Ch 8.3-8.4: Contraction and Metabolism of Skeletal Muscle

A Quick Review Fasicles Sarcomere Fibers Myofibrils Actin Myosin

Case Study # 1 Case Study # 2 Case Study # 3 Signs and Symptoms: Respiratory Acidosis Accelerated oxygen consumption Extreme heat production Case Study # 2 Signs and Symptoms: Muscle weakness Easily fatigued Muscles eventually cease to function Case Study # 3 Signs and Symptoms: Uncoordinated movements Jerky to-and-fro motion of trunk and limbs

How Muscles Work with the Nervous System Neuromuscular Junction: where a nerve and muscle fiber come together Motor neuron Axon terminal Motor end plate A single motor neuron stimulates many muscle fibers Motor Unit Axon of motor neuron Axon terminal Neuromuscular junction (NMJ) Sarcolemma Myofibril

How Muscles Work with the Nervous System Axon terminal Nerve impulse Synaptic Cleft: space between axon terminal and sarcolemma Axon terminals contain synaptic vesicles filled with neurotransmitters Acetylcholine (Ach) This is what activates the muscle Synaptic vesicle containing acetylcholine (ACh) Sarcolemma Motor end plate Synaptic cleft (space)

How Muscles Work with the Nervous System 1 ACh is released from synaptic vesicle 4 ACh is broken down - Acetylcholinesterase 2 ACh binds to ACh receptor -Opens ion channels Na+ 3 Muscle action potential is produced

The Sliding Filament Mechanism (Theory) How a muscle contracts Thin filaments (actin) slide past the thick filaments (myosin) Myosin heads pull on actin molecules Sarcomere shortens but filament size remains the same  

Physiology of Contraction Calcium (Ca2+) and Energy (ATP) are necessary for contraction to occur Action potential causes sarcoplasmic reticulum to rapidly release Ca2+ Ca2+ binds to troponin → tropomyosin moves away from myosin-actin binding site

The Contraction Cycle 1 Myosin heads hydrolyze ATP and become reoriented and energized Key: = Ca2+ 2 Myosin heads bind to actin, forming cross-bridges ADP P P ATP ADP ATP ADP 4 As myosin heads bind ATP, the cross-bridges detach from actin 3 Myosin cross-bridges rotate toward center of sarcomere (power stroke)

Pg 206 1 Nerve impulse arrives at axon terminal of motor neuron and triggers release of acetylcholine (ACh). Nerve impulse Muscle action potential Ca2+ 2 ACh diffuses across synaptic cleft, binds to its receptors in the motor end plate, and triggers a muscle action potential (AP). Transverse tubule 4 Muscle AP traveling along transverse tubule opens Ca2+ release channels in the sarcoplasmic reticulum (SR) membrane, which allows calcium ions to flood into the sarcoplasm. ACh receptor Acetylcholinesterase in synaptic cleft destroys ACh so another muscle action potential does not arise unless more ACh is released from motor neuron. Synaptic vesicle filled with ACh 3 SR Ca2+ 9 Muscle relaxes. 8 Troponin–tropomyosin complex slides back into position where it blocks the myosin binding sites on actin. 5 Ca2+ binds to troponin on the thin filament, exposing the binding sites for myosin. Elevated Ca2+ Ca2+ active transport pumps 7 Ca2+ release channels in SR close and Ca2+ active transport pumps use ATP to restore low level of Ca2+ in sarcoplasm. 6 Contraction: power strokes use ATP; myosin heads bind to actin, swivel, and release; thin filaments are pulled toward center of sarcomere.

Metabolism of Skeletal Muscle Three sources of energy (ATP) production: Creatine Phosphate: energy rich molecule unique to muscle fibers Allows muscle to contract up to 15 seconds Anaerobic Cellular Respiration: without oxygen Glycolysis Enough energy for about 30-40 seconds Aerobic Cellular Respiration: requires oxygen - Allows muscle activity lasting longer than 30 seconds