops
π ExcitationβContraction Coupling
β Sequence linking nerve excitation to muscle contraction
β Troponin & tropomyosin act as the switch controlling contraction
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Central of muscle force:
π§ Central Nervous System (CNS) Control
β CNS adjusts force to suit the task
β Large force (e.g. kicking)
β Small force (e.g. writing)
π’ Motor Unit Recruitment Methods
π Size Principle
β Small motor units recruited first
β Larger motor units added as force demand increases
β May be less effective for very large forces
β‘ Frequency (Rate) Coding
β Force increased by β rate of motor unit activation
β Higher firing frequency β greater muscle force
β‘ Key Idea
β Muscle force controlled by:
Which motor units are recruited
How often they are activated
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