Physiology
Topic: Mechanics of single fiber contraction
Supervised by:
Dr.Tabish Ali
Compiled by:
Dr. Ali Mansoor
Mechanics of single fiber contraction
Muscle fiber:
A cylindrical, multinucleate cell composed of numerous myofibril that contract when stimulated
Myofibril:
Ø Densely packed rod like elements
Ø 80% of cell volume
Ø Exhibit striation perfectly aligned repeating series of dark A band and light I band
Contraction:
Ø The generation of force
Ø Does not necessarily cause shortening of fiber
Ø Shorting occurs when tensions generated by cross bridge on the filaments exceed force opposing shorting
Requirement for muscle contraction:
Activation;
Ø Neural stimulation at a neuro muscular junction
Ø excitation contraction coupling
Ø generation and propagation of an action potential along the sarcolema
Final trigger;
Ø a brief rise in intracellular ca+2 level
Mechanics of fiber contraction
Force exerted by an object on a contracting muscle is called load. These are opposing forces and whether exertion of force leads to fiber shorting depending on relative magnitude of tension and load. For a fiber to shorten and move a load, tension must be greater than load.
When a muscle develops tension but does not shorten contraction is called isometric contraction. (Isometric means “constant length”).Seen when a muscle supports a load or attempts to move a load that is greater than the tension. During such a contraction bound cross bridges dose not move.
A contraction in which the muscle shortens while load remains constant is called isotonic (constant tension). In such a contraction the cross bridges bound to actin move, shortening the fibers. Before an isotonic shortening there is a period of isometric contraction during which muscle develops tension (increases).
A lengthening contraction occurs when a load on a muscle is greater then the tension and the load lengthens the muscle. Not an active process but a result of an external force on the muscle .In a lengthening contraction, cross bridges are pulled towards Z –line
Events taking place;
1. Discharge of motor neuron
↓
2. Release of acetyl-choline at motor end-plate
↓
3. Binding of acetyl-choline to nicotine acetyl-choline receptors
↓
4. Increased sodium Na+ and potassium K+ conductance in end-plate membrane
↓
5. Generation of end-plate potential
↓
6. Generation of action potential in muscle fibers
↓
7. Inward spread of depolarization a long T-tubules
↓
8. Release of Ca+2 from terminal cisterns of sarcoplasmic reticulum and diffusion to thick and thin filaments.
↓
9. Binding of calcium to troponin uncovering myosin binding sites onactin
↓
10. Formation of cross- linkage between actin and myosin and sliding of thin on thick filaments producing movement )
↓
11. Myosin binds to actin and slides
↓
12. Pulling of 2 lines closer together
↓
13. Reducing width of I bands
(Filament length is not changed, it is shortening of sarcomere . as long fiber remains activated sliding mechanism continues)
Explanation;
Stimuli received by nervous system through sensory neurons are analyzed and the response encoded in the form of an impulse traveling through motor neurons to the effectors.
The neuro muscular junction is the synapse between an alpha motor neuron axon and a muscle fiber,
Ø Each axon can form synapses with several muscle fibers (forming a motor unit).
Ø The precision of muscle control is related to motor unit size.
· Small precise movements of the hand.
· Large movements of the legs.
Ø Ach is the neuromuscular junction transmitter
· Release of Ach produces large end-plate potential.
· Voltage changes open calcium channel open
Ø Calcium entry triggers myosin –actin intraction (rowing action)
Ø Movements of myosin bridges shorten muscle fibers. Ach produces large end-plate potential which spreads inward depolarization along the T-tubules.
This spread of depolarization causes the release of calcium from cisterns of SR. calcium diffuse in to actin and myosin where binding of calcium and troponin take place.
Binding of calcium to troponin causes the uncovering of myosin binding sites on actin filaments.
Formation of actin and myosin cross bridges takes place and contraction starts.
Energy for contraction:
ATP for muscle action;
Ø ATP is regenerated by;
(a) Direct phosphorylation of ADP by creatine phosphate.
(b) Aerobic respiration
(c) Anaerobic pathway
(a) Direct phosphorylation:
Coupled reaction of CP and ADP
Energy source; CP (creatine phosphate)
CP + ADP
↓ ↓ Creatine kinase
CREATINE ATP
Oxygen use: None
Products: 1 ATP per CP, creatine
Duration f energy provision: 15 sec.
(b) Aerobic pathway:
Produces 95% of ATP during rest and light to moderate exercise
Fuels: storage glycogen, then blood borne glucose, pyruvic acid from glycolysis and free fatty acid.
Ø Aerobic cellular respiration
Energy source:
Glucose, pyruvic acid free fatty acids from adipose tissue, amino acid from protein catabolism.
Glucose from glycogen breakdown
Or delivered from blood
↓
Pyruvic acid
↓ O2
Aerobic respiration in mitochondria
↓ ↓ ↓
H2O Co2 32 ATP (net gain per glucose)
Oxygen use: Required
Products: 32 ATP/Glucose, carbon dioxide, water.
Duration of energy provision: Hours
(c) Anaerobic pathway:
Ø At 70% of the maximum contractile activity;
· Bulging muscle compress blood vessels
· Oxygen delivery is impaired
· Pyruvic acid is converted into lactic acid
Lactic acid:
· Diffuses into blood stream
· Used as a fuel by liver, kidneys an heart
· Converted back into pyruvic acid by liver
(c) Anaerobic pathway:
Glycolysis and lactic acid formation
Energy source: Glucose .
GLUCOSE (from glycogen breakdown or delivered from blood
↓ ↓
2ATP Pyruvic acid
2ATP Pyruvic acid
↓
Lactic acid
↓
Release to blood
Oxygen use: None
Product: 2 ATP per Glucose, Lactic acid
Duration of energy provision: 60 sec. or slightly more
References:
2: Gyton and hall medical physiology chapter 6( general mechanism of contraction)
3:K.Sembulingam- Essentials of medical physiology, 6th edition- section 3( types of contraction)
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