HomeCells & MoleculesDiseasesEcosystemHuman BiologyAQA BIOL1AQA HBIO1AQA HBIO2AQA HBIO4AQA HBIO5
Human Biology > Skeletal Muscle
Welcome, Guest!
Login with Facebook | Login
Video tutorials

Supplemental Videos

Click here to watch video tutorials for exam board specific videos by A* students

The Sliding-Filament Theory

Gross and Microscopic Structure of Skeletal Muscle Including Ultrastructure of a Myofibril

  • Skeletal muscle is joined to bone by inelastic tendons
    • Muscle contraction / pulls on tendons / bone moves
  • Each muscle is made of bundles of muscle fibres surrounded by connective tissue
  • An individual muscle fibre
    • Has many nuclei → muscle fibre develops from fusion of many cells
    • Sarcoplasm (cytoplasm) filled by parallel myofibrils
    • Sarcolemma (surface membrane) forms deep tubes (T tubules) into the sarcoplasm along its length
    • Network of membranes called sarcoplasmic reticulum (ER)

Roles of Actin, Myosin, Calcium Ions and ATP in Myofibril Contraction

Striations In Skeletal Muscle Are Caused By Filaments Of Two Protein Actin And Myosin

  • Actin filament / thinner than myosin → lighter striations
  • Myosin filament / thicker than actin filament → darker striation
  • Distance between 2 adjacent Z lines: sarcomere / actin filament is attached to Z lines and extended into sarcomeres on either side
  • Striation of actin alone → I band
  • Striation of myosin alone → H zone
  • Length of myosin → A band
  • Central thickening of each myosin filament → M line

Structure Of Actin And Myosin Filament

  • Actin filament: 2 actin strands twisted around each other
    • Troponin-tropomyosin-actin complex blocks binding site for myosin
  • Myosin filament: bundles of myosin molecules
    • Bundle of myosin tails form a central stalk
    • Globular heads attach to specific sites on actin filaments
    • Myosin heads contain ATPase that hydrolyses ATP

Neuromuscular Junction

  • Synapse between motor neurone and muscle fibre
  • \ skeletal muscle fibres are stimulated by motor neurones
  • IMPULSE REACHES NEUROMUSCULAR JUNCTION
  • Influx of Ca2+ / synaptic vesicles fuse with presynaptic membrane
  • Release of acetylcholine (ACh) into synaptic cleft by exocytosis
  • Neurotransmitter diffuses across cleft
  • Binds with receptors on motor end plate (→postsynaptic membrane of muscle fibre)
  • Depolarises sarcolemma
  • Threshold stimulates wave of depolarisation along muscle fibre
  • Changes permeability of sarcoplasmic reticulum to Ca2+
  • Ca2+ move into sarcoplasm / causes contraction of myofibril

 

Muscles As Effectors

  • Motor neurones stimulate glands and muscles into action
  • Respond to a stimulus → are effectors

Role of ATP and Phosphocreatine in Providing the Energy Supply During Muscle Contraction

Stimulation Of Muscle Fibres By The Nervous System

  • CONTRACTION → myosin heads attach to actin binding sites / form temporary cross bridges / bridges rapidly break and reform / new cross bridges form further along actin filament / causing shortening of each sarcomere
  • WHEN STIMULATION STOPS → Ca2+actively taken up by sarcoplasmic reticulum / myosin head detaches from actin / cross bridges reform / muscle relaxes
  • NO ATP AVAILABLE → cross bridges cannot detach / muscle becomes stiff / unable to relax / extreme form: rigor mortis / occurs after death

Cycle Of Events During Contraction Of A Myofibril

  • Ca2+ ions enter sarcoplasm during wave of depolarisation
  • Bind to troponin / changes shape of protein / removes block of tropomyosin / exposes actin binding sites
  • ATP binds to myosin / stimulates ATPase / RELEASES ENERGY
  • Allows myosin heads to form cross bridges with actin
  • Allows POWER STROKE: myosin head changes angle / pulls on actin filaments
    • Width of I band, H zone decrease → filaments overlap increases
    • Z lines move closer together → length of sarcomere decreases
    • No change to A band → lengths of filaments stay constant
  • Allows Ca2+ ions to be pumped back in by active transport
  • New ATP binds to myosin / allows detachment from actin
  • Myosin head changes to original position (cross bridges reform)
  • Next attachment to actin filament and power stroke can occur
    • Ca2+ and ATP required for cycle to continue

Energy In Active Muscle Cells

  • Breakdown of phosphocreatine / releases PI + energy / attach to ADP / forms ATP
    • PHOSPHOCREATINE + ADP → CREATINE + ATP
    • ATP is used faster than it can be supplied by respiration
    • Phosphocreatine allows regeneration of ATP without respiration
  • Thus, Muscle cells continue exercise until slower pathways synthesis ATP
    • Breakdown of glycogen in muscle cells / aerobic respiration of glucose
    • Aerobic respiration of glucose, fatty acids from bloodstream / fatty acids last longer
  • Prolonged exercise / not enough O2 for aerobic respiration
    • Anaerobic respiration continues
    • Lactate may cause cramps

Table 16-9-1: Structure, location and general properties of slow and fast skeletal muscle fibres


Feature

Fast muscle

Slow muscle

FUNCTIONAL
- Role in body

- Rapid, powerful movements
- Short-lasting

- Slow movement
- Long-lasting

STRUCTURAL
- Diameter of fibres
- Capillaries
- Sarcoplasmic reticulum
- Mitochondria


- Large
- Few
- High
- Few


- Small
- Many
- Low
- Many (ETC, Krebs cycle)

MECHANICAL
- Speed of contraction
- Rate of pumping Ca2+


- Fast
- High


- Slow
- Slower

BIOCHEMICAL
- ATPase activity
- Respiration
- Glycogen content
- Myoglobin content
- Resistance to fatigue


- High, split ATP quickly
- Anaerobic
- High
- Low
- Low


- Low, split ATP slowly
- Aerobic
- Low
- High
- High

LOCATION

Arms and legs
(running and throwing)

Back and neck
(postural muscles)

Slow muscles contain myoglobin in sarcoplasm → appears bright red