10. • Myosin 2 globular heads & long tail
• Head of myosin contains actin-binding site & catalytic site
that hydrolize ATP
11. • Thin filaments two chains of actin
• Tropomyosin in the groove of actin
• Troponin: T binds other troponin to tropomyosin
I inhibits the interaction of myosin & actin
C contains the binding sites for Ca+2
12. • Sarcotubular system = T system + sarcoplasmic reticulum
• T system of tubules + adjacent terminal cisternae = triad
• T system rapid transmission of action potentials from
the cell membrane to the fibrils
13. • The resting membrane potential of muscle = -90 mV
• The action potential = 2 – 4 ms
• The speed along the muscle = 5 m/s
• The absolute refractory period = 1 – 3 ms
• The distribution of ions nerve cells
• Depolarization = Na+
influx
• Repolarization = K+
efflux
• Depolarization starts at motor end plate transmitted
along the fiber contractile response
14. Sequence of events during transmission from the motor
nerve the muscles = transmission in synapses between
neurons
15. Sequence of Events in Contraction and Relaxation of
Skeletal Muscle
Steps in Contraction:
1. Discharge of motor neuron end of motor neuron Ca+2
enters the endings
16. 2. Release of transmitter (acetylcholine) at motor end-plate
3. Binding of acetylcholine to nicotinic acetylcholine
receptors (concentrated at the tops of the junctional folds)
18. 4. Increased Na+
and K+
conductance in end-plate membrane
5. Generation of end-plate potential
6. Generation of action potential in muscle fibers
19. 7. Inward spread of depolarization along T tubules
excitation – contraction coupling
8. Release of Ca+2
from terminal cisterns of sarcoplasmic
reticulum and diffusion to thick and thin filaments
20. 9. Binding of Ca+2
to troponin C, uncovering myosin-binding
sites on actin (at resting, troponin I is tightly bound to actin
and tropomyosin covers the sites where myosin heads bind
to actin)
• ATP is then split ADP + Pi contraction
21. 10. Formation of cross-linkages between actin and myosin
and sliding of thin on thick filaments, producing movement
22.
23.
24. Steps in Relaxation:
1. Ca+2
pumped back into sarcoplasmic reticulum
diffuses into the terminal cisterns, ready to be released
by next action potential
2. Release of Ca+2
from troponin
3. Cessation of interaction between actin and myosin
27. Production of ATP in Muscle Fibers (Tortora & Derrickson,
2006)
• 3 ways of ATP production:
1. From creatine phosphate
2. Anaerobic cellular respiration (ATP-producing reactions
not requiring oxygen)
3. Aerobic cellular respiration (ATP-producing reactions
requiring oxygen, in mitochondria)
28. 1. Creatine Phosphate
• Creatine: small amino acid-like molecule formed in liver,
kidneys, pancreas transported to muscles
• Relaxed muscles creatine phosphate 3-4x > ATP
• Relaxation: ATP + creatine creatine phosphate + ADP
(by creatine kinase)
• Contraction: creatine phosphate + ADP ATP + creatine
(by creatine kinase)
• For 15 seconds contraction (100-m dash)
29. 2. Anaerobic Cellular Respiration
• Creatine phosphate is depleted then:
• Glucose (from blood or from the breakdown of glycogen in
muscles) glycolysis 2 pyruvic acid + 2 ATP (produces
4 ATP but net gain of 2 ATP)
• Pyruvic acid mitochondria, aerobic respiration ATP
• No oxygen (anaerobic) in cytosol: 80% Pyruvic acid
lactic acid blood (becomes acid) liver convert back
into glucose
• For 30 - 40 seconds activity (400-m race)
30. 3. Aerobic Cellular Respiration
• Sources of ATP: pyruvic acid, fatty acid (breakdown of
triglycerides; yields > 100 ATP), amino acids (breakdown
of proteins)
• Sufficient oxygen: Pyruvic acid mitochondria
oxydized ATP + CO2 + H2O + heat
• Slower than glycolysis, but yields 36 ATP
• Sources of oxygen: hemoglobin & myoglobin
• For > 10 minutes activity (marathon race)
31. Energy Sources (Ganong, 2005)
ATP + H2O ADP + H3PO4 + 7.3 kcal
Phosphorylcreatine + ADP ↔ Creatine + ATP
Rest & light exercise:
FFA CO2 + H2O + ATP
Increased intensity of exercise
Glucose + 2 ATP (or glycogen + 1 ATP) 2 Lactic acid + 4 ATP
(anaerobic)
Glucose + 2 ATP (or glycogen + 1 ATP) 6CO2 + 6H2O + 40ATP
(aerobic)
32. • 100-m dash (10 seconds) 85% of energy is derived
anaerobically
• 2-mile race (10 minutes) 20% of energy is derived
anaerobically
• long-distance race (60 minutes) 5% of energy is derived
anaerobically
33. • Muscle fatigue: The inability of muscle to maintain force
of contraction after prolonged activity, caused by:
• Inadequate release of Ca+2
from sarcoplasmic
reticulum
• Depletion of creatine phosphate
• ATP levels = resting levels
• Insufficient oxygen
• Depletion of glycogen
• Buildup of lactic acid & ADP
• Failure of action potentials in releasing ACh
34. Oxygen Consumption after Exercise
• Oxygen debt added oxygen, over and above the
resting oxygen consumption, taken into the body after
exercise
1. Convert lactic acid glycogen stores in liver (small
amount)
2. Resynthesize creatine phosphate & ATP
3. Replace the oxygen removed from myoglobin
• Much of lactic acid pyruvic acid for ATP production
(heart, liver, kidneys, skeletal muscles)
• Better term: recovery oxygen uptake ( chemical
reactions, heart & muscles still working, recovery
processes)
36. Types of Contraction
• Isometric (“same length”) contraction: Contraction occurs
without an appreciable decrease in the length of the whole
muscle do not work (work = force x distance)
37. • Isotonic (“same tension”) contraction: Contraction against
a constant load do work
39. Muscle twitch: brief contraction followed by relaxation of all
muscle fibers in a motor unit caused by a single action
potential in its motor neuron
• “Fast” muscle fibers: fine movements (7.5 ms)
• “Slow” muscle fibers: gross movements (100 ms)
40. Summation of Contractions
• No refractory period such as in neuronsin muscle fibers
• Repeated stimulation summation of contractions
• Tetanus (tetanic contraction) continuous contraction:
• Fused (complete) tetanus
• Unfused (incomplete) tetanus
41.
42. Type I
Type I Type II
Type II
Other names
Other names Slow, oxidative,
Slow, oxidative,
red muscles
red muscles
Fast;
Fast;
glycolytic;
glycolytic;
white muscles
white muscles
Myosin isoenzyme ATPase rate
Myosin isoenzyme ATPase rate Slow
Slow Fast
Fast
Ca
Ca+2
+2
pumping capacity of
pumping capacity of
sarcoplasmic reticulum
sarcoplasmic reticulum
Moderate
Moderate High
High
Diameter
Diameter Moderate
Moderate Large
Large
Glycolytic capacity
Glycolytic capacity Moderate
Moderate High
High
Oxidative capacity (content of
Oxidative capacity (content of
mitochondria, capillary
mitochondria, capillary
density, myoglobin content)
density, myoglobin content)
High
High Low
Low
Examples
Examples Long muscles of
Long muscles of
the back
the back
Estraocular
Estraocular
Types of Muscle Fibers
43. Type I
Type I
(Red muscles)
(Red muscles)
Type II
Type II
(White muscles)
(White muscles)
Charateristics
Charateristics Slow response;
Slow response;
long latency;
long latency;
adapted for
adapted for
long, slow
long, slow
contractions
contractions
Short twitch
Short twitch
durations
durations
Functions
Functions Posture
Posture
maintenance
maintenance
Fine, skilled
Fine, skilled
movements
movements
Examples
Examples Long muscles in
Long muscles in
the back
the back
Extraocular
Extraocular
muscles, hand
muscles, hand
muscles
muscles
48. Disorders and Abnormalities
• Myasthenia gravis: skeletal muscles are weak and tire
easily; caused by autoantibodies destroying nicotinic
acetylcholine receptors
• Lambert-Eaton syndrome: muscle weakness; caused by
antibodies against Ca+2
channels in the nerve endings
• Denervation hypersensitivity
• Contracture: No relaxation due to the inhibition of Ca+2
transport into the reticulum
49. Disorders and Abnormalities
• Hypotonia: decreased or lost muscle tone
• Flaccid paralysis loss of muscle tone, loss/ reduction
of tendon reflexes, atrophy, degeneration of muscles
(disorders of nervous system; electrolytes imbalances
(Na+
, Ca+2
, Mg+2
)
• Hypertonia: increased muscle tone
• Spastic paralysis increased muscle tone, tendon
reflexes, pathological reflexes (Babinski sign)
• Rigidity increased muscle tone, not reflexes
(tetanus)
50. Disorders and Abnormalities
• Muscular dystrophy: progressive weakness of skeletal
muscle caused by mutations in genes for muscle proteins
• Duchene’s muscular dystrophy dystrophin protein is
absent from muscle; X-linked; fatal by 30 y/o
• Metabolic myopathies (e.g. McArdle’s syndrome)
mutations in genes of enzymes involved in carbohydrates,
fats, and proteins, metabolism
• Myotonia muscle relaxation is prolonged after
contraction; abnormal genes in chromosomes 7, 17, or 19,
which produce abnormalities of Na+
or Cl-
channels
51. References
1. Ganong WF (2005). Review of Medical Physiology, 22nd
ed. Chapter 3, Pages: 65-78; Chapter 4, Pages: 116-120
2. Tortora GJ & Derrickson B (2006). Principles of Anatomy
and Physiology, 11th
ed. Chapter 10, Pages: 290-314.
