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Chapter 12- Muscles (Part 1)
Use this summary in addition to your EOC assignments and your LRG questions. Where indicated, you will need to fill in some blanks and draw in representative diagrams found in your textbook. Please come by if you need help.
Types of Muscle Tissue
Skeletal Muscle Tissue - Attached to bones. Striated and voluntary.
Cardiac M.T. - Wall of heart. Striated and involuntary.
Smooth (Visceral) M.T. - In viscera, blood vessels, & arrector pili muscles. Non-striated (smooth) and involuntary.
Functions of Muscle Tissue
· Motion
è Move the body by pulling on bones of the skeleton.
è Heart pushes blood thru the circulatory system.
è Smooth muscle pushes food and solids through the digestive tract. It also regulates the diameter of small arteries and causes piloerection (goose bumps).
· Posture and body support
è Gives the body form and support around flexible joints.
è Certain muscles are active postural muscles whose primary function is to work in opposition to gravity. (Ever experienced a “rubber neck-head bob”, while nodding off in class?)
· Heat production
è Only 30-40 % of energy used from Glucose to make ATP; 60-70% lost as heat
è As you exercise strenuously, the rate of heat production increases immensely. (Ever jumped up and down to keep warm?)
Characteristics of Muscle Tissue
EXCITABILITY (irritability) - ability to respond to certain stimuli by producing electrical signals called action potentials (impulses).
CONTRACTILITY - ability to shorten & thicken (contract), generating force to do work.
ELASTICITY - ability to be extended (stretched) w/o damage.
EXTENSIBILITY - ability to return to original shape after contraction or extension.
Motor Unit
= A single motor neuron may
innervate 10-2000 muscle
fibers (ave. 150)
Skeletal Muscle
Functions of Skeletal Muscle
· Highly specialized for contraction.
· Produces skeletal movement, range of motion, and generates force.
è Skeletal muscle contractions pull on tendons and move the bones of the skeleton.
è Effects range from simple motions (extending the arm) to highly coordinated movements (skiing, swimming, typing, running).
· Stabilizing body positions.
è Tension in muscles also maintains body posture – holding the head in position when reading your physiology book or balancing the weight of the body above your feet while walking from building to building on ASU’s campus.
è Without constant muscular activity you would not be able to sit upright at the Rambell’s basketball games without collapsing into a heap or stand in line for a soda at the Ram’s football games without topping over.
· Support soft tissues.
è The abdominal wall and the floor of the pelvic cavity consist of layers of skeletal muscle.
è These muscles:
§ Support the weight of visceral organs
§ Shield internal tissues from injury
· Guard entrances and exits.
è Openings of the digestive & urinary tracts are encircled by skeletal muscle.
è These muscles provide voluntary control over swallowing, defecation, & urination.
· Generation of heat & maintenance of body temperature.
è Muscle contractions require energy.
è Whenever energy is used in the body some of it is converted to heat.
è Heat released by working muscles keeps body temperature in the range required for normal homeostasis.
Somatic Motor Neurons
è A motor neuron transmits nerve impulse (ap’s) to skeletal muscles.
è Acetylcholine (ACh) release by motor neuron triggers a muscle action potential
Anatomy Review: Be sure to be familiar with the structure of skeletal muscle and the sarcomere: see figures 12-3 & 12-5 in your text and draw the pictures below.
Sarcomere Organization
è Myofibrils are bundles of actin and myosin filaments.
o The actin is found in the thin filaments
o The myosine is found in the THICK filaments.
è Myofilaments are organized in repeating functional units called sarcomeres.
è A-band = the length of a typical THICK filament.
o Divided into several subdivisions:
o M line = THICK filaments linked with accessory proteins
o H zone = THICK filaments only
o Zone of overlap = Outer edge of A band, where THICK & thin filaments overlap
è I-band = extends from A-band of one sarcomere to A-band of adjacent sarcomere
o Thin filaments only
o Center contains Z-disk
è Z-disk = boundary line between adjacent sarcomeres (1 sarcomere extends from z-disk to z-disk)
o Attachment site for thin filaments
Thin Filaments (~5-6 nm diam.) = ACTIN
è Contains 3 different proteins, F-actin, tropomyosin, & troponin:
o F-actin = double twisted strand of 300-400 globular molecules of G-actin.
o G-actin contains active sites that are covered by strands of tropomyosin to prevent actin-myosin interaction during muscle relaxation
o Tropomyosin is bound to one molecule of troponin midway along its length.
o A contraction cannot occur unless there is a change in the position of the troponin-tropomysin complex that exposes the active site.
THICK Filaments = MYOSIN
è Contains a pair of myosin subunits twisted around one another
o Long attached tail bound to other myosin molecules
o Free globular head projecting outward toward the nearest thin filament.
§ Head is hinged at its connection with the tail
§ Also called a cross-bridge due to the connection formed with the thin filaments during contraction
Titian & Nebulin
è Titian provides elasticity (returns stretched muscle to resting length) and stabilized the myosin by spanning the distance from one Z disk to the next M line.
è Nebulin helps align actin.
Skeletal Muscle Physiology
è The force created by the contracting muscle is called the muscle tension.
è The load is a weight or force that opposes contraction of a muscle.
è For example, in order to pick up a book your muscle must generate enough muscle tension (force) to overcome load it is trying to lift (the weight of the book)
è Also, you are unable to push over the wall of this building because the muscle tension (force) you are generating is not large enough to overcome the load (weight of the wall) you are trying to push.
Neuromuscular Junction/Myoneural Junction
è Skeletal muscle fibers contract only under the control of the nervous system.
è Communication between the nervous system and skeletal muscle fibers occurs at NMJ’s.
Overview of Contraction-Relaxation
o The link between the generation of an action potential in the sarcolemma and the start of a muscle contraction is called excitation-contraction coupling.
Steps
Events at the neuromuscular junction:
1. Action potential in somatic motor neuron arrives at axon terminal.
2. Voltage-gated calcium channels open. Calcium triggers exocytsosis
3. Causing synaptic vesicles to release ACh (acetylcholine)
4. ACh diffuses across the synaptic cleft at the NMJ and binds to nicotinic receptors on the sarcolemma
5. Sarcolemma depolarizes and causes a muscle action potential in the sarcolemma
Excitation-contraction coupling:
6. The impulse travels over the surface of the muscle cell where it is diverted into the interior of the cell through the T-
tubules to the sarcoplasmic reticulum.
5. Calcium released from the SR into the sarcoplasm.
7. Ca++ ions combine w/ troponin causing it to pull on the tropomyosin and change its orientation, thus exposing the myosin-
binding sites on actin.
Sliding Filament Theory:
8. Once the binding sites on actin are exposed upon the influx of calcium, the following events occur in rapid succession:
· Cross bridge attachment: The activated myosin heads are strongly attracted to the exposed binding sites on actin and cross bridge binding occurs.
9. Power Stroke:
· As a myosin head binds, it changes from its high-energy conformation (shape) to its bent, low-energy shape, which
causes the head to pull on the thin filament, sliding it toward the center of the sarcomere.
· At the same time, ADP and inorganic phosphate (Pi) generated during the prior contraction cycle are released from the myosin head.
10. Cross-bridge Attachment: As a new ATP molecule binds to the myosin head, the myosin cross-bridge is released from
actin.
11. “Cocking” of the Myosin Head. Hydrolysis of ATP to ADP and Pi by ATPase provides the energy needed to return the
myosin head to its high-energy, or “cocked,” position, which gives it the potential energy needed for the next attachment-power stroke sequence. Now we are back where we started, the cycle is repeated, and the myofibrils shorten.
12. A single power stroke of all the cross bridges in a muscle results in a shortening of only about 1%. Since contracting
muscles routinely shorten 35% to 50% of their total resting length, it is obvious that each myosin crossbridge attaches and
detaches many time during the course of a single contraction.
· It has been estimated that only half of the myosin heads of a thick filament are actively exerting a pulling force at
the same instant: the remaining are randomly seeking their next binding site.
· Sliding of thin filaments continues as long as the calcium signal is present.
· Removal of calcium ion from the sarcoplasm, by the sarcoplasmic reticulum, restores the tropomyosin inhibition,
contraction ends, and the muscle fiber relaxes.
13. Relaxation occurs when ACh is broken down by the enzyme acetylcholinesterase (AChE) and Ca++ is moved back into the
sarcoplasmic reticulum by active calcium transport pumps and a calcium binding protein called calsequestrin
14. Linkages between actin and myosin are disengaged.
15. Troponin and tropomyosin inhibt interaction between actin and myosin
16. Actin and myosin slide apart and muscle returns to resting length/relaxes aided by titian (at the moleclular level) and
connective tissue components.
Draw a summary diagram of these processes here (Use Fig. 12-9, 12-10, & 12-11 to assist you):
Rigor Mortis = state of muscular rigidity following death. Results from a lack of ATP to split myosin-actin cross bridges; therefore, the muscles remain “locked” in a contracted state. (Ca++ leaks out to initiate troponin) (last about 24 hours).
Remember…it takes ATP for muscles to relax.
Muscle Metabolism
On demand, skeletal muscle fibers can step up ATP production
Energy utilization:
è The primary function of ATP is the transfer of energy from one location to another, rather than the long-term storage of energy.
è At rest skeletal muscles fibers produce more ATP than they need, and under these conditions ATP transfers energy to another high-energy compound, creatine phosphate.
o This reaction can be summarized as:
§ At rest ……….ATP from metabolism + creatine à ADP + creatine phosphate
è During a contraction each myosin cross-bridge breaks down ATP, producing ADP and a phosphate group.
è The energy stored in creatine phosphate is then used to “recharge” ADP, converting it back to ATP thru the reverse reaction.
o This reaction can be summarized as:
§ During work/contraction….ADP + creatine phosphate ------creatine phosphokinase------> ATP & creatine
è See Fig. 12-13 (creatine kinase)
è When muscle cells sustain serious damaged, CPK leaks across the cell membrane and into the circulation. What would a high blood concentration of CPK indicate?
è Aerobic metabolism (w/O2) à glucose à glycolysis à Krebs cycle à ETC…..lots of ATP.
è Anaerobic metabolism (w/o O2 ) à glucose à lactic acid cycle….not at much ATP, but quicker.
Use the following 4 terms and filling the correct blanks below.
1) ATP --very little stored
2) CP --- creatine phosphate
3) aerobic respiration
4) anaerobic respiration
5) oxygen debt
1. ______- (aka phosphocreatine) can transfer its high-energy phosphate group to ADP to make ATP.
Can power maximal contractions for up to 15 sec.
2. ______- generates ATP from the partial catabolism (break-down) of glucose anaerobically.
Provides power for ~30-40 sec
Hhmmmm? Why does this pathway occur, if aerobic system is so much more energetically efficient?
Hint--what happens to blood vessels when the muscle is contracting powerfully?
3. ______. Muscular activity lasting more than 30 seconds requires oxygen. The aerobic system will provide enough ATP for prolonged activity as long as O2 & nutrients are available.
4. Elevated O2 use after exercise is called ______. In such a situation the muscles can continue to break down glucose to liberate energy for a short time using anaerobic respiration. This partial breakdown produces lactic acid, which results in a sensation of fatigue when it reaches certain levels in the muscles and the blood. This explains why it is possible to run faster in a sprint than over longer distances. During the sprint, the muscles can respire anaerobically. Once the vigorous muscle movements cease, the body breaks down the accumulated lactic acid on top of the ‘normal’ breakdown of glucose in aerobic respiration, using up extra oxygen to do so. Panting after exercise is an automatic mechanism to ‘pay off’ the oxygen debt.
Muscle Fatigue (this is different than muscle pain)
è Inability of a muscle to maintain its strength of contraction or tension
è Causes Peripheral Fatigue:
o depletion of glycogen stores, ATP, PCr
o buildup of lactic acid, hydrogen ions, inorganic phosphate
o K+ efflux (decreasing Ca+2 release)
o depletion of ATP
o interference w/availability of Ca+2 (usually due to interference of Ach events @ myoneural jxn) thus decreaseing calcium-troponin interaction
è Central Fatigue
o Subjective feelings of tiredness and loss of desire to exercise--usually precedes physiological fatigue
o cause???????? maybe Serotonin (a brain neurotransmitter related)?
è See Fig. 12-11 (if you can explain this….you know PF and CF)
Muscle Tone:
è Results from a sustained partial contraction
è Maintains posture
è Hypotonia (aka atrophy)- decreased or lost muscle tone (flaccid muscles)
o Skeletal muscle is not stimulated by a motor neuron on a regular basis (i.e. not stimulation, no contraction) à results in loss of muscle tone and mass.
o The muscle may reduce in size, tone, and power (not able to contract forcefully à loss of muscle tension)
o Spinal cord injuries or other damage to the NS will gradually lead to loss in muscle tone and size in the affected area
o Temporary reduction in muscle use can lead to hypotonia. Have you ever worn a cast on your arm or leg for a period of time? What was the muscle like before the cast? What was it like after? Did you have to go to physical therapy?