L7-8: Skeletal Muscle Physiology I-II Flashcards
Describe/define the following:
a. ) Sarcolemma
b. ) Sarcomere
c. ) Sarcoplasmic reticulum
d. ) T-tubule
e. ) Muscle fiber
f. ) Myofibril
g. ) Titin
h. ) Dystrophin
i. ) Ryanodine receptor
j. ) DHP receptor
- a.) Plasma membrane of the muscle fiber (cell)
- b.) Functional subunit of a muscle fiber that contains proteins for contraction
- c.) Specialized endoplasmic reticulum in muscle that contains high concentration of calcium necessary for contraction to occur
- d.) Invaginations of sarcolemma into the muscle fiber, spreads APs
- e.) Muscle fiber is the muscle cell
- f.) Cylindrical structure made up of an end-to-end chain of repeating units (aka sarcomeres) containing thick and thin filaments
- g.) Protein that holds thick filaments in place and connects them to the Z-disk
- h.) Protein that connects F-actin (thin filament) to the transmembrane proteins that connect the muscle fibers to the strong CT
- i.) Aka calcium release channels in SR through which calcium travels from SR to sarcoplasm
- j.) Aka L-type calcium channel embedded in T-tubule membrane that is coupled with some of the ryanodine receptors – conveys AP to SR and ultimately causes ryanodine receptors to open up
Describe sliding filament theory of contraction and explain cross-bridge cycle. Include roles of myosin, actin, tropomyosin and troponin subunits
- Myosin = thick filament, actin=thin filament, tropomyosin=attached to actin, covers active site on actin filament where myosin binds. Troponin with subunits; TnI = affinity to actin, TnC = affinity to calcium and TnT = affinity to tropomyosin
1. ) ATP binds to head of myosin heavy chain causing release of myosin from actin
2. ) ATP hydrolyzed to ADP and Pi causing myosin head to be placed in cocked position and myosin head now lined up with new actin monomer. ADP-Pi still attached
3. ) Cross-bridge formation occurs when Ca binds TnC on tropomyosin causing conformational change and exposing myosin binding site on actin. Now, myosin associated with ADP-Pi binds to actin
4. ) Pi released from myosin triggers power stroke and actin pulled further over myosin
5. ) ADP released from myosin completes cycle. Actomyosin complex remains until ATP binds to myosin again to start another cycle
Describe role of ATP in skeletal muscle contraction
- ATP is necessary to bind to the myosin head to cause release of myosin from actin. It also pumps Ca back into SR via Ca/H ATPase to allow muscle to relax until a new AP is received
Describe role of Calcium in skeletal muscle contraction
- Calcium binds troponinC causing tropomyosin to move and exposing myosin binding site on actin. Upon pumping of calcium back into the SR, reversal of this action occurs and myosin binding site on actin is covered up by tropomyosin
Explain role of SR in skeletal muscle contraction and relaxation. What is role of SR Ca ATPase? What is role of calsequestrin?
- SR stores high levels of calcium, releases it into the sarcoplasm for contraction in response to AP and resequesters it via ATPase pump for relaxation to result. It contains calreticulin and calsequestrin, which are calcium binding proteins. By having these proteins, the concentration gradient of Ca is not too steep so that the Ca/H ATPase pump can still work to bring calcium in during resequestration period.
Explain rigor mortis and describe why it occurs
- This is a stiffness to muscle a while after death as a result of no further ATP to detach myosin from actin
Describe EC coupling. How do APs spread throughout skeletal muscle? What are roles of L-type Ca channel (DHP receptor) and Ca release channel (ryanodine receptor)?
- EC coupling refers to AP generated at NMJ to be transferred into the cell to allow for mechanical contraction.
- APs spread through cell via T-tubule system. L-type Ca channels (DHP) in T-tubules act as voltage sensors and are mechanically coupled to Ca release channels (ryanodine) in SR causing Ca to leave SR and flow into sarcoplasm
Explain how relative durations of skeletal muscle cell action potential and single muscle cell twitch and related to concept of frequency summation and tetanization.
- The duration of a single muscle AP is much shorter than the duration of the contraction (muscle twitch). As a result, in order to increase tension from the myofibrils controlled by a motor neuron, another AP can be fired, while Calcium level in myofibril is still increasing from first leading to a further increase in tension. Further APs will continue to cause this to occur until tetanization, which is the continuous state of full activation – no further tension develops
Roles of phosphocreatine, creatine kinase and glycogen in regenerating ATP for muscle contraction
- Muscles contain (from creatine) phosphocreatine, which serve as a source of phosphate group for creatine kinase to phosphorylate ADP to ATP quickly. By product of this process is creatinine
- Glycogen represents large numbers of polymers of glucose for glycolysis and TCA cycle provided o2 available or if not to lactate production.
Describe motor unit and state which size are expected in muscles requiring fine control (eg. EOM) or less fine control (large postural muscles).
- Motor unit = motor neuron plus all the myofibers it innervates
- Small motor units are small motor neurons and its few myofibers
- Large motor units are large motor neurons and its many myofibers
- EOM can have hundreds of the small motor units, which confer fine motor control
- Postural muscles can have large motor units (in varying number), yet recruitment of a few will be sufficient to activate thousands of muscle fibers
Explain how muscles produce graded and sustained muscle contractions
- ) Increase number of motor units at any one time
2. ) Increase the rate of stimulation of a single motor unit to drive the myofibers towards tetanization
Describe relationship between dystrophin-glycoprotein complex and muscular dystrophies
- Dystrophin is the protein that forms a rod connecting thin actin to the transmembrane protein complex, adding strength to muscles by connecting fibrils to EC matrix
- DMD: severe reduction in dystrophin in skeletal and cardiac muscle, X-linked recessive usually fatal by age 30
- Becker muscular dystrophy: less severe since functional dystrophin is present, but altered or reduced in amount
- Limb-girdle dystrophies: different types associated with mutation in genes encoding other compoments of this complex or other muscle proteins
What is the difference between isometric and isotonic contractions?
- Isometric: muscle doesn’t shorten, but tension increases
- Isotonic: muscle shortens while tension on muscle remains constant
