1. Ch 8.3-8.4: Contraction and Metabolism of Skeletal Muscle

2. A Quick Review
Fasicles
Sarcomere
Fibers
Myofibrils
Actin
Myosin

3. 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

4. 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

5. 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)

6. How Muscles Work with the Nervous System1
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

7. 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

9. 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

10. 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)

11. 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.

12. 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 seconds
Aerobic Cellular Respiration: requires oxygen
- Allows muscle activity lasting longer than 30 seconds