Unit 5.

5 Skeletal muscles are stimulated to contract by nerves and act as effectors Know the gross and microscopic structure of skeletal muscle Understand the roles of actin/myosin/calcium ions/ and ATP in the sliding filament theory of muscle contraction. Appreciate the ATP/PC system in providing more immediate energy for contraction. Know the structure, location and properties of slow and fast muscle fibres. Appreciate a response to a stimulus s achieved through an effector e.g. muscle.

Key words Actin, myosin, troponin, tropmyosin, sacromere, fast twitch, slow twitch, Z line, A band, I band. Muscle histology:

Actin filaments are attached to the dark Z lines at the ends of the sacromere. The thick myosin filaments are attached at the centre of the sacromere to the M line. Where there are myosin filaments the sacromere looks darker than at the ends where there are only actin filaments. The darkest zones are where the filaments overlap. If you were to cut across one of the darkest zones you would see a mixture of thin and thick filaments.

The sliding filament theory of muscle contraction; Muscle contraction requires calcium ions (Ca2+) and energy (in the form of ATP) in order for the thick and thin filaments to slide past each other. The steps are; The binding sites of the actin molecule are blocked by a complex of two molecules: tropmyosin and troponin. Prior to muscle contraction, ATP binds to the heads of the myosin molecules, priming them in an erect high energy state. Arrival of an action potential causes a release of Ca2+ from the sacroplasmic reticulum. The Ca2+ binds to the troponin and causes the blocking molecules to move so that the myosin binding sites on the actin filaments become exposed. The heads of the crossbridging myosin molecules attach to the binding sites on the actin filament. Release of energy from the hydrolysis of ATP accompanies the cross bridge formation. The energy released from ATP hydrolysis causes a change in shape of the myosin cross bridge, resulting in a bending action (the power stroke). This causes the actin filaments to slide past the myosin filaments towards the centre of the sacromere. Fresh ATP attaches to the myosin molecules, releasing them from the binding sites and repriming hem for a repeat movement. They become attached further along the actin chain as long as ATP and Ca2+ are available.

Muscle contraction Impulse reaches the neuro-muscular junction(end plate), synaptic vesicles fuse with the end plate membrane and release a transmitter substance (e.g. acetylcholine). Acetylcholine depolarises the sarcolemma, acetylcholine is hydrolysed by acetylcholinesterase. Proved the threshold value is exceeded, an action potential (wave of depolarisation) us created in the muscle fibre. Calcium ions are released from the T-system and sarcoplasmic reticulum. Calcium ions bind to troponin, changing its shape. Troponin displaces tropomyosin which has been blocking the actin filament. The myosin heads now become attached to the actin filament, ATP is hydrolysed and the energy released causes the myosin head to change position, causing the actin filaments to slide past the stationary myosin ones, there ADP + Pi fall off the myosin head, then an ATP molecule becomes fixed to the myosin head, causing it to become detached from the actin (breaks the cross bridge) Hydrolysis of ATP provides energy for the myosin head to be cocked The myosin head becomes reattached further along the actin filament The muscle contracts by means of this ratchet mechanism The following changes in muscle occur: o I(isotropic bands) band shortens o Z lines move closer together i.e. the sarcomere shortens o H zone shortens Calcium ions are actively absorbed back into the T-system Troponin reverts to its original shape, allowing tropomyosin to again block the actin filament. Aerobic respiration is used to regenerate ATP

Energy supply during muscle contraction ATP Used in the movement of the myosin heads And the reabsorption of calcium ions into the endoplasmic reticulum by active transport. Anaerobic respiration uses phosphocreatine o Regenerates ADP o Stored in muscles and acts as a reserve supply of phosphate, which is available immediately to combine with ADP and so re-form ATP. o The phosphocreatine store is replenished using phosphate from ATP when the muscle is relaxed. o o

The neuro-muscular junction;

Events at the neuromuscular junction Nerve impulse arrives at end plate Acetylcholine is released from vesicles Neurotransmitter (acetylcholine) diffuses across synapse. Acetylcholine fits into receptors on the sarcolemma Sarcolemma (membrane around muscle) is depolarised by entry of Na+ ions If threshold is exceeded then an action potential is generated in muscle fibres Calcium ions released from T-system tubules Calcium ions bind to troponin Actin filament slides past myosin, muscle contracts.

Slow twitch muscle characteristics: Smaller store of calcium ions in tubules Many large mitochondria Slow rate of ATP hydrolysis in myosin heads Resistant to fatigue Large amounts of myoglobin Long contraction relaxation cycle Dense network of blood capillaries around fibres ATP largely obtained from aerobic respiration.

Fast twitch muscle characteristics Large store of calcium ions and more tubules in the reticulum Fewer smaller mitochondria High rate of ATP hydrolysis in myosin heads Lactate accumulates rapidly. Quickly becomes fatigued. Very little myoglobin Short contraction relaxation cycle Fewer blood capillaries around fibres ATP largely obtained from anaerobic respiration