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)
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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
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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
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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
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Muscles As Effectors |
- Motor neurones stimulate glands and muscles into action
- Respond to a stimulus → are effectors
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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
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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
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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
- \ 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
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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 |
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