Skeletal Muscle Contraction

Question 1

skeletal muscle

Answer 1

• 40% of the body – a big chunk of our body is made up of muscle weight
• Can only contract – this is all the skeletal muscles can do! This is why we have oppositional muscle groups
• A muscle can flex or extend a joint but it can’t do both

Question 2

microscopic anatomy of muscle

Answer 2

• Bundles (fascicles) of bundles (fibers)
• The fibers are bundles of myofibrils (muscle proteins)
• Individual cells contain myofibrils
• Sarcolemma surrounds muscle cell
• Myofibrils are contractile elements containing myofilaments (smaller proteins)
• Mitochondria (2% of the volume in skeletal whereas it is 25% in cardiac cells)
• Sarcoplasmic reticulum stores calcium

Question 3

Myofilaments

Answer 3

• Actin (thin) – represents the thin filaments
• Actin is a helical coil of actin subunits (light blue balls)
• Arranged in long polymers )2 long polymers are coiled around each other)
• Myosin (thick) – has head group with two hinges (one at the attachment of head group and one on the tail region)
• Tail region is coil of two proteins
• Many myosin subunits are put together to form thick filaments
• Troponin are the bright pink comp

Question 4

mechanism of contraction

Answer 4

• Begins with stimulation by nervous system in skeletal muscle
• Skeletal muscle doesn’t contract unless stimulated by a nerve cell
• Each fiber must be stimulated by a nerve though one nerve does not stimulate all fibers (why not?)
• “motor unit” – the individual motor nerve fibers and all the muscle fibers innervated by that nerve
• If you have a muscle with all its fibers that has a lot of motor units, you have a lot more options for how you contract the muscle
• Gives you a lot more dexterity
• The larger muscles that move the limbs tend to have larger motor units because you don’t need as refined movements

Question 5

Neuromuscular Junction

Answer 5

• Union between nervous and muscular systems
• Uses acetylcholine as NT
• Binding of receptor opens a sodium channel and may trigger action potential
• Sarcoplasmic reticulum releases its store of calcium

Question 6

sliding filament

Answer 6

• Sliding filaments – thick and thin filaments are going to slide over each other
• Myosin, each composed of 6 polypeptide chains (head region and tail region)
• Protein heads (“Cross bridges”) extend away from the body of the filament
• Successive heads offset by 120 degrees

Question 7

actin filaments

Answer 7

• Actin (thin) filaments made of 2 helically coiled F-actin strands
• F-actin strands made of G-actin which is attached to one ADP molecule which may act as a site of cross bridge binding
• One end attached to Z-disc while the other protrudes between thick filaments

Question 8

tropomyosin filaments

Answer 8

• Tropomyosin connect loosely within F-actin coils (composed of G actin subunits)
• Each tropomyosin molecule spirals around F-actin covering approximately 7 ADP sites
• Troponin made of 3 protein subunits
• TI binds actin
• TT binds tropomyosin
• TC binds calcium (calcium is in the SR waiting to be released when the muscle undergoes an action potential

Question 9

troponin/tropomyosin complexes

Answer 9

• Troponin/tropomyosin complexes inhibit binding of cross bridges by physically blocking binding sites that the myosin head groups want to bind to
• Calcium release inhibits blockade by removing complexes from binding sites
• Calcium binds to the TC subunit which pulls the myosin off
• Uncovering sites on actin exposes them to myosin binding and “walk-along”

Question 10

role of ATP

Answer 10

• Binds head of the cross bridge – hydrolyzed and causes the myosin head group to reset to an open posture
• That open myosin head group has the ADP and Pi still attached so that opening up of the head group is considered potential energy (storing energy from hydrolysis of ATP)
• When the myosin attaches to the thin filament, the energy is released
• Is cleaved by ATPase activity of the cross bridge to ADP + Pi which remain attached
• Energy stored by hydrolysis is released when myosin heads bind to actin
• ADP+Pi are released with conformational change and new ATP is bound resulting in release of actin site and return of head

Question 11

single fibers

Answer 11

• Increasing tension developed with stretch (maximum at approx. 110% of normal sarcomere width)
• Maximum tension is achieved when the thin filaments are pulled to the end of the thick filaments – generate the most force of contraction when it draws the thin filaments together (up to 10% of myosin width)
• Limited by the ends of the myosin filaments
• Shortening sarcomeres limits tension as z-lines contact myosin filaments
• No cross bridges at myosin centers

Question 12

whole muscle

Answer 12

• Similar tension/stretch relationships as single fibers
• Normal resting length very near length for maximal tension development
• Velocity of contraction inversely related to load – the greater the load, the lower the velocity
• Work = Load x Distance moved

Question 13

energy for contraction

Answer 13

• ATP required in large amounts
• Muscle sequester short supply
• ADP must be phosphorylated and returned to high energy ATP state
• Creatine phosphate (phosphocreatine) stored in muscle provides, fast but short-lived source of phosphate. Stored in levels about 5x greater than raw ATP
• It can phosphorylate very quickly but can’t keep up very long
• Glycogen: storage form of sugars in muscle which can be liberated and broken down to pyruvate for glycolytic cycling.

Question 14

oxidative phosphorylation

Answer 14

-Oxidative phosphorylation: dietary sugars broken down first through glycolysis and the Krebs cycle then combine with oxygen as part of an enzymatic cascade producing ATP as a by-product

Question 15

comparison of energy sources

Answer 15

• CP: 4M/min ATP produced for seconds
• Glycogen/lactic acid (anaerobic): 2.5M/min for minutes
• Oxidative phosphorylation: 1M/min as long as the food holds out!
• You can do this forever as you have glucose

Question 16

contraction of whole muscle

Answer 16

• Term denotes development of tension, separate from “shortening”
• Isometric = “same length.” Tension = Load
• Isotonic = Tension > load
• Lengthening contraction = Tension < Load

Question 17

muscle structure

Answer 17

• Fast Fibers: large fibers, very strong. Large SR = large, fast Ca ion release. Large supply of glycolytic enzymes. Oxidative metabolism less important, blood supply reduced, fewer mitochondria – can generate a great deal of strength but Fatigue quickly.
• Slow Fibers: smaller, more extensive blood supply, increased mitochondria, large myoglobin content, slow fatiguing.
• Much more dependent on circulating sugars

Question 18

spatial summation

Answer 18

• Size does matter: Size principle
• Smaller motor units contract first (like the low gear on a car), but with growth of signal strength, larger motor units are recruited (smaller motor neurons are more excitable)
• Smooth contraction ensured by alternating stimulation of various motor units

Question 19

temporal summation

Answer 19

• Alteration of frequency of stimulation
• At some level contractions fuse into state of sustained contraction referred to as “tetanus.”
• Nearly every movement involves tetany

Question 20

strength of contraction

Answer 20

• Can achieve values of 4kg/cm2 or 50psi
• Step like increase in strength of contraction after period of rest (staircase effect). May occur due to flooding of the sarcoplasm with calcium

Question 21

muscle tone

Answer 21

• Resting tension on the muscle
• Results from low baseline rate of nerve impulses and neurotransmitter release from the spinal cord and causes a trophic effect that maintains the bulk of musculature
• Low level of release of neurotransmitter which provides low level of muscle tone

Question 22

fatigue

Answer 22

• Increases in proportion to the loss of glycogen stores
• Transmission of nerve impulses at the NMJ also reduced after prolonged stimulation – due to inability to keep up with recycling of neurotransmitter

Question 23

lever system

Answer 23

• Muscles apply tension at insertion points on bone
• Work with joints to affect movement of the skeleton – muscles can only move the skeleton if the skeleton is flexible – always crosses a joint
• Force related to the distance of the attachment from the fulcrum, the length of the lever arm to be moved and the original position of the lever.
• Force estimated by: (cross sectional area) x50psi

Question 24

muscle alteration

Answer 24

• Almost continuous process
• Fiber number changes rare
• Fiber hypertrophy by addition of myofibrils
• New sarcomeres added with stretch
• Increase in metabolic enzyme and glycogen storage, blood supply with sustained aerobic activity

Question 25

denervation

Answer 25

• Muscle atrophy begins immediately
• Most fibers destroyed and replaced by fibrous or fatty tissues or the muscle just sort of deteriorates
• Neighboring motor units can sprout new branches to re-innervate muscle fibers resulting in “macromotor units.”
• Micromotor units have less dexterity than the original motor unit

Question 26

dystrophies

Answer 26

• Genetic disorders (> 30 defects known)
• Mixed muscle atrophy, hypertrophy and necrosis
• Muscle fibers replaced by fat and fibrotic material (psuedohypertrophy)
• Characterized by insidious, progressive weakness

Question 27

duchenne MD

Answer 27

• Heritable absence of dystrophin (protein required for muscle structure)
• Males, females have 50% chance of carrying/passing mutation
• Onset of progressive weakness leading to paralysis at 3-5 yr, most lose ability to walk by 12 yo
• Becker MD similar but less severe disorder of dysfunctional dystrophin

Question 28

adult MD

Answer 28

• Fascioscapulohumeral MD – slowly progressive disorder of face, arms, shoulder beginning in teens
• Myotonic – MC adult form characterized by cardiac abnormalities and cataracts, swan neck, drooping eyelids

Question 29

MD

Answer 29

• Mostly affects boys (rarely girls).
• Often brothers or male relatives have same problem.
• First signs appear around ages 3 to 5: the child may seem awkward or clumsy, or he begins to walk ‘tiptoe’ because he cannot put his feet flat. Runs strangely. Falls often.
• Problem gets steadily worse over the next several years.
• Muscle weakness first affects feet, fronts of thighs, hips, belly, shoulders, and elbows. Later, it affects hands, face, and neck muscles. “Walk up” from seated/lying position.
• Most children become unable to walk by age 10.
• May develop a severe curve of the spine.
• Heart and breathing muscles also get weak. Child usually dies before age 20 from heart failure or pneumonia.