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 Slow muscles contain myoglobin in sarcoplasm → appears bright red Feature Fast muscle Slow muscle FUNCTIONAL Role in body - Rapid, powerful movements - Short-lasting - Slow movement - Long-lasting STRUCTURAL Diameter of fibres Large Small Capillaries Few Many Sarcoplasmic reticulum High Low Mitochondria Few Many (ETC, Krebs cycle) MECHANICAL Speed of contraction Fast Slow Rate of pumping Ca2+ High Slower BIOCHEMICAL ATPase activity High, split ATP quickly Low, split ATP slowly Respiration Anaerobic Aerobic Glycogen content High Low Myoglobin content Low High Resistance to fatigue Low High LOCATION Arms and legs (running and throwing) Back and neck (postural muscles)