1. Muscles Unit 4 option C by CSE November 2006

2. Types of muscle Skeletal / striped / striated /voluntary Smooth / unstriated / involuntary Cardiac

3. Striated Attached to bones Movement of parts of the body or locomotion Long fibres with cross striations Control by voluntary nervous system Contracts readily but fatigues easily

4. Smooth Present in walls of tubular organs eg gut, uterus, bladder, blood vessels, diaphragm Movement of materials in the body Short spindle shaped cells with no cross striations Control by involuntary (autonomic) nervous system Contracts slowly but can be maintained for long periods

5. Cardiac Only found in heart walls Pumping of heart maintains blood circulation Branched cells forming a linked network Allows waves of electrical excitation to pass easily between them Toughened cell membranes between cells Contraction is myogenic (self initiated) but rate changed by autonomic system Contraction manitained without fatigue

6. Skeletal muscle Each muscle made of large numbers of specialised cells called myofibrils Myofibrils are grouped into bundles with connective tissue and each bundle is called a muscle fibre Myofibrils are very long cells with lots of nuclei which lie close to the surface Fibre bounded by sarcolemma, infolded to form T tubules which penetrate into the cell. Sarcoplasm – lots of mitochondria, sarcoplasmic reticulum which stores calcium ions

7. Myofibril structure Made of 2 types of filament – thin and thick Thicker filaments made of a protein called myosin Thinner filaments made of actin protein Myofibril split into repeating units called sarcomeres.

8. Arrangement of proteins Actin filaments are attached to bands of connective tissue called Z lines Sarcomere -= distance between 2 Z lines Myosin filaments found in central part of each sarcomere In middle of myosin is a band of connective tissue called M line For part of their length, actin and myosin lie between each other (overlap) – looks dark Near Z line, only have thin actin filaments so looks light. In centre of sarcomere, only myosin so intermediate colour

10. Contraction Actin pulled between myosin filaments Greater overlap area I bands and H zones narrower Sarcomere shorter Z lines closer A bands stay same length Sliding of filaments not shortening of filaments

11. Contraction detail 1 Myosin molecule has a long rod shaped tail made of fibrous protein and 2 roundish heads of globular protein Heads face outwards and link to actin during contraction Actin made of 2 long helical chains of small globular protein molecules twisted round each other Actin associated with 2 other proteins – tropomyosin and troponin Tropomyosin forms long thin strands wound over actin so blocks sites where myosin attach Troponin binds to calcium ions during contraction initiation

12. Contraction detail 2 Nerve impulse causes contraction (NMJ) Action potential spreads along sarcolemma and down T tubules Sarcoplasmic reticulum becomes more permeable to calcium ions which diffuse out into myofibrils Calcium ions cause a change in position of tropomyosin and unblock actin binding sites Myosin heads attach to binding sites forming actomyosin cross bridges Myosin head changes angle, pulling actin over myosin towards sarcomere centre

13. Contraction detail 3 A molecule of ATP attaches to each myosin head Hydrolysis of ATP releases energy which is used to detach myosin head from actin and to reposition head further along chain Myosin head changes position and pulls actin again Cycle repeated many times – myosin head walks along actin until the fibre end.

14. Relaxation Nerve stimualtion stops Calcium ions pumped out of myofibrils and back into sarcoplasmic reticulum – needs energy With no calcium ions, tropomyosin changes position and blocks binding sites on actin Myosin heads can’t bind with actin Muscle relaxed and can be extended by contraction of antagonistic muscle

15. Interesting facts Muscle contraction 25% efficient – rest lost as heat Rigor mortis – stiffening of muscles due to ATP not available to break cross bridges between actin and myosin so muscle can’t relax. Appears 4 hours after death but after 24 hours muscles loosen as enzymes destroy muscle proteins Cycle of myosin heads binding, detachng and repositioning repeated 50 –100 times per second and moves actin 10nm

16. Fast twitch muscle fibresSlow twitch muscle fibres White muscleRed muscle Little myoglobin presentLarge amount of myoglobin Rapid short term contraction - sprinters have 62% Slower sustained contraction – marathon runners have 82% Energy from anaerobic respAerobic respiration Few mitochondriaMany mitochondria Large amounts creatine phosphate Little creatine phosphate Less extensive blood supplyExtensive blood supply Fatigues quicklyFatigues more slowly

17. Creatine phosphate – reserve store of phosphate and energy. Provides phosphate to add to ADP.When broken down, releases energy which used to regenerate ATP. When muscle relaxes, P from ATP used to regenerate CP. Myoglobin – protein fond in muscle. Similar structure to haemoglobin. Can attach to oxygen and store it in muscles. Release when oxygen supply gets low. Glycogen – carbohydrate store in muscle.

18. Helpful hints Actin has less letters than myosin so actin is thin fibre Actin begins with A (1 st letter of alphabet) has a Z line (last letter) Myosin is thick fibres Myosin middle of sarcomere Myosin mid line = M line Light part = only actin (near Z line) called I band (lIght) Intermediate colour = only myosin = H zone Dark part = Actin + myosin = A band (dArk)

19. Neuromuscular junction Specialised synapse between motor neurone and skeletal muscle Allows motor neurones to stimulare muscle contraction End of axon membrane and sarcolemma membrane of muscle are highly folded Functions like normal excitatory synapse Axon end contains vesicles with acetylcholine + many mitochondria Sodium ions diffuse into sarcolemma causes a change in potential difference and if above threshold causes an action potential which spreadsto muscle and causes contraction.

20. Synapse working Nerve impulse travels down axon causing Ca channels to open in membrane so Ca ions diffuse rapidly into bulb from surrounding tissue Causes Ach vesicles to move to and fuse with membrane, so Ach goes into cleft by exocytosis Ach binds with receptors on muscle fibre, causing Na channels to open so Na+ into muscle sarcolemma. Inside less negative, causing an action potential if larger than threshold value Ach broken down by cholinesterase and shape change means the acetyl and choline are released from receptors and diffuse back into presynaptic membrane where reform Ach using energy

21. Training Proportions of fast and slow twitch fibres can not be changed much by training Regular training programs where muscle made to do work against a load eg weight training - stimulates muscle growth, larger cross sectional area due to an increase in number of myofibrils. - Number of mitochondria increase - Amount creatine phosphate increases - Amount ATP increases - cells more tolerant to lactic acid build up Useful in power events eg throwers and sprinters

22. Endurance events training Involves steadier work over longer time Muscle bulk not increase Increase glycogen store Heart increases in size allowing blood to be delivered to muscles more quickly and efficiently Allow more potential for aerobic respiration